Obesity 1 degree according to microbial 10. Obesity - the principles of treatment. Principles of obesity treatment

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2014

Other forms of obesity (E66.8), Extreme obesity accompanied by alveolar hypoventilation (E66.2), Obesity, unspecified (E66.9), Obesity due to excessive intake of energy resources (E66.0)

Endocrinology

general information

Short description

Expert Council of RSE on REM "Republican Center for Health Development"

Ministry of Health and Social Development of the Republic of Kazakhstan

Obesity- a chronic, relapsing disease characterized by excessive deposition of fat in the body.

Body mass index(BMI) (BMI) is a value that allows you to assess the degree of correspondence between a person’s weight and his height, and thereby assess whether the mass is insufficient, normal or overweight.

Body mass index is calculated by the formula:

I = --------------------

M is body weight in kilograms;

H - height in meters.

And it is measured in kg/m².

The body mass index was developed by the Belgian sociologist and statistician Adolphe Quetelet in 1869.

Up to 19 kg / m 2 - weight deficit;

19-24.9 kg / m 2 - normal weight;

25-29.9 kg / m 2 - overweight;

30 kg / m 2 and above - obesity.

BMI greater than or equal to 25 - overweight;

BMI greater than or equal to 30 - obesity;

BMI greater than or equal to 35 - severe obesity;

BMI greater than or equal to 40 - morbid obesity;

BMI greater than or equal to 50 - super-obese (super-obese);

BMI over 60 kg / m 2 - super-super-obesity.

bariatric surgery(metabolic surgery, weight loss surgery) is a branch of surgery that treats overweight people and includes surgical weight loss by limiting the intake of nutrients and / or reducing their absorption in the gastrointestinal tract. Bariatric surgery does not include cosmetic (body contouring) surgery, and is aimed at improving health.

The bariatric effect is expressed in (Exess weight loss - EWL%) - the percentage of excess weight loss in kg of excess body weight.

Types of operations used in the treatment of obesity:

Restrictive surgery- the bariatric effect is achieved by reducing the volume of the stomach, in connection with which the quantitative food intake decreases with maximum and accelerated irritation of the bariatric receptors;

Malabsorption surgery- bariatric effect is achieved by reducing the absorption surface of the gastrointestinal tract.

Mixed type of operation- the bariatric effect is achieved in a combined way: restrictive surgery on the stomach and by reducing the absorption surface of the gastrointestinal tract.

I. INTRODUCTION

Protocol name: Morbid obesity. metabolic syndrome.

Protocol code:

ICD 10 code:

E66.0 Obesity due to excessive intake of energy resources;

E66.2 Extreme obesity accompanied by alveolar hypoventilation (Pickwick syndrome);

E66.8 Other forms of obesity Morbid (morbid) obesity;

E66.9 Obesity, unspecified

Abbreviations used in the protocol:

BP - arterial pressure;

ALT - alanine aminotransferase;

ASAT - aspartate aminotransferase;

APTT - activated partial thromboplastin time;

GDZ - hepato-duodenal zone;

GERD-gastroesophageal reflux disease;
HH - hiatal hernia;

VC - vital capacity of the lungs;

ZHKB - cholelithiasis;

GIT - gastrointestinal tract;

BMI - body mass index;

CT - computed tomography;

LGP - laparoscopic gastroplication;

HDL - high density lipoproteins;

LDL - low density lipoproteins;

MPU - medical and preventive institutions;

INR - international normalized ratio;

MRI - magnetic resonance imaging;

MS - metabolic syndrome;

KLA - complete blood count;

OAM - urinalysis;

OB - volume of the hips

OT - waist size

PT - prothrombin time;

PHC - primary health care;

PLV% - % excess weight loss;

RCT - randomized clinical trial;

DM 2 - type 2 diabetes mellitus;

TAG - triacylglyceride;

PE - pulmonary embolism;

LE - level of evidence;

Ultrasound - ultrasound examination;

CSBH - Centers of Excellence in Bariatric Surgery;

ECG - electrocardiogram;

BMI -Body Mass Index (Body Mass Index);

EWL% - Exess Weight Loss.

IFSO - International Federation for the Surgery of Obesity and Metabolic Disorders (International Federation for the Surgery of Obesity and Metabolic Syndrome);

MRSA - Methicillin-resistant Staphylococcus aureus (Resistant Staphylococcus aureus)

Protocol development date: year 2014.

Protocol Users: surgeon, general practitioner, therapist, endocrinologist, cardiologist, gastroenterologist, hepatologist, neuropathologist.

This protocol uses the Oxford system of "evidence-based medicine", with levels of evidence (Table 1), which are determined by the analysis of scientific literature, and the choice of grade of recommendation (Table 2), which in turn depends on the level of evidence. In 2010, in a joint clinical guideline developed by the American Association of Clinical Endocrinologists, the Society of Bariatric and Metabolic Surgeons, a gradation of the level of evidence similar to the Oxford system was used to assess the evidence base.

Table 1 Levels of evidence

Level	Therapy / Prevention, Etiology / Risk
1a	Systematic Reviews (Meta-analyses) of Randomized Clinical Trials (RCTs)
1b	Selected RCTs
1c	Series of “all-or-none results” cases
2a	Systematic Reviews (with Homogeneity) of Cohort Studies
2b	Individual cohort trials (including low-quality RCTs such as<80% follow-up)
2c	Research reports. Environmental studies
3a	Systematic reviews (with homogeneity) of case-control studies
3b	Selected case-control studies
4	Case series (and low-quality cohorts and case-control studies)
5	Expert opinion without precise critical evaluation, or based on physiology and other principles

It should be noted that in determining the grade of recommendation, there is no direct relationship between the level of evidence and the grade of recommendation. Evidence from randomized controlled trials does not always rank as grade A recommendations in case there are flaws in methodology or inconsistencies between published results from multiple studies. Also, the lack of high-level evidence does not exclude the possibility of making a grade A recommendation if there is rich clinical experience and consensus. In addition, there may be exceptional situations where confirmatory studies cannot be performed, perhaps for ethical or other reasons, in which case precise recommendations are considered useful.

Note:

"Extrapolation" is when data are used in a situation where there may be clinically significant differences than are unambiguously confidently described in the original studies.

Classification

obesity classification

According to etiology and pathogenesis:

1. primary obesity(alimentary-constitutional or exogenous-constitutional) (in 95% of cases):

Gynoid (lower type, gluteal-femoral);

Android (upper type, abdominal, visceral);

With individual components of the metabolic syndrome;

With advanced symptoms of metabolic syndrome;

With severe eating disorders;

With night eating syndrome;

With seasonal affective fluctuations;

With hyperphagic stress response;

With Pickwick's syndrome;

With secondary polycystic ovaries;

With sleep apnea syndrome;

With puberty-youthful dispituitarism.

2. Symptomatic (secondary) obesity(in 5% of cases):

With an established genetic defect:

As part of known genetic syndromes with multiple organ damage;

Genetic defects of the structures involved in the regulation of fat metabolism.

Cerebral:

. (adiposogenital dystrophy, Babinski-Pehkranz-Froelich syndrome)

Tumors of the brain, other cerebral structures;

Dissemination of systemic lesions, infectious diseases;

Hormonally inactive pituitary tumors, "empty" sella syndrome, "pseudotumor" syndrome;

Against the backdrop of mental illness.

Endocrine:

hypothyroid;

Hypoovarian;

In diseases of the hypothalamic-pituitary system;

In diseases of the adrenal glands.

Classification of obesity according to the course of the disease:

stable;

progressive;

Residual.

Classification of obesity by body mass index

Degrees of obesity by BMI:

Obesity I degree: BMI from 30 to 34.9 kg / m 2;

Obesity II degree: BMI from 35 to 39.9 kg / m 2;

Obesity III degree: BMI from 40 kg / m 2 and above.

Classification of obesity according to the type of deposition of adipose tissue:

Abdominal (android, central) obesity;

Gluteal-femoral (gynoid) obesity;

mixed obesity.
To determine the type of deposition of adipose tissue, the ratio of OT and OB is used. Obesity is considered abdominal if women have OT/OB > 0.85, men - > 1.0.

Table #3 Waist circumference and the risk of complications of obesity

An increase in waist circumference is a sign of an increased risk of complications, even with normal BMI values.

Waist circumference is measured in a standing position, midway between the bottom edge chest and the iliac crest along the mid-axillary line (not in the maximum size and not at the level of the navel), the circumference of the hips - in their widest area at the level of the greater trochanter.

Indicators of high risk of comorbidities (in terms of waist circumference): in men > 102 cm, in women > 88 cm.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

The main (mandatory) diagnostic examinations carried out at the outpatient level:

UAC deployed;

Biochemical blood test (urea, creatinine, total protein, AlAT, AsAT, glucose, total bilirubin, HDL, LDL, cholesterol, thymol test, alkaline phosphatase);

Glycemic profile;

GDZ ultrasound;

Endocrinologist consultation;

Hepatologist consultation;

Therapist's consultation.

Additional diagnostic examinations performed at the outpatient level:

Definition of VC;

CT scan of the brain;

Ultrasound of the thyroid gland.

The minimum list of examinations that must be carried out when referring to planned hospitalization:

Coagulogram (PV, fibrinogen, APTT, INR);

Biochemical blood test (urea, creatinine, total protein, ALT, AST, total bilirubin, HDL, LDL, cholesterol, thymol test, alkaline phosphatase);

blood sugar;

Microreaction;

Determination of blood for viruses hepatitis B, C;

GDZ ultrasound;

Fluorography;

Consultation of a therapist to identify contraindications to surgical treatment;

The main (mandatory) diagnostic examinations carried out at the hospital level:

Coagulogram (PV, fibrinogen, APTT, INR);

Biochemical blood test (urea, creatinine, total protein, AlAT, AsAT, total bilirubin);

blood sugar;

Group and Rh - blood factor;

R - scan (graph) of the stomach with barium.

Additional diagnostic examinations carried out at the hospital level:

ultrasound abdominal cavity.

Diagnostic measures carried out at the ambulance stage emergency care: not performed.

Diagnostic criteria

Complaints and anamnesis

Complaints:

Overweight;

Pain in the joints - pelvic, knee, ankle;

Shortness of breath when walking;

Palpitation when walking;

Increased blood pressure;

Pain in the chest;

Violation of the menstrual cycle in women of childbearing age;

Infertility.

Anamnesis:

The presence of concomitant diseases (arterial hypertension, type 2 diabetes mellitus, arthropathy);

Family predisposition to the development of obesity;

Sedentary lifestyle;

Violation of the diet;

Stress.

Physical examination:

Measurement of body weight;

Height measurement;

Calculation of BMI;

Measurement of chest volume;

Waist measurement;

Measuring the volume of the hips;

Measurement of VC.

Laboratory research

Table No. 4. Criteria for diagnosing metabolic syndrome

Criteria for laboratory tests	Index
Elevated levels of triacylglycerols (esters of glycerol and higher fatty acids—TAGs) or LDL fractions (beta-lipoproteins)	greater than or equal to 1.7 mmol/l or specific treatment for these lipid disorders.
Reduced cholesterol Decreased high-density lipoprotein (HDL)	less than 1.03 mmol/l in men; less than 1.29 mmol/l in women; or specific treatment for these lipid disorders.
Elevated plasma glucose	Fasting plasma glucose greater than or equal to 5.6 mmol/L or previously diagnosed type 2 diabetes mellitus; If fasting plasma glucose is less than 5.6 mmol/l, a glucose tolerance test is recommended, although this is not required to confirm the presence of the metabolic syndrome itself.

Instrumental research:

Ultrasound of the liver - to detect dystrophic changes in the liver in the form of fatty hepatosis;

Ultrasound of the liver - to detect stones in gallbladder to determine possible simultaneous surgical treatment;

EFGDS - detection of GERD and / or HH.

Indications for consultation of narrow specialists:

Consultation with a general practitioner/cardiologist to clarify the general somatic condition;

Consultation with an endocrinologist to exclude obesity associated with endocrine diseases;

Consultation of a neuropathologist/neurosurgeon for patients with a history of traumatic brain injury, neuroendocrine diseases;

Consultation of a psychotherapist is indicated for patients with eating disorders (attacks of compulsive eating at certain intervals of time, lack of a feeling of satiety, taking large amounts of food without feeling hungry, in a state of emotional discomfort, sleep disturbance with nighttime meals in combination with morning anorexia);

Consultation of a geneticist in the presence of signs of genetic syndromes.

Differential Diagnosis

Table No. 5 Differential diagnosis for morbid obesity

Types of obesity	Etiology	Clinical manifestations	Diagnostics
Alimentary - constitutional	Availability of food and overeating from early childhood; Reflexes related to time and amount of food; Assimilated types of nutrition (national traditions); Hypodynamia, predisposing heredity to obesity; The constitution of adipose tissue; The activity of fat metabolism; The state of the hypothalamic centers of satiety and appetite; Dishormonal conditions (pregnancy, childbirth, lactation, menopause) are often predisposing to the development of obesity.		BMI; FROM/OB; Elevated levels of triacylglycerols; Increase in cholesterol; triglycerides in the blood; Elevated plasma glucose.
Cerebral	Skull injuries; neuroinfections; brain tumors; Prolonged increase in intracranial pressure.	even distribution of subcutaneous fat throughout the body	CT scan of the brain; MRI of the brain.
Endocrine	. primary pathology of the endocrine glands (hypercorticism, hypothyroidism, hypogonadism, insulinoma)	the upper type is typical for hypothalamic obesity of the type of Itsenko-Cushing's disease with adrenal obesity and in fact with Itsenko-Cushing's disease;	Increase in the content of ACTH, cortisol; Increasing the level of 17KS, 170KS;. Decrease in the content of thyroid hormones (TK, T4, TSH); Decreased levels of HTG, estrogen, progesterone, testosterone, inherent in hypogonadal obesity. These hormonal changes provide lipogenesis.
Medicinal	Formed at long-term use of drugs that increase appetite or activate liposynthesis	Uniform distribution of subcutaneous fat throughout the body	BMI; FROM/OB; Elevated levels of triacylglycerols; Increase in cholesterol Triglycerides in the blood Elevated plasma glucose

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Treatment

Treatment goals:

Achieving the most stable (at least 5 years) and gradual weight loss (no more than 0.5-1 kg per week).

Achievement of target values ​​of metabolic parameters:

BP less than or equal to 130/85 mm Hg. Art.;

Fasting glycemia less than or equal to 5.6 mmol/l;

Triglycerides less than or equal to 1.7 mmol/L;

HDL more than 1.03 mmol/l in men and more than 1.29 mmol/l in women;

Total cholesterol is less than or equal to 5.2 mmol/L.

Treatment tactics

Not drug treatment (mode, diet, etc.):

Diet therapy;

Physical activity.

Medical treatment

Ampicillin/sulbactam (1.5 g, IV);

Amoxicillin/clavulanate (1.2 g, IV);

Cefazolin (2 g, i.v.);

Cefuroxime (1.5 g, IV).

From 1-3 days of the postoperative period - with a duration of surgery of more than 4 hours, if there are technical difficulties during the operation, especially when performing hemostasis, as well as at the risk of microbial contamination.

(depending on the results of the microbiological examination):

Ampicillin/sulbactam:

With a mild course of infection - 1.5 g 2 r / day IV, the duration of treatment is up to 3-5 days;

In moderate course -1.5 g 4 r / day in / in, the duration of treatment is 5-7 days;

In severe cases -3 g 4 r / day in / in, the duration of treatment is up to 7-10 days.

Amoxicillin/clavulanate(calculation for amoxicillin):

With a mild infection: 1 g IV, 3 times a day, the duration of treatment is up to 3-5 days;

Cefazolin:

With a mild infection: 0.5-1 g IV, 3 times a day, the duration of treatment is up to 3-5 days;

In severe infection: 2 g IV, 3 times a day, the duration of treatment is 5-10 days.

Cefuroxime:

With a mild infection: 0.75 g IV, 3 times a day, the duration of treatment is up to 3-5 days;

In severe infection: 1.5 g IV, 3 times a day, the duration of treatment is 5-10 days.

Metronidazole:

With a mild infection: 500 mg IV, drip, 3 times a day, the duration of treatment is up to 5-7 days;

In severe infection: 1000 mg IV, 2-3 times a day, the duration of treatment is 5-10 days.

Vancomycin:

For beta-lactam allergy, documented case of MRSA colonization: 7.5 mg/kg every 6 hours or 15 mg/kg every 12 hours IV. Duration of treatment - 7-10 days;

Ciprofloxacin 200 mg IV 2 times a day, Duration of treatment - 5-7 days

macrolides:

Azithromycin 500 mg once a day IV. The course of treatment - no more than 5 days. After the end of the intravenous administration, it is recommended to prescribe azithromycin orally at a dose of 250 mg until the completion of the 7-day general course of treatment.

Crystalloid solutions in a total volume of up to 1500-2000 ml.

Sodium chloride/sodium acetate solution;

Sodium chloride/potassium chloride/sodium bicarbonate solution;

Sodium acetate trihydrate/sodium chloride/potassium chloride solution;

Dextrose solution 5%.

Antimycotic therapy:

Fluconazole 50-400 mg once a day, depending on the risk of developing a fungal infection.

:

Synthetic opioids:

Tramadol in / in, in / m, s / c at 50-100 mg to 400 mg per day, orally at 50 mg to 0.4 g per day) no more than every 4-6 hours.

Narcotic analgesics

List of essential medicines (having 100% probability of use): not carried out.

List of additional medicines (less than 100% probability of use): not carried out.

Antibacterial therapy is carried out with the aim of:

Prevention of infectious complications:

Ampicillin / sulbactam (1.5g, IV),

Amoxicillin / clavulanate (1.2g, IV),

Cefazolin (2g, IV)

Cefuroxime (1.5g, IV).

Terms of antibacterial prophylaxis:

One time (intraoperatively);

From 1-3 days of the postoperative period - with a duration of surgery of more than 4 hours, if there are technical difficulties during the operation, especially when performing hemostasis, as well as at the risk of microbial contamination.

Treatment of infectious complications(depending on the results of the microbiological examination)

Ampicillin/sulbactam:

With a mild course of infection -1.5 g, 2 r / day in / in, the duration of treatment is up to 3-5 days;

With a moderate course -1.5 g, 4 r / day in / in, the duration of treatment is 5-7 days;

In severe cases -3 g, 4 r / day in / in, the duration of treatment is up to 7-10 days.

Amoxicillin/clavulanate(calculation for amoxicillin):

With a mild infection: 1 g, IV, 3 times a day, the duration of treatment is up to 3-5 days;

Cefazolin:

With a mild infection: 0.5-1 g, intravenously, 3 times a day, the duration of treatment is up to 3-5 days;

In severe infection: 2 g, iv, 3 times a day, duration of treatment 5-10 days.

Cefuroxime:

With a mild infection: 0.75 g, intravenously, 3 times a day, the duration of treatment is up to 3-5 days;

In severe infection: 1.5 g, iv, 3 times a day, duration of treatment 5-10 days.

Metronidazole:

With a mild infection: 500 mg, intravenously, drip, 3 times a day, the duration of treatment is up to 5-7 days;

In severe infection: 1000 mg, iv, 2-3 times a day, the duration of treatment is 5-10 days.

Vancomycin: (for beta-lactam allergy, documented case of MRSA colonization).

7.5 mg/kg every 6 hours or 15 mg/kg every 12 hours IV. Duration of treatment - 7-10 days

Ciprofloxacin 200 mg IV 2 times a day, Duration of treatment - 5-7 days

macrolides:

Azithromycin 500 mg once a day IV. The course of treatment is no more than 5 days. After the end of the intravenous administration, it is recommended to prescribe azithromycin orally at a dose of 250 mg until the completion of the 7-day general course of treatment.

Infusion - detoxification therapy: carried out for the purpose of treating intoxication syndrome, preventing infectious complications, in the provision of emergency medical care - with active bleeding.

Crystalloid solutions in a total volume up to 1500-2000 ml:

Sodium chloride solution 0.9%;

Sodium chloride solution 0.9%/sodium acetate;

Sodium chloride solution 0.9% / potassium chloride / sodium bicarbonate;

Sodium acetate trihydrate/sodium chloride solution 0.9%/potassium chloride;

Dextrose solution 5%.

Antimycotic therapy:

Fluconazole 50-400 mg once a day, depending on the risk of developing a fungal infection.

Prevention of thromboembolic complications carried out for 3 days with low molecular weight heparins:

Dalteparin, 0.2 ml, 2500 IU, s.c.;

Enoxaparin, 0.4 ml (4000 Anti-Xa MO), s.c.;

Nadroparin, 0.3 ml (9500 IU / ml 3000 Anti-Xa MO), s / c;

Reviparin, 0.25 ml (1750 anti-Xa ME), s.c.;

Certoparin sodium 0.4 ml (3000 Anti-Xa MO), s.c.

For pain relief:

Non-steroidal anti-inflammatory drugs:

Ketoprofen, IM, IV, 100 mg/2 ml up to 4 times a day;

Ketorolac inside, in / m, in / in 10-30 mg up to 4 times a day;

Diclofenac, 75-150 mg per day IM up to 3 times a day.

Synthetic opioids:

Tramadol, i.v., i.m., s.c. 50-100mg up to 400mg per day, orally 50mg up to 0.4g per day) no more than every 4-6 hours.

Narcotic analgesics with severe pain during the early postoperative period:

Trimeperidine, 1.0 ml of 1% or 2% solution i / m;

Morphine, 1.0 ml of 1% i.m. solution.

Medical treatment provided on an outpatient basis:

List of essential medicines: not carried out.

Medical treatment provided at the inpatient level

List of essential medicines:

Cefazolin, powder for the preparation of an injection solution for intravenous administration 500 and 1000 mg;

Ketoprofen, ampoules 100 mg / 2 ml;

enoxaparin, disposable syringe 0.4 ml (4000 Anti-Ha MO).

List of additional medicines:

Ampicillin / sulbactam, powder for solution for intravenous and intramuscular injection 1.5 g;

Amoxicillin / clavulanate, powder for the preparation of an injection solution for intravenous administration 1.2g; 600mg;

Cefuroxime, powder for the preparation of an injection solution for intravenous administration 750 mg and 1500 mg;

Metronidazole, solution 500 mg, 100.0 ml for IV infusion;

Azithromycin, powder for the preparation of an injection solution for intravenous administration 500 mg; tablet 250 mg;

Ciprofloxacin, solution 200 mg, 100.0 ml for IV infusion;

Dalteparin, disposable syringe 0.2 ml, 2500 IU, s.c.;

Nadroparin, disposable syringe 0.3 ml (9500 IU / ml 3000 Anti-Xa MO), s / c;

Reviparin, disposable syringe 0.25 ml (1750 anti-Xa ME), s.c.;

Certoparin sodium disposable syringe 0.4 ml (3000 Anti-Xa MO), s / c;

Sodium chloride solution 0.9%, 400.0 ml;

Solution, sodium chloride 0.9%/sodium acetate 400.0 ml;

Solution, sodium chloride 0.9% / potassium chloride / sodium bicarbonate 400.0 ml;

Sodium acetate trihydrate / sodium chloride solution 0.9% / potassium chloride, 400.0 ml;

Dextrose solution 5%, 400.0 ml;

Fluconazole, 50 or 150 mg capsules;

Ketorolac tab. 10 mg each, 30 mg/ml solution 1.0 ml;

Diclofenac 75 mg, 3.0 ml;

Tramadol, ampoule, 50 mg 1.0 ml

Trimeperidine, 1.0 ml of 1% or 2% solution;

Morphine, 1.0 ml of 1% solution;

Drug treatment provided at the stage of emergency emergency care: not carried out.

Other treatments

Endoscopic application of an intragastric balloon

Indications for the installation of an intragastric balloon:

BMI 30 kg/m2, when conservative therapy methods were not effective;

As a preoperative preparation for the main bariatric treatment of obesity, in extreme forms of obesity.

Contraindications to the installation of an intragastric balloon are:

Diaphragmatic hernia and gastroesophageal reflux disease;

Erosions and ulcers of the esophagus, stomach and duodenum in the acute stage;

Taking hormonal and anticoagulant drugs;

Alcohol and drug addiction;

Previously performed operations on the stomach;

Mental disorders;

Pregnancy.

The percentage of excess weight loss is approximately 10.9%, and the decrease in BMI is most often in the range from 2 to 6 kg/m2 (LE: 1b).

Other types of treatment provided at the outpatient level: not available.

Other types provided at the stationary level: not carried out.

Other types of treatment provided at the stage of emergency emergency care: not available.

Surgical intervention

Methods of surgical treatment of MO and MS(LE 1a):

Laparoscopic gastric banding;

Laparoscopic plication of the greater curvature of the stomach;

Laparoscopic longitudinal (sleeve, tubular, sleeve) resection of the stomach;

Roux-en-Y laparoscopic gastric bypass;

Minigastric bypass (single-anastomous gastric bypass, Ω-shaped gastric bypass);

Method of biliopancreatic shunting (N.Scopinaro operation);

Biliopancreatic shunting in the Hess-Marceau modification (Biliopancreatic Diversion/Duodenal Switch).

Contraindications to surgical treatment for all methods are as follows:

The patient's age is less than 20 years / more than 70 years;

Diseases of the cardiovascular system;

mental illness;

Drug addiction, alcoholism;

The patient has esophageal pathology such as severe esophagitis, esophageal varices;

The patient has portal hypertension;

The presence of cirrhosis of the liver;

The presence of a stomach or duodenal ulcer;

The presence of chronic pancreatitis;

Presence of pregnancy;

The presence of a chronic infection in the body;

Continuous use of steroid hormones;

The presence of autoimmune diseases of the connective tissue.

Surgical intervention provided on an outpatient basis: not performed.

Surgical intervention provided in a hospital setting

Laparoscopic gastric banding(LE 2b)

Indications for gastric banding:

BMI of 30 kg/m2 or more, when the methods of conservative therapy were not effective and the patient still has associated psychological problems.

Specific complications:

Dysphagia;

Esophageal dilatation;

The effect of "slip";

Difficulties in adjusting the port to regulate the inner hole;

Discomfort from having a device;

Device migration;

Erosion formation;

Bedsores of the stomach wall.

Laparoscopic plication of the greater curvature of the stomach(LE 2b) :

Indications for laparoscopic plication of the greater curvature of the stomach:

BMI of 30 kg/m2 or more, when conservative therapy methods have not been effective and the patient has associated psychological problems.

Specific indications:

When MO is combined with GERD and HH. (LE 3) .

The method of laparoscopic longitudinal (sleeve, tubular, sleeve) resection of the stomach(level 1b)

Indications for laparoscopic longitudinal resection of the stomach:

BMI 35 kg/m2 or more;

BMI 45 - 50 kg/m2, as the first stage of treatment, in the future to prepare for biliopancreatic bypass surgery.

Complications:

Inconsistency of seams on the stomach;

Development of peptic ulcers;

Bleeding;

Reflux - esophagitis.

Roux-en-Y Laparoscopic Gastric Bypass Method(LE 1a)

Indications for laparoscopic Roux-en-Y gastric bypass:

BMI from 40 kg/m2.

Specific contraindications for Roux-en-Y gastric bypass:

BMI less than 30 kg/m2.

Metabolic Complications:

Hypoproteinemia;

Anemia;

Manifestations of deficiency of fat-soluble vitamins (A, D, E, K).

Mini-gastric bypass (single-anastomous gastric bypass, Ω-shaped gastric bypass)(LE 1a) [:

Indications for laparoscopic mini gastric bypass surgery:

BMI from 35 kg/m2, with concomitant pathology of type 2 diabetes;

BMI from 40 kg/m2.

Specific contraindications for minigastric bypass:

BMI less than 30 kg/m2.

Complications:

Inconsistency of the sutures of the anastomoses;

Stenosis of the outlet section from a small part of the stomach;

Development of peptic ulcers;

Bleeding.

Metabolic Complications:

Manifestations of calcium deficiency;

Manifestations of iron deficiency;

Manifestations of vitamin deficiency.

Method of biliopancreatic shunting (N.Scopinaro operation) .

BMI from 45 kg/m2;

Specific contraindications to the bilipancreatic shunt method:

BMI less than 40 kg/m2.

Biliopancreatic shunting in the Hess-Marceau modification (Biliopancreatic Diversion/Duodenal Switch)(LE 1b) :

Indications for the bilipancreatic shunt method:

BMI from 45 kg/m2, with concomitant pathology of type 2 diabetes;

Specific contraindications to the bilipancreatic shunt method:

BMI less than 50 kg/m2.

Complications:

uncontrolled weight loss;

Bleeding from the site of anastomoses;

Manifestations of basal metabolic disorders requiring replacement therapy.

Preventive measures (prevention of complications)

Bariatric surgery in patients with excessive accumulation of adipose tissue has a high likelihood of complications, and therefore requires active preventive measures (LE: 1a, 1b):

Type of complication	Intraoperative prophylaxis	Postoperative prophylaxis
The failure of the seams on gastrointestinal tract, peritonitis	Peritonization of a mechanical staple suture with a manual suture	Nasogastric tube
Bleeding from gastrointestinal sutures	Careful hemostasis	Coagulation time control, drainage tube control
TELA	Passive by using the system: scd express thromboembolism prevention system (COVIDIEN), elastic bandage and elastic stockings on the lower limbs	Passive and active prophylaxis use of anticoagulants
cholelithiasis	Preventive cholecystectomy	-
Postoperative hernia	Closure of trocar wounds	-
Unacceptable weight loss; Re-increase in body weight.	Choice of the most effective method	Regulation of regimen and diet

Further management ( postoperative management, dispensary activities indicating the frequency of visits to PHC doctors and narrow specialists, primary rehabilitation carried out at the hospital level)

In the early postoperative period:

Monitoring of surgical complications, including leakage or bleeding from the anastomosis and other areas of organ stapling;

Prescribing parenteral nutrition in patients at high risk of suture failure on the gastrointestinal tract and / or following a liquid diet during the first week, a semi-liquid diet during the second week;

Maintain appropriate blood glucose levels; use of an insulin analog, if indicated;

Vancomycin (Vancomycin) Dalteparin (Dalteparin) Dextrose (Dextrose) Diclofenac (Diclofenac) Potassium chloride (Potassium chloride) Ketoprofen (Ketoprofen) Ketorolac (Ketorolac) Clavulanic acid Metronidazole (Metronidazole) Morphine (Morphine) Nadroparin calcium (Nadroparin calcium) Sodium acetate Sodium acetate trihydrate Sodium bicarbonate (Sodium hydrocarbonate) Sodium chloride (Sodium chloride) Reviparin sodium (Reviparin sodium) Sulbactam (Sulbactam) Tramadol (Tramadol) Trimeperidine (Trimeperidine) Fluconazole (Fluconazole) Certoparin sodium (Certoparin sodium) Cefazolin (Cefazolin) Cefuroxime (Cefuroxime) Ciprofloxacin (Ciprofloxacin) Enoxaparin sodium (Enoxaparin sodium)

Hospitalization

1. 1. Oxford sed Medicine - Levels of Evidence (March 2009). 2. Mechanick JI, Kushner RF, Sugerman HJ, Gonzalez-Campoy JM, Collazo-Clavell ML, Guven S, Spitz AF, Apovian CM, Livingston EH, Brolin R, Sarwer DB, Anderson WA, Dixon J. American Association of Clinical Endocrinologists, the Obesity Society, and American Society for Metabolic & Bariatric Surgery Medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support . Endocr Practice. 2008 Jul-Aug;14(Suppl 1):1-83. 3. WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. WHO Technical Report Series 854. Geneva: World Health Organization, 1995. 4. WHO. Obesity: preventing and managing the global epidemic. Report of a WHO Consultation. WHO Technical Report Series 894. Geneva: World Health Organization, 2000. 5. WHO/IASO/IOTF. The Asia-Pacific perspective: redefining obesity and its treatment. Health Communications Australia: Melbourne, 2000. 6. James WPT, Chen C, Inoue S. Appropriate Asian body mass indices? Obesity Review, 2002; 3:139. 7. WHO expert consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. The Lancet, 2004; 157-163. 8. Lee WJ, Chong K, Chen CY, et al. Diabetes remission and insulin secretion after gastric bypass in patients with body mass index

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of protocol developers:

1. Ospanov Oral Bazarbaevich - Doctor of Medical Sciences, Professor, Head of the Department of Endosurgery of the Faculty of Continuous Professional Development and Additional Education of JSC "Astana Medical University". Astana, President of the Republican Public Association "Society of Bariatric and Metabolic Surgeons of Kazakhstan". Kazakhstan Respublikasynyn enbek sinirgen önertapkyshy.

2. Namaeva Karlygash Abdimalikovna - Assistant of the Department of Endosurgery of the Faculty of Continuous Professional Development and Additional Education of JSC "Astana Medical University"

3. Akhmadyar Nurzhamal Sadyrovna - Doctor of Medical Sciences, Senior Clinical Pharmacologist of JSC "National Scientific Medical Center for Motherhood and Childhood"

Indication of no conflict of interest: no conflict of interest.

Reviewers:

Tashev Ibragim Akzholovich - Doctor of Medical Sciences, Professor, Head of the Surgical Department of JSC "National Scientific Medical Center", Astana.

Indication of the conditions for revising the protocol: Review protocol after 3 years and/or when new diagnostic/treatment methods become available with a higher level of evidence.

Annex to the protocol

Conditions for the possibility of surgical treatment of patients with obesity:

Due to the high operational risk and complexity of weight loss operations in conditions of excess fat, the International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) makes the following demands on surgeons, equipment and medical institutions: requirements:

Surgeon requirements:

1. Availability of a certificate (certificate) issued in training centers accredited by the IFSO or national affiliates of the World Federation of Obesity Societies (IFSO);

2. Have good skills in performing endosurgical tissue stapling (confirming document for passing the exam on a virtual simulator) and trained in working with stapling devices.

3. Able to perform surgical intervention for complications both openly and laparoscopically;

4. Annually attending scientific conferences and congresses on bariatric issues, writing articles about their bariatric experience (IFSO mandatory requirement);

5. Additionally, it is required to pass a training cycle of advanced training for teachers - members of the Republican public association "Society of Bariatric and Metabolic Surgeons of Kazakhstan", lasting at least 216 hours, and it is necessary to have experience in performing standard laparoscopic resection of the stomach according to B-2. and have experience in assisting at least 30 bariatric surgeries for each major type of surgery (gastric drain-resection and gastric bypass).

Equipment requirements:

Equipment necessary for obese patients such as scales, height rod, operating room tables, instruments and Consumables specially designed for obesity and for use in both laparoscopic and open surgery, laparoscopic video endo-surgical units (racks), wheelchairs, various other furniture and mechanical lifts that can accommodate a stretcher for obese patients, as well as an equipped room intensive care(Recovery room);

The medical gurney and operating table should be designed for the maximum weight of the patient and should be multifunctional, and the operating table should be able to change the position of the patient and accessories for fixing him in various positions;

Working laparoscopic instruments (trocars, clamps, etc.) and staplers should be of maximum length (elongated);

For the prevention of thromboembolic complications, means of intraoperative and postoperative compression of the veins of the lower extremities should be used.

Gradation of IFSO facilities where bariatric surgery can be performed:

1. Initially created bariatric medical organizations - where there are trained and certified medical personnel, equipment with special equipment and tools (listed above). Cardiologists, pulmonologists, psychotherapists, nutritionists, anesthesiologists with experience in treating bariatric patients should be easily available for consultations in health facilities. These medical institutions cannot accept patients with superobesity during the first period (1-2 years) in their practice. In addition, during this period, simpler operations (LBZH, LGP, LRZh) should be limited. After two years, these restrictions are removed only if at least 50 operations are performed);

2. Operating bariatric institutions - if bariatric operations are performed from 50 to 100 operations per year, or most of those performed more than 100 - only restrictive);

3. TsSBH (excellence centers) if there are at least 100 bariatric surgeries per year, most of which are GSh and BPSh). Have at least one bariatric surgeon certified in the IFSO unit, trained in other CSSCs, having publications in leading international journals based on their own bariatric experience. Maintain a register of patients and their observation covering at least 75% of those operated on. In such centers, educational and pedagogical work and accreditation for doctors and paramedical personnel should be carried out.

Attached files

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Class IV. Diseases of the endocrine system, eating disorders and metabolic disorders (E00-E90)

Note. All neoplasms (both functionally active and inactive) are included in class II. Appropriate codes in this class (for example, E05.8, E07.0, E16-E31, E34.-) can be used as additional codes, if necessary, to identify functionally active neoplasms and ectopic endocrine tissue, as well as hyperfunction and hypofunction of the endocrine glands, associated with neoplasms and other disorders classified elsewhere.
Excludes: complications of pregnancy, childbirth and the puerperium (O00-O99), symptoms, signs and abnormal findings from clinical and laboratory investigations, not elsewhere classified (R00-R99), transient endocrine and metabolic disorders, specific for fetus and newborn (P70-P74)

This class contains the following blocks:
E00-E07 Diseases of the thyroid gland
E10-E14 Diabetes mellitus
E15-E16 Other disorders of glucose regulation and pancreatic endocrine secretion
E20-E35 Disorders of other endocrine glands
E40-E46 Malnutrition
E50-E64 Other types of malnutrition
E65-E68 Obesity and other types of malnutrition
E70-E90 Metabolic disorders

The following categories are marked with an asterisk:
E35 Disorders of the endocrine glands in diseases classified elsewhere
E90 Nutritional and metabolic disorders in diseases classified elsewhere

THYROID DISEASES (E00-E07)

E00 Congenital iodine deficiency syndrome

Includes: endemic conditions associated with environmental iodine deficiency natural environment as directly,
and due to iodine deficiency in the mother's body. Some of these conditions cannot be considered true hypothyroidism, but are the result of inadequate secretion of thyroid hormones in the developing fetus; there may be a connection with natural goiter factors. If necessary, identify the associated delay mental development use an additional code (F70-F79).
Excludes: subclinical hypothyroidism due to iodine deficiency (E02)

E00.0 Syndrome of congenital iodine deficiency, neurological form. Endemic cretinism, neurological form
E00.1 Syndrome of congenital iodine deficiency, myxedematous form.
Endemic cretinism:
. hypothyroid
. myxedematous form
E00.2 Syndrome of congenital iodine deficiency, mixed form.
Endemic cretinism, mixed form
E00.9 Congenital iodine deficiency syndrome, unspecified.
Congenital hypothyroidism due to iodine deficiency NOS. Endemic cretinism NOS

E01 Thyroid disorders associated with iodine deficiency and related conditions

Excludes: congenital iodine deficiency syndrome (E00.-)
subclinical hypothyroidism due to iodine deficiency (E02)

E01.0 Diffuse (endemic) goiter associated with iodine deficiency
E01.1 Multinodular (endemic) goiter associated with iodine deficiency. Nodular goiter associated with iodine deficiency
E01.2 Goiter (endemic) associated with iodine deficiency, unspecified. Endemic goiter NOS
E01.8 Other thyroid diseases associated with iodine deficiency and related conditions.
Acquired hypothyroidism due to iodine deficiency NOS

E02 Subclinical hypothyroidism due to iodine deficiency

E03 Other forms of hypothyroidism

Excludes: hypothyroidism associated with iodine deficiency (E00-E02)
hypothyroidism following medical procedures (E89.0)

E03.0 congenital hypothyroidism with diffuse goiter.
Goiter (non-toxic) congenital:
. NOS
. parenchymal
E03.1 Congenital hypothyroidism without goiter. Aplasia of the thyroid gland (with myxedema).
Congenital:
. atrophy of the thyroid gland
. hypothyroidism NOS
E03.2 Hypothyroidism caused by drugs and other exogenous substances.
If it is necessary to identify the cause, use an additional external cause code (class XX).
E03.3 Post-infectious hypothyroidism
E03.4 Thyroid atrophy (acquired).
Excludes: congenital atrophy of thyroid gland (E03.1)
E03.5 Myxedema coma
E03.8 Other specified hypothyroidisms
E03.9 Hypothyroidism, unspecified. Myxedema NOS

E04 Other forms of non-toxic goiter

Excludes: congenital goiter:
. NOS )
. diffuse ) (E03.0)
. parenchymal)
goiter associated with iodine deficiency (E00-E02)

E04.0 Non-toxic diffuse goiter.
Goiter non-toxic:
. diffuse (colloidal)
. simple
E04.1 Non-toxic single nodular goiter. Colloidal node (cystic) (thyroid).
Non-toxic mononodous goiter. Thyroid (cystic) nodule NOS
E04.2 Non-toxic multinodular goiter. Cystic goiter NOS. Polynodous (cystic) goiter NOS
E04.8 Other specified forms of non-toxic goiter
E04.9 Nontoxic goiter, unspecified. Goiter NOS. Nodular goiter (nontoxic) NOS

E05 Thyrotoxicosis [hyperthyroidism]

Excludes: chronic thyroiditis with transient thyrotoxicosis (E06.2)
neonatal thyrotoxicosis (P72.1)

E05.0 Thyrotoxicosis with diffuse goiter. Exophthalmic or toxic call NOS. Graves' disease. Diffuse toxic goiter
E05.1 Thyrotoxicosis with toxic single-nodular goiter. Thyrotoxicosis with toxic mononodous goiter
E05.2 Thyrotoxicosis with toxic multinodular goiter. Toxic nodular goiter NOS
E05.3 Thyrotoxicosis with ectopic thyroid tissue
E05.4 Thyrotoxicosis artificial
E05.5 Thyroid crisis or coma
E05.8 Other forms of thyrotoxicosis. Hypersecretion of thyroid-stimulating hormone.

E05.9 Thyrotoxicosis, unspecified. Hyperthyroidism NOS. Thyrotoxic heart disease (I43.8)

E06 Thyroiditis

Excludes: postpartum thyroiditis (O90.5)

E06.0 Acute thyroiditis. Thyroid abscess.
Thyroiditis:
. pyogenic
. purulent
If necessary, an additional code (B95-B97) is used to identify the infectious agent.
E06.1 Subacute thyroiditis.
Thyroiditis:
. de Quervain
. giant cell
. granulomatous
. nonpurulent
Excludes: autoimmune thyroiditis (E06.3)
E06.2 Chronic thyroiditis with transient thyrotoxicosis.
Excludes: autoimmune thyroiditis (E06.3)
E06.3 Autoimmune thyroiditis. Hashimoto's thyroiditis. Chasitoxicosis (transient). Lymphoadenomatous goiter.
Lymphocytic thyroiditis. Lymphomatous struma
E06.4 Medical thyroiditis
E06.5 Thyroiditis:
. chronic:
. NOS
. fibrous
. woody
. Riedel
E06.9 Thyroiditis, unspecified

E07 Other thyroid disorders

E07.0 hypersecretion of calcitonin. C-cell hyperplasia of the thyroid gland.
Hypersecretion of thyrocalcitonin
E07.1 Dishormonal goiter. Family dyshormonal goiter. Syndrome Pendred.
Excludes: transient congenital goiter with normal function (P72.0)
E07.8 Other specified diseases of the thyroid gland. Tyrosine-binding globulin defect.
hemorrhage)
Heart attack) (in) the thyroid gland (s)
Syndrome of impaired euthyroidism
E07.9 Thyroid disease, unspecified

DIABETES (E10-E14)

If necessary, identify medicinal product that caused diabetes use an additional external cause code (class XX).

The following fourth characters are used with categories E10-E14:
.0 Coma
Diabetic:
. coma with or without ketoacidosis (ketoacidotic)
. hypermolar coma
. hypoglycemic coma
Hyperglycemic coma NOS

1 With ketoacidosis
Diabetic:
. acidosis)
. ketoacidosis) with no mention of coma

2 With kidney damage
Diabetic nephropathy (N08.3)
Intracapillary glomerulonephrosis (N08.3)
Kimmelstiel-Wilson syndrome (N08.3)

3 With ocular lesions
Diabetic:
. cataract (H28.0)
. retinopathy (H36.0)

4 With neurological complications
Diabetic:
. amyotrophy (G73.0)
. autonomic neuropathy (G99.0)
. mononeuropathy (G59.0)
. polyneuropathy (G63.2)
. autonomous (G99.0)

5 With peripheral circulatory disorders
Diabetic:
. gangrene
. peripheral angiopathy (I79.2)
. ulcer

6 With other specified complications
Diabetic arthropathy (M14.2)
. neuropathic (M14.6)

7 With multiple complications

8 With unspecified complications

9 No complications

E10 Insulin-dependent diabetes mellitus

[cm. the above headings]
Includes: diabetes (diabetes):
. labile
. with onset at a young age
. prone to ketosis
. type I
Excludes: diabetes mellitus:
. newborns (P70.2)
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)

E11 Non-insulin dependent diabetes mellitus

Includes: diabetes (diabetes) (non-obese) (obese):
. with onset in adulthood
. not prone to ketosis
. stable
. type II
Excludes: diabetes mellitus:
. associated with malnutrition (E12. -)
. neonates (P70.2)
. during pregnancy, during childbirth and postpartum
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
postoperative hypoinsulinemia (E89.1)

E12 Diabetes mellitus associated with malnutrition

[cm. above subheadings]
Includes: diabetes mellitus associated with malnutrition:
. insulin dependent
. non-insulin dependent
Excludes: diabetes mellitus during pregnancy, during childbirth
and in the puerperium (O24.-)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
neonatal diabetes mellitus (P70.2)
postoperative hypoinsulinemia (E89.1)

E13 Other specified forms of diabetes mellitus

[cm. above subheadings]
Excludes: diabetes mellitus:
. insulin dependent (E10.-)
. associated with malnutrition (E12. -)
. neonatal (P70.2)
. during pregnancy, during childbirth and postpartum
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
postoperative hypoinsulinemia (E89.1)

E14 Diabetes mellitus, unspecified

[cm. above subheadings]
Includes: diabetes NOS
Excludes: diabetes mellitus:
. insulin dependent (E10.-)
. associated with malnutrition (E12. -)
. neonates (P70.2)
. non-insulin dependent (E11.-)
. during pregnancy, during childbirth and postpartum
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
postoperative hypoinsulinemia (E89.1)

OTHER DISORDERS OF GLUCOSE AND INTERNAL SECRETION REGULATION

PANCREAS (E15-E16)

E15 Non-diabetic hypoglycemic coma. Non-diabetic insulin coma caused by drugs
means. Hyperinsulinism with hypoglycemic coma. Hypoglycemic coma NOS.
If necessary, identify medicine that caused non-diabetic hypoglycemic coma, use an additional external cause code (class XX).

E16 Other disorders of internal secretion of the pancreas

E16.0 Medical hypoglycemia without coma.
If it is necessary to identify the medicinal product, use an additional code for external causes (class XX).
E16.1 Other forms of hypoglycemia. Functional non-hyperinsulinemic hypoglycemia.
Hyperinsulinism:
. NOS
. functional
Hyperplasia of pancreatic islet beta cells NOS. Encephalopathy after hypoglycemic coma
E16.2 Hypoglycemia, unspecified
E16.3 Increased secretion of glucagon.
Pancreatic islet cell hyperplasia with glucagon hypersecretion
E16.8 Other specified disorders of the internal secretion of the pancreas. Hypergastrinemia.
Hypersecretion:
. growth hormone releasing hormone
. pancreatic polypeptide
. somatostatin
. vasoactive intestinal polypeptide
Zollinger-Ellison Syndrome
E16.9 Violation of the internal secretion of the pancreas, unspecified. Islet cell hyperplasia NOS.
Hyperplasia of pancreatic endocrine cells NOS

DISORDERS OF OTHER ENDOCRINE GLANDS (E20-E35)

Excludes: galactorrhea (N64.3)
gynecomastia (N62)

E20 Hypoparathyroidism

Excludes: Di George syndrome (D82.1)
hypoparathyroidism following medical procedures (E89.2)
tetany NOS (R29.0)
transient hypoparathyroidism of the newborn (P71.4)

E20.0 Idiopathic hypoparathyroidism
E20.1 Pseudohypoparathyroidism
E20.8 Other forms of hypoparathyroidism
E20.9 Hypoparathyroidism, unspecified. Parathyroid tetagy

E21 Hyperparathyroidism and other disorders of the parathyroid [parathyroid] gland

Excludes: osteomalacia:
. in adults (M83.-)
. in childhood and adolescence (E55.0)

E21.0 Primary hyperparathyroidism. Hyperplasia of the parathyroid glands.
Generalized fibrous osteodystrophy [Recklinghausen's bone disease]
E21.1 Secondary hyperparathyroidism, not elsewhere classified.
Excludes: secondary hyperparathyroidism of renal origin (N25.8)
E21.2 Other forms of hyperparathyroidism.
Excludes: familial hypocalciuric hypercalcemia (E83.5)
E21.3 Hyperparathyroidism, unspecified
E21.4 Other specified violations parathyroid gland
E21.5 Disease of the parathyroid glands, unspecified

E22 Hyperfunction of the pituitary gland

Excludes: Itsenko-Cushing's syndrome (E24.-)
Nelson's syndrome (E24.1)
hypersecretion:
. adrenocorticotropic hormone [ACTH], unrelated
with Itsenko-Cushing's syndrome (E27.0)
. pituitary ACTH (E24.0)
. thyroid-stimulating hormone (E05.8)

E22.0 Acromegaly and pituitary gigantism.
Arthropathy associated with acromegaly (M14.5).
Hypersecretion of growth hormone.
Excluded: constitutional:
. gigantism (E34.4)
. high growth(E34.4)
hypersecretion of growth hormone-releasing hormone (E16.8)
E22.1 Hyperprolactinemia. If necessary, to identify the drug that caused hyperprolactinemia, use an additional code of external causes (class XX).
E22.2 Syndrome of inappropriate secretion of antidiuretic hormone
E22.8 Other states of hyperfunction of the pituitary gland. Precocious puberty of central origin
E22.9 Hyperfunction of the pituitary gland, unspecified

E23 Hypofunction and other disorders of the pituitary gland

Includes: listed conditions due to diseases of the pituitary and hypothalamus
Excludes: hypopituitarism following medical procedures (E89.3)

E23.0 Hypopituitarism. Fertile eunuchoid syndrome. Hypogonadotropic hypogonadism.
Idiopathic growth hormone deficiency.
Isolated deficiency:
. gonadotropin
. growth hormone
. other pituitary hormones
Kalmann syndrome
Short stature [dwarfism] Loreina-Levi
Pituitary necrosis (postpartum)
Panhypopituitarism
Pituitary :
. cachexia
. insufficiency NOS
. short stature [dwarfism]
Sheehan's syndrome. Simmonds disease
E23.1 Medical hypopituitarism.
E23.2 Diabetes insipidus.
Excludes: nephrogenic diabetes insipidus (N25.1)
E23.3 Hypothalamic dysfunction, not elsewhere classified.
Excludes: Prader-Willi syndrome (Q87.1), Russell-Silver syndrome (Q87.1)
E23.6 Other diseases of the pituitary gland. Abscess of the pituitary gland. Adiposogenital dystrophy
E23.7 Pituitary disease, unspecified

E24 Itsenko-Cushing's syndrome

E24.0 Itsenko-Cushing's disease of pituitary origin. Hypersecretion of ACTH by the pituitary.
Hyperadrenocorticism of pituitary origin
E24.1 Nelson syndrome
E24.2 Drug Itsenko-Cushing's syndrome.
If necessary, to identify the medicinal product, use an additional external cause code (class XX).
E24.3 Ectopic ACTH syndrome
E24.4 Cushingoid syndrome caused by alcohol
E24.8 Other Conditions Characterized by Cushingoid Syndrome
E24.9 Itsenko-Cushing syndrome, unspecified

E25 Adrenogenital disorders

Includes: adrenogenital syndromes, virilization or feminization acquired or due to hyperplasia
adrenal glands, which is a consequence of congenital enzyme defects in the synthesis of hormones
female(s):
. adrenal false hermaphroditism
. heterosexual precocious false genitalia
maturity
male(s):
. isosexual precocious false genitalia
maturity
. early macrogenitosomia
. premature puberty with hyperplasia
adrenal glands
. virilization (female)

E25.0 Congenital adrenogenital disorders associated with enzyme deficiency. Congenital adrenal hyperplasia. Deficiency of 21-hydroxylase. Congenital adrenal hyperplasia causing salt loss
E25.8 Other adrenogenital disorders. Idiopathic adrenogenital disorder.
If necessary, to identify the drug that caused the adrenogenital disorder, use an additional code of external causes (class XX).
E25.9 Adrenogenital disorder, unspecified. Adrenogenital syndrome NOS

E26 Hyperaldosteronism

E26.0 Primary hyperaldosteronism. Conn's syndrome. Primary aldosteronism due to hyperplasia of the supra-
kidney (bilateral)
E26.1 Secondary hyperaldosteronism
E26.8 Other forms of hyperaldosteronism. Barter syndrome
E26.9 Hyperaldosteronism, unspecified

E27 Other adrenal disorders

E27.0 Other types of hypersecretion of the adrenal cortex.
Hypersecretion of adrenocorticotropic hormone [ACTH] not associated with Itsenko-Cushing's disease.
Excludes: Itsenko-Cushing's syndrome (E24.-)
E27.1 Primary adrenal insufficiency. Addison's disease. Autoimmune inflammation of the adrenal glands.
Excludes: amyloidosis (E85.-), Addison's disease of tuberculous origin (A18.7), Waterhouse-Friderichsen syndrome (A39.1)
E27.2 Addisonian crisis. Adrenal crisis. adrenocortical crisis
E27.3 Drug insufficiency of the adrenal cortex. If necessary, to identify the medicinal product, use an additional external cause code (class XX).
E27.4 Other and unspecified insufficiency of the adrenal cortex.
Adrenal(th):
. bleeding
. heart attack
Adrenocortical sufficiency NOS. Hypoaldosteronism.
Excludes: adrenoleukodystrophy [Addison-Schilder] (E71.3), Waterhouse-Friderichsen syndrome (A39.1)
E27.5 Hyperfunction of the adrenal medulla. Hyperplasia of the adrenal medulla.
Catecholamine hypersecretion
E27.8 Other specified disorders of the adrenal glands. Impaired cortisol-binding globulin
E27.9 Adrenal gland disease, unspecified

E28 Ovarian dysfunction

Excludes: isolated gonadotropic insufficiency (E23.0)
ovarian failure following medical procedures (E89.4)

E28.0 Excess estrogen. If necessary, to identify the drug that caused the excess estrogens, use an additional code of external causes (class XX).
E28.1 An excess of androgens. Hypersecretion of ovarian androgens. If necessary, to identify the drug that caused the androgen excess, use an additional code of external causes (class XX).
E28.2 Polycystic ovarian syndrome. Sclerocystic ovarian syndrome. Stein-Leventhal syndrome
E28.3 Primary ovarian failure. Low estrogen content. Premature menopause NOS.
Persistent ovarian syndrome.
Excl.: menopause and female climacteric status (N95.1)
pure gonadal dysgenesis (Q99.1)
Turner's syndrome (Q96.-)
E28.8 Other types of ovarian dysfunction. Ovarian hyperfunction NOS
E28.9 Ovarian dysfunction, unspecified

E29 Testicular dysfunction

azoospermia or oligospermia NOS (N46)
isolated gonadotropic insufficiency (E23.0)
Klinefelter's syndrome (Q98.0-Q98.2, Q98.4)
testicular hypofunction following medical procedures (E89.5)
testicular feminization (syndrome) (E34.5)

E29.0 Testicular hyperfunction. Hypersecretion of testicular hormones
E29.1 Testicular hypofunction. Impaired biosynthesis of testicular androgen NOS
5-alpha reductase deficiency (with male pseudohermaphroditism). Testicular hypogonadism NOS.
If necessary, to identify the drug that caused testicular hypofunction, use an additional
external cause code (class XX).
E29.8 Other types of testicular dysfunction
E29.9 Testicular dysfunction, unspecified

E30 Disorders of puberty, not elsewhere classified

E30.0 Delayed puberty. Constitutional delay in puberty.
Delayed puberty
E30.1 Precocious puberty. Premature menstruation.
Excludes: Albright(-McCune)(-Sternberg) syndrome (Q78.1)
precocious puberty of central origin (E22.8)
female heterosexual precocious false puberty (E25.-)
male isosexual precocious false puberty (E25.-)
E30.8 Other disorders of puberty. Premature thelarche
E30.9 Disorder of puberty, unspecified

E31 Polyglandular dysfunction

Excludes: telangiectatic ataxia [Louis Bar] (G11.3)
myotonic dystrophy [Steinert] (G71.1)
pseudohypoparathyroidism (E20.1)

E31.0 Autoimmune polyglandular insufficiency. Schmidt syndrome
E31.1 Polyglandular hyperfunction.
Excludes: multiple endocrine adenomatosis (D44.8)
E31.8 Other polyglandular dysfunction
E31.9 Polyglandular dysfunction, unspecified

E32 Diseases of the thymus

Excludes: aplasia or hypoplasia with immunodeficiency (D82.1), myasthenia gravis (G70.0)

E32.0 Persistent hyperplasia of the thymus. Hypertrophy of the thymus
E32.1 Abscess of the thymus
E32.8 Other diseases of the thymus
E32.9 Thymus disease, unspecified

E34 Other endocrine disorders

Excludes: pseudohypoparathyroidism (E20.1)

E34.0 carcinoid syndrome.
Note. If necessary, to identify the functional activity associated with a carcinoid tumor, you can use an additional code.
E34.1 Other conditions of hypersecretion of intestinal hormones
E34.2 Ectopic hormonal secretion, not elsewhere classified
E34.3 Short stature [dwarfism], not elsewhere classified.
Short stature:
. NOS
. constitutional
. laron type
. psychosocial
Excludes: progeria (E34.8)
Russell-Silver syndrome (Q87.1)
limb shortening with immunodeficiency (D82.2)
short stature:
. achondroplasty (Q77.4)
. hypochondroplastic (Q77.4)
. with specific dysmorphic syndromes
(code these syndromes; see index)
. alimentary (E45)
. pituitary (E23.0)
. renal (N25.0)
E34.4 Constitutional tallness. Constitutional gigantism
E34.5 Syndrome of androgen resistance. Male pseudohermaphroditism with androgen resistance.
Violation of peripheral hormonal reception. Reifenstein syndrome. Testicular feminization (syndrome)
E34.8 Other specified endocrine disorders. Dysfunction of the pineal gland. Progeria
E34.9 Endocrine disorder, unspecified.
Violation:
. endocrine NOS
. hormonal NOS

E35 Disorders of endocrine glands in diseases classified elsewhere

E35.0 Thyroid disorders in diseases classified elsewhere.
Thyroid tuberculosis (A18.8)
E35.1 Adrenal disorders in diseases classified elsewhere.
Addison's disease of tuberculous etiology (A18.7). Waterhouse-Friderichsen syndrome (meningococcal) (A39.1)
E35.8 Disorders of other endocrine glands in diseases classified elsewhere

malnutrition (E40-E46)

Note. The degree of malnutrition is usually assessed in terms of body weight, expressed in standard deviations from the mean value for the reference population. Lack of weight gain in children or evidence of decreased
A decrease in body weight in children or adults with one or more previous body weight measurements is usually an indicator of malnutrition. If there is evidence from only a single measurement of body weight, the diagnosis is based on assumptions and is not considered definitive unless other clinical and laboratory studies are performed. In exceptional cases, when there is no information about body weight, clinical data are taken as the basis. If an individual's body weight is below the mean for the reference population, then severe malnutrition is highly likely when the observed value is 3 or more standard deviations below the mean for the reference group; moderate malnutrition if the observed value is 2 or more but less than 3 standard deviations below the mean, and mild malnutrition if the observed body weight is 1 or more but less than 2 standard deviations below the mean for the reference group.

Excludes: intestinal malabsorption (K90.-)
nutritional anemia (D50-D53)
consequences of protein-energy malnutrition (E64.0)
wasting disease (B22.2)
starvation (T73.0)

E40 Kwashiorkor

Severe malnutrition accompanied by alimentary edema and pigmentation disorders of the skin and hair

E41 Alimentary insanity

Severe malnutrition accompanied by insanity
Excluded: senile kwashiorkor (E42)

E42 Marasmic kwashiorkor

Severe protein-energy malnutrition [as in E43]:
. intermediate form
. with symptoms of kwashiorkor and marasmus

E43 Severe protein-energy malnutrition, unspecified

Severe weight loss in a child or adult or no weight gain in a child that results in detectable weight being at least 3 standard deviations below the mean for the reference group (or similar weight loss reflected by other statistical methods) . If only a single measurement of body weight is available, severe wasting is highly likely when the detected body weight is 3 or more standard deviations below the mean for the reference population. hungry edema

E44 Moderate and mild protein-energy malnutrition

E44.0 Moderate protein-energy insufficiency. Weight loss in children or adults or lack of weight gain in a child that results in detectable body weight below the mean
for a reference population by 2 standard deviations or more but less than 3 standard deviations (or
similar weight loss reflected by other statistical methods). If only a single measurement of body weight is available, then moderate protein-energy malnutrition is highly likely when the detected body weight is 2 or more standard deviations below the mean for the reference population.

E44.1 Mild protein-energy malnutrition. Weight loss in children or adults or lack of weight gain in a child that results in detectable body weight below the mean
for a reference population by 1 or more but less than 2 standard deviations (or similar weight loss reflected by other statistical methods). If data from only a single measurement of body weight are available, then mild protein-energy malnutrition is highly likely when the detected body weight is 1 or more, but less than 2 standard deviations, below the mean for the reference population.

E45 Developmental delay due to protein-energy malnutrition

Alimentary:
. short stature (dwarfism)
. growth retardation
Delayed physical development due to malnutrition

E46 Protein-energy malnutrition, unspecified

Malnutrition NOS
Protein-energy imbalance NOS

OTHER MALNUTRITIONS (E50-E64)

Excludes: nutritional anemia (D50-D53)

E50 Vitamin A deficiency

Excludes: consequences of vitamin A deficiency (E64.1)

E50.0 Vitamin A deficiency with conjunctival xerosis
E50.1 Vitamin A deficiency with Byto's plaques and conjunctival xerosis. Bitot's plaque in a young child
E50.2 Vitamin A deficiency with corneal xerosis
E50.3 Vitamin A deficiency with corneal ulceration and xerosis
E50.4 Vitamin A deficiency with keratomalacia
E50.5 Vitamin A deficiency with night blindness
E50.6 Vitamin A deficiency with xerophthalmic corneal scars
E50.7 Other ocular manifestations of vitamin A deficiency. Xerophthalmia NOS
E50.8 Other manifestations of vitamin A deficiency.
Follicular keratosis) due to insufficiency
Xeoderma) vitamin A (L86)
E50.9 Vitamin A deficiency, unspecified. Hypovitaminosis A NOS

E51 Thiamine deficiency

Excludes: consequences of thiamine deficiency (E64.8)

E51.1 Take it.
Take take:
. dry form
. wet form (I98.8)
E51.2 Wernicke's encephalopathy
E51.8 Other manifestations of thiamine deficiency
E51.9 Thiamine deficiency, unspecified

E52 Nicotinic acid deficiency [pellagra]

Failure:
. niacin (-tryptophan)
. nicotinamide
Pellagra (alcoholic)
Excludes: consequences of nicotinic acid deficiency (E64.8)

E53 Deficiency of other B vitamins

Excludes: consequences of vitamin B deficiency (E64.8)
vitamin B12 deficiency anemia (D51.-)

E53.0 Riboflavin deficiency. Ariboflavinosis
E53.1 Pyridoxine deficiency. Vitamin B6 deficiency.
Excludes: pyridoxine-responsive sideroblastic anemia (D64.3)
E53.8 Deficiency of other specified B vitamins.
Failure:
. biotin
. cyanocobalamin
. folate
. folic acid
. pantothenic acid
. vitamin B12
E53.9 B vitamin deficiency, unspecified

E54 Ascorbic acid deficiency

Vitamin C deficiency. Scurvy.
Excludes: anemia due to scurvy (D53.2)
consequences of vitamin C deficiency (E64.2)

E55 Vitamin D deficiency

osteoporosis (M80-M81)
effects of rickets (E64.3)

E55.0 Rickets is active.
Osteomalacia:
. children's
. youthful
Excludes: rickets:
. intestinal (K90.0)
. Crown (K50.-)
. inactive (E64.3)
. renal (N25.0)
. vitamin D-resistant (E83.3)
E55.9 Vitamin D deficiency, unspecified. Avitaminosis D

E56 Deficiency of other vitamins

Excludes: consequences of other vitamin deficiencies (E64.8)

E56.0 Vitamin E deficiency
E56.1 Vitamin K deficiency.
Excludes: clotting factor deficiency due to vitamin K deficiency (D68.4)
vitamin K deficiency in newborn (P53)
E56.8 Deficiency of other vitamins
E56.9 Vitamin deficiency, unspecified

E58 Nutritional calcium deficiency

Excludes: disorders of calcium metabolism (E83.5)
consequences of calcium deficiency (E64.8)

E59 Alimentary deficiency of selenium

Keshan disease
Excludes: sequelae of selenium deficiency (E64.8)

E60 Nutritional zinc deficiency

E61 Insufficiency of other batteries

If necessary, to identify the medicinal product that caused the failure, use an additional external cause code (class XX).
Excludes: disorders of mineral metabolism (E83.-)
thyroid dysfunction associated with iodine deficiency (E00-E02)

E61.0 copper deficiency
E61.1 iron deficiency.
Excludes: iron deficiency anemia (D50.-)
E61.2 Magnesium deficiency
E61.3 Manganese deficiency
E61.4 Chromium deficiency
E61.5 Molybdenum deficiency
E61.6 Vanadium deficiency
E61.7 Deficiency of many nutrients
E61.8 Deficiency of other specified nutritional elements
E61.9 Deficiency of batteries, unspecified

E63 Other malnutrition

Excludes: dehydration (E86)
growth disorders (R62.8)
feeding problems of the newborn (P92. -)
consequences of malnutrition and other nutritional deficiencies (E64. -)

E63.0 Deficiency of essential fatty acids
E63.1 Unbalanced intake of food elements
E63.8 Other specified malnutrition
E63.9 Malnutrition, unspecified. Cardiomyopathy due to malnutrition NOS+ (I43.2)

E64 Sequelae of malnutrition and deficiencies of other nutrients

E64.0 Consequences of protein-energy insufficiency.
Excludes: developmental delay due to protein-energy malnutrition (E45)
E64.1 Consequences of vitamin A deficiency
E64.2 Consequences of vitamin C deficiency
E64.3 Consequences of rickets
E64.8 Consequences of other vitamin deficiencies
E64.9 Sequelae of nutritional deficiencies, unspecified

OBESITY AND OTHER OVERNUTRITION (E65-E68)

E65 Localized fat deposition

Fat pads

E66 Obesity

Excludes: adiposogenital dystrophy (E23.6)
lipomatosis:
. NOS (E88.2)
. painful [Dercum's disease] (E88.2)
Prader-Willi syndrome (Q87.1)

E66.0 Obesity due to excess intake of energy resources
E66.1 Obesity caused by medication.
If necessary, to identify the medicinal product, use an additional external cause code (class XX).
E66.2 Extreme obesity accompanied by alveolar hypoventilation. pickwick syndrome
E66.8 Other forms of obesity. Morbid obesity
E66.9 Obesity, unspecified. Simple obesity NOS

E67 Other types of power redundancy

Excludes: overeating NOS (R63.2)
consequences of overnutrition (E68)

E67.0 Hypervitaminosis A
E67.1 Hypercarotenemia
E67.2 Syndrome of megadoses of vitamin B6
E67.3 Hypervitaminosis D
E67.8 Other specified forms of overnutrition

E68 Consequences of oversupply

METABOLIC DISORDERS (E70-E90)

Excludes: androgen resistance syndrome (E34.5)
congenital adrenal hyperplasia (E25.0)
Ehlers-Danlos syndrome (Q79.6)
hemolytic anemias due to enzyme disorders (D55.-)
Marfan syndrome (Q87.4)
5-alpha-reductase deficiency (E29.1)

E70 Disorders of aromatic amino acid metabolism

E70.0 Classic phenylketonuria
E70.1 Other types of hyperphenylalaninemia
E70.2 Tyrosine metabolism disorders. Alkaptonuria. Hypertyrosinemia. Ochronosis. Tyrosinemia. Tyrosinosis
E70.3 Albinism.
Albinism:
. ophthalmic
. dermo-ocular
Syndrome:
. Chediaka (-Steinbrink) -Higashi
. cross
. Hermanski-Pudlaka
E70.8 Other metabolic disorders of aromatic amino acids.
Violations:
. histidine metabolism
. tryptophan metabolism
E70.9 Disorders of aromatic amino acid metabolism, unspecified

E71 Disorders of branched-chain amino acid metabolism and fatty acid metabolism

E71.0 Maple Syrup Disease
E71.1 Other types of metabolic disorders of branched chain amino acids. Hyperleucine isoleucinemia. Hypervalinemia.
Isovaleric acidemia. Methylmalonic acidemia. propionic acidemia
E71.2 Disorders of branched-chain amino acid metabolism, unspecified
E71.3 Fatty acid metabolism disorders. Adrenoleukodystrophy [Addison-Schilder].
Deficiency of muscle carnitine palmityltransferase.
Excludes: Refsum's disease (G60.1)
Schilder's disease (G37.0)
Zellweger syndrome (Q87.8)

E72 Other disorders of amino acid metabolism

Excludes: abnormal without evidence of disease (R70-R89)
violations:
. aromatic amino acid metabolism (E70. -)
. branched-chain amino acid metabolism (E71.0-E71.2)
. fatty acid metabolism (E71.3)
. metabolism of purines and pyrimidines (E79. -)
gout (M10.-)

E72.0 Amino acid transport disorders. cystinosis. Cystinuria.
Fanconi syndrome (-de Toni) (-Debre). Hartnap's disease. Low's syndrome.
Excludes: disorders of tryptophan metabolism (E70.8)
E72.1 Metabolic disorders of sulfur-containing amino acids. Cystationinuria.
Homocystinuria. Methioninemia. Deficiency of sulfite oxidase.
Excludes: transcobalamin II deficiency (D51.2)
E72.2 Urea cycle metabolic disorders. Argininemia. Argininosuccinic aciduria. Citrullinemia. Hyperammonemia.
Excludes: disorders of ornithine metabolism (E72.4)
E72.3 Metabolic disorders of lysine and hydroxylysine. Glutaric aciduria. Hydroxylysinemia. Hyperlysinemia
E72.4 Ornithine metabolism disorders. Ornithinaemia (types I, II)
E72.5 Glycine metabolism disorders. Hyperhydroxyprolinemia. Hyperprolinemia (types I, II). Non-ketone hyperglycinemia.
Sarcosinemia
E72.8 Other specified disorders of amino acid metabolism.
Violations:
. beta amino acid metabolism
. gamma-glutamyl cycle
E72.9 Amino acid metabolism disorders, unspecified

E73 Lactose intolerance

E73.0 Congenital lactase deficiency
E73.1 Secondary lactase deficiency
E73.8 Other types of lactose intolerance
E73.9 Lactose intolerance, unspecified

E74 Other disorders of carbohydrate metabolism

Excludes: increased secretion of glucagon (E16.3)
diabetes mellitus (E10-E14)
hypoglycemia NOS (E16.2)
mucopolysaccharidosis (E76.0-E76.3)

E74.0 Diseases of glycogen storage. Cardiac glycogenosis.
Disease:
. Andersen
. Corey
. Forbes
. Gersa
. McArdle
. pompe
. Tauri
. Gierke
Liver phosphorylase deficiency
E74.1 Fructose metabolism disorders. Essential fructosuria.
Fructose-1,6-diphosphatase deficiency. hereditary fructose intolerance
E74.2 Disorders of galactose metabolism. Galactokinase deficiency. Galactosemia
E74.3 Other disorders of absorption of carbohydrates in the intestine. Malabsorption of glucose-galactose.
Deficiency of sucrose.
Excludes: lactose intolerance (E73.-)
E74.4 Disorders of pyruvate metabolism and gluconeogenesis.
Failure:
. phosphoenolpyruvate carboxykinase
. pyruvate:
. carboxylase
. dehydrogenases
Excludes: with anemia (D55.-)
E74.8 Other specified disorders of carbohydrate metabolism. Essential pentosuria. Oxalosis. Oxaluria.
Renal glucosuria
E74.9 Disorder of carbohydrate metabolism, unspecified

E75 Disorders of sphingolipid metabolism and other lipid storage diseases

Excludes: mucolipidosis types I-III (E77.0-E77.1)
Refsum's disease (G60.1)

E75.0 Gangliosidosis-GM2.
Disease:
. Sendhoff
. Thea-Saxa
GM2 gangliosidosis:
. NOS
. adults
. juvenile
E75.1 Other gangliosidoses.
Gangliosidosis:
. NOS
. GM1
. GM3
Mucolipidosis IV
E75.2 Other sphingolipidoses.
Disease:
. Fabri(-Anderson)
. Gaucher
. Crabbe
. Niman-Peak
Faber syndrome. Metachromatic leukodystrophy. sulfatase deficiency.
Excludes: adrenoleukodystrophy (Addison-Schilder) (E71.3)
E75.3 Sphingolipidosis, unspecified
E75.4 Lipofuscinosis of neurons.
Disease:
. Batten
. Bilshovsky-Yansky
. Kufsa
. Spielmeier-Vogt
E75.5 Other disorders of lipid accumulation. Cerebrotendinous cholesterosis [Van Bogart-Scherer-Epstein]. Volman disease
E75.6 Lipid storage disease, unspecified

E76 Disorders of metabolism of glucosaminoglycans

E76.0 Mucopolysaccharidosis, type I.
Syndromes:
. Gurler
. Gurler-Sheie
. Sheye
E76.1 Mucopolysaccharidosis, type II. Gunther's syndrome
E76.2 Other mucopolysaccharidoses. Deficiency of beta-glucuronidase. Mucopolysaccharidoses types III, IV, VI, VII
Syndrome:
. Maroto-Lami (light) (heavy)
. Morchio (-similar) (classic)
. Sanfilippo (type B) (type C) (type D)
E76.3 Mucopolysaccharidosis, unspecified
E76.8 Other disorders of glycosaminoglycan metabolism
E76.9 Disorder of glycosaminoglycan metabolism, unspecified

E77 Disorders of glycoprotein metabolism

E77.0 Defects in post-translational modification of lysosomal enzymes. Mucolipidosis II.
Mucolipidosis III [Hurler pseudopolydystrophy]
E77.1 Defects in the degradation of glycoproteins. Aspartyl glucosaminuria. Fucosidosis. Mannosidosis. Sialidosis [mucolipidosis I]
E77.8 Other disorders of glycoprotein metabolism
E77.9 Disorders of glycoprotein metabolism, unspecified

E78 Disorders of lipoprotein metabolism and other lipidemias

Excludes: sphingolipidosis (E75.0-E75.3)
E78.0 pure hypercholesterolemia. Familial hypercholesterolemia. Hyperlipoporteinemia Fredrickson, type Iia.
Hyper-beta-lipoproteinemia. Hyperlipidemia, group A. Hyperlipoproteinemia with low-density lipoprotein
E78.1 pure hyperglyceridemia. endogenous hyperglyceridemia. Hyperlipoporteinemia Fredrickson, type IV.
Hyperlipidemia, group B. Hyperpre-beta-lipoproteinemia. Hyperlipoproteinemia with very low lipoproteins
density
E78.2 Mixed hyperlipidemia. Extensive or floating beta-lipoproteinemia.
Hyperlipoporteinemia Fredrickson, types IIb or III. Hyperbetalipoproteinemia with pre-beta lipoproteinemia.
Hypercholesterolemia with endogenous hyperglyceridemia. Hyperlipidemia, group C. Tuboeruptive xanthoma.
Tuberous xanthoma.
Excludes: cerebrotendinous cholesterosis [Van Bogart-Scherer-Epstein] (E75.5)
E78.3 Hyperchylomicronemia. Hyperlipoporteinemia Fredrickson, types I or V.
Hyperlipidemia, group D. Mixed hyperglyceridemia
E78.4 Other hyperlipidemias. Familial combined hyperlipidemia
E78.5 Hyperlipidemia, unspecified
E78.6 Lack of lipoproteins. A-beta-lipoproteinemia. Deficiency of high density lipoproteins.
Hypo-alpha-lipoproteinemia. Hypo-beta-lipoproteinemia (familial). Deficiency of lecithincholesterol acyltransferase. Tangier disease
E78.8 Other disorders of lipoprotein metabolism
E78.9 Disorders of lipoprotein metabolism, unspecified

E79 Disorders of purine and pyrimidine metabolism

Excludes: kidney stone (N20.0)
combined immunodeficiencies (D81.-)
gout (M10.-)
orotaciduric anemia (D53.0)
xeroderma pigmentosum (Q82.1)

E79.0 Hyperuricemia without signs of inflammatory arthritis and gouty nodes. Asymptomatic hyperuricemia
E79.1 Lesch-Nychen syndrome
E79.8 Other metabolic disorders of purines and pyrimidines. hereditary xanthinuria
E79.9 Disturbance of purine and pyrimidine metabolism, unspecified

E80 Disorders of porphyrin and bilirubin metabolism

Includes: catalase and peroxidase defects

E80.0 Hereditary erythropoietic porphyria. Congenital erythropoietic porphyria.
Erythropoietic protoporphyria
E80.1 Porphyria cutaneous slow
E80.2 Other porphyrias. hereditary coproporphyria
Porfiria:
. NOS
. acute intermittent (hepatic)
If it is necessary to identify the cause, use an additional external cause code (class XX).
E80.3 Catalase and peroxidase defects. Acatalasia [Takahara]
E80.4 Gilbert's syndrome
E80.5 Crigler-Najjar Syndrome
E80.6 Other disorders of bilirubin metabolism. Dubin-Johnson Syndrome. Rotor syndrome
E80.7 Disorder of bilirubin metabolism, unspecified

E83 Disorders of mineral metabolism

Excludes: malnutrition (E58-E61)
parathyroid disorders (E20-E21)
vitamin D deficiency (E55.-)

E83.0 Copper metabolism disorders. Menkes disease [curly hair disease] [steel hair]. Wilson's disease
E83.1 Iron metabolism disorders. Hemochromatosis.
Excludes: anemia:
. iron deficiency (D50. -)
. sideroblastic (D64.0-D64.3)
E83.2 Disorders of zinc metabolism. Enteropathic acrodermatitis
E83.3 Phosphorus metabolism disorders. Acid phosphatase deficiency. Familial hypophosphatemia. Hypophosphatasia.
Vitamin D resistant:
. osteomalacia
. rickets
Excl.: adult osteomalacia (M83.-)
osteoporosis (M80-M81)
E83.4 Magnesium metabolism disorders. Hypermagnesemia. Hypomagnesemia
E83.5 Calcium metabolism disorders. Familial hypocalciuric hypercalcemia. Idiopathic hypercalciuria.
Excludes: chondrocalcinosis (M11.1-M11.2)
hyperparathyroidism (E21.0-E21.3)
E83.8 Other disorders of mineral metabolism
E83.9 Mineral metabolism disorder, unspecified

E84 Cystic fibrosis

Includes: cystic fibrosis

E84.0 Cystic fibrosis with pulmonary manifestations
E84.1 Cystic fibrosis with intestinal manifestations. Meconium ileus(P75)
E84.8 Cystic fibrosis with other manifestations. Cystic fibrosis with combined manifestations
E84.9 Cystic fibrosis, unspecified

E85 Amyloidosis

Excludes: Alzheimer's disease (G30.-)

E85.0 Hereditary familial amyloidosis without neuropathy. Familial Mediterranean fever.
hereditary amyloid nephropathy
E85.1 Neuropathic hereditary familial amyloidosis. Amyloid polyneuropathy (Portuguese)
E85.2 Hereditary familial amyloidosis, unspecified
E85.3 Secondary systemic amyloidosis. Amyloidosis associated with hemodialysis
E85.4 limited amyloidosis. Localized amyloidosis
E85.8 Other forms of amyloidosis
E85.9 Amyloidosis, unspecified

E86 Reducing the volume of liquid

Dehydration. Decreased volume of plasma or extracellular fluid. hypovolemia
Excludes: dehydration of newborn (P74.1)
hypovolemic shock:
. NOS (R57.1)
. postoperative (T81.1)
. traumatic (T79.4)

E87 Other disorders of water-salt metabolism or acid-base balance

E87.0 Hyperosmolarity and hypernatremia. Excess sodium. Sodium overload
E87.1 Hypoosmolarity and hyponatremia. Sodium deficiency.
Excludes: syndrome of impaired secretion of antidiuretic hormone (E22.2)
E87.2 Acidosis.
Acidosis:
. NOS
. lactic acid
. metabolic
. respiratory
Excludes: diabetic acidosis (E10-E14 with common fourth character.1)
E87.3 Alkalosis.
Alkalosis:
. NOS
. metabolic
. respiratory
E87.4 Mixed acid-base imbalance
E87.5 Hyperkalemia. Excess potassium [K]. Potassium overload [K]
E87.6 Hypokalemia. Potassium deficiency [K]
E87.7 Hypervolemia.
Excludes: edema (R60.-)
E87.8 Other disorders of water-salt balance, not elsewhere classified.
Electrolyte imbalance NOS. Hyperchloremia. Hypochloremia

E88 Other metabolic disorders

Excludes: histiocidosis X (chronic) (D76.0)
If necessary, to identify the drug that caused the metabolic disorder, use an additional code of external causes (class XX).

E88.0 Disorders of plasma protein metabolism, not elsewhere classified. Alpha-1 antitrypsin deficiency.
Bis-albuminemia.
Excludes: disorders of lipoprotein metabolism (E78.-)
monoclonal gammopathy (D47.2)
polyclonal hyper-gamma globulinemia (D89.0)
Waldenström's macroglobulinemia (C88.0)
E88.1 Lipodystrophy, not elsewhere classified. Lipodystrophy NOS.
Excludes: Whipple's disease (K90.8)
E88.2 Lipomatosis, not elsewhere classified.
Lipomatosis:
. NOS
. painful [Derkum's disease]
E88.8 Other specified metabolic disorders. Adenolipomatosis Lonua-Bansod. Trimethylaminuria
E88.9 Metabolic disorder, unspecified

E89 Endocrine and metabolic disorders following medical procedures, not elsewhere classified

E89.0 Hypothyroidism following medical procedures.
Radiation-induced hypothyroidism. Postoperative hypothyroidism
E89.1 Hypoinsulinemia after medical procedures. Hyperglycemia after removal of the pancreas.
Hypoinsulinemia postoperative
E89.2 Hypoparathyroidism following medical procedures. Parathyroid tetany
E89.3 Hypopituitarism after medical procedures. Radiation-induced hypopituitarism
E89.4 Ovarian dysfunction following medical procedures
E89.5 Testicular hypofunction following medical procedures
E89.6 Hypofunction of the adrenal cortex (medulla) after medical procedures
E89.8 Other endocrine and metabolic disorders resulting from medical procedures
E89.9 Endocrine and metabolic disorder occurring after medical procedures, unspecified

Obesity(lat. adipositas- literally: "obesity" and lat. obesitas- literally: fullness, obesity, fattening) - the deposition of fat, an increase in body weight due to adipose tissue. Adipose tissue can be deposited both in places of physiological deposits, and in the area of ​​​​the mammary glands, hips, and abdomen.

Obesity is divided into degrees (according to the amount of adipose tissue) and types (depending on the reasons that led to its development). Obesity leads to an increased risk of developing diabetes, hypertension and other diseases associated with being overweight. The causes of excess weight also affect the distribution of adipose tissue, the characteristics of adipose tissue (softness, firmness, percentage of fluid content), as well as the presence or absence of skin changes (stretching, enlarged pores, the so-called "cellulite").

What Causes Obesity:

Obesity can develop as a result of:

• imbalance between food intake and energy expended, that is, increased food intake and reduced energy expenditure;
• obesity of non-endocrine pathology appears due to disorders in the systems of the pancreas, liver, small and large intestines;
• genetic disorders.

Predisposing Factors for Obesity

• Sedentary lifestyle
• Genetic factors, in particular:
  • Increased activity of lipogenesis enzymes
  • Decreased activity of lipolysis enzymes
• Increased intake of easily digestible carbohydrates:
  • drinking sweet drinks
  • a diet rich in sugars
• Certain diseases, in particular endocrine diseases (hypogonadism, hypothyroidism, insulinoma)
• Eating disorders (for example, binge eating disorder), in Russian literature called eating disorders, a psychological disorder leading to an eating disorder
• Tendency to stress
• sleep deprivation
• Psychotropic drugs

In the process of evolution, the human body has adapted to accumulate a supply of nutrients in conditions of an abundance of food in order to use this reserve in conditions of a forced absence or restriction of food - a kind of evolutionary advantage that made it possible to survive. In ancient times, fullness was considered a sign of well-being, prosperity, fertility and health. An example is the sculpture "Venus of Willendorf" (Venus of Willendorf), dated to the 22nd millennium BC. e. (perhaps the earliest known illustration of obesity).

Viruses

Human infection with adenovirus-36 (Ad-36) ( for a long time was considered the causative agent of respiratory and eye diseases) converts mature stem cells of adipose tissue into fat cells; moreover, those cells in which the virus was not detected remained unchanged.

Pathogenesis (what happens?) during Obesity:

The regulation of the deposition and mobilization of fat from fat depots is carried out by a complex neurohormonal mechanism (cerebral cortex, subcortical formations, sympathetic and parasympathetic nervous system and endocrine glands). The main role in the pathogenesis of obesity is played by dysfunctions of the central nervous mechanisms - the cerebral cortex and hypothalamus (hypothalamus), where the centers that regulate appetite are located. Disruption of coordination between energy consumption and appetite, which determines the arrival of energy material and the intensity of metabolic processes, causes the accumulation of fat. Apparently, the functional state of the centers that regulate eating behavior may have congenital features or acquired (brought up) from childhood in connection with the lifestyle of the family, the nature of nutrition, etc. Disturbances in the functional state of the hypothalamic centers that regulate appetite may also be a consequence of inflammatory process or injuries, accompanied by damage to the hypothalamus.

In the pathogenesis of obesity, one cannot but attach importance to the endocrine organs and, above all, to the pituitary gland, adrenal glands, pancreatic islet apparatus, thyroid and gonads.

An increase in the functional activity of the pituitary - adrenal cortex and insular apparatus of the pancreas contributes to the accumulation of fat in fat depots. A decrease in the somatotropic activity of the adenohypophysis, accompanied by a weakening of the processes of fat mobilization from the depot and its subsequent oxidation in the liver, also acts as a pathogenetic factor, especially in the alimentary-constitutional form of obesity. A certain pathogenetic role in hypothalamic-pituitary obesity is played by the thyroid gland (due to a lack of thyroid hormones, the release of fat from fat depots and its oxidation in the liver is inhibited).

Reduced production of adrenaline - an active lipolytic factor - is essential in reducing fat mobilization and is one of the pathogenetic factors of obesity. The role of the gonads in the pathogenesis of primary obesity has not been studied enough.

Obesity Symptoms:

Clinical manifestations of different types of obesity are basically similar. There are differences in the distribution of excess body fat and in the presence or absence of symptoms of damage to the nervous or endocrine system.

Most common alimentary obesity, usually in individuals with a hereditary predisposition to be overweight. It develops in cases where the caloric content of food exceeds the energy expenditure of the body, and is observed, as a rule, in several members of the same family. This type of obesity is more common in middle-aged and older women, leading sedentary image life. When collecting an anamnesis with a detailed clarification of the daily diet, it is usually established that patients systematically overeat. For alimentary obesity is characterized by a gradual increase in body weight. Subcutaneous adipose tissue is distributed evenly, sometimes accumulates to a greater extent in the abdomen and thighs. There are no signs of damage to the endocrine glands.

hypothalamic obesity observed in diseases of the central nervous system with damage to the hypothalamus (with tumors, as a result of injuries, infections). This type of obesity is characterized by the rapid development of obesity. The deposition of fat is noted mainly on the abdomen (in the form of an apron), buttocks, thighs. Often there are trophic changes in the skin: dryness, white or pink stretch marks (stretch marks). Clinical symptoms (eg. headache, sleep disorders) and the data of a neurological examination of the patient usually manages to establish the pathology of the brain. As a manifestation of hypothalamic disorders, along with obesity, various signs of autonomic dysfunction are observed - increased blood pressure, impaired sweating, etc.

endocrine obesity develops in patients with certain endocrine diseases (for example, hypothyroidism, Itsenko-Cushing's disease), the symptoms of which predominate in clinical picture. On examination, along with obesity, which is usually characterized by uneven deposition of fat on the body, other signs of hormonal disorders (for example, masculinization or feminization, gynecomastia, hirsutism) are revealed, and striae are found on the skin.

A peculiar type of obesity is the so-called painful lipomatosis(Derkum's disease), which is characterized by the presence of fatty nodes, painful on palpation.

In patients obesity II-IV degrees there are changes in the cardiovascular system, lungs, digestive organs. Often observed tachycardia, muffled heart tones, increased blood pressure. Sometimes respiratory failure and chronic cor pulmonale develop due to the high standing of the diaphragm. Most obese patients have a tendency to constipation, the liver is enlarged due to fatty infiltration of its parenchyma, symptoms of chronic cholecystitis and pancreatitis are often detected. Pain in the lower back, arthrosis of the knee and ankle joints are noted. Obesity is also accompanied by menstrual irregularities, amenorrhea is possible. Obesity is a risk factor for the development of diabetes mellitus, atherosclerosis, hypertension, coronary heart disease, with which it is often combined.

Obesity in children, as in adults, develops against the background of hereditary characteristics or as a result of acquired metabolic and energy disorders. Obesity is most often observed in the 1st year of life and at 10-15 years. As in adults, exogenous-constitutional obesity is more common in children, which is based on a hereditary (constitutional) predisposition to excessive fat deposition, often combined with family tendencies to overeat and overfeed children. Excess fat deposition usually begins as early as the 1st year of life and is not equally common in boys and girls. Girls are born with already more developed subcutaneous adipose tissue than boys; with age, this difference increases, reaching a maximum in adults, and causes a greater incidence of obesity in girls and women.

In children aged 10-15 years, the most common cause of obesity is the hypothalamic syndrome of puberty, which is characterized by the appearance of thin striae on the skin of the thighs, mammary glands, buttocks, and the inner surface of the shoulders. There is usually a transient increase in blood pressure; in some cases, signs of increased intracranial pressure are found. Less often, the cause of hypothalamic obesity in children is the consequences of a traumatic brain injury, neuroinfection.

Obesity Diagnosis:

The most commonly used diagnostic criterion for obesity is the determination of excess total body weight in relation to the norm, established statistically. However, to determine the severity of the disease, it is not so much an excess of total body weight that is important, but an excess of adipose tissue mass, which can differ significantly even in individuals of the same age, height and body weight. In this regard, the development and implementation in the clinic of diagnostic methods for determining body composition and specifically fat mass is quite relevant.

The starting point in determining the degree of obesity is the concept of normal body weight. Normal body weight is determined according to special tables, taking into account gender, height, body type and age, and is the average value corresponding to each group.

Along with the concept of normal body weight, the concept of ideal body weight is of great importance in the clinic. This indicator was developed by order of health insurance companies and was supposed to determine at what body weight insured events (illness or death) are the least likely. It turned out that the body weight at which life expectancy is maximum is about 10% less than normal body weight. The ideal body weight is determined taking into account the human constitution (normosthenic, asthenic and hypersthenic). Exceeding this value is considered overweight. Obesity is said to be in cases where excess body weight is more than 10%.

A number of methods have been proposed for calculating ideal body weight. The simplest formula was proposed by the anthropologist and surgeon Brock (1868):

Mi = R- 100 ,

Where Mi- ideal body weight, kg, R- height, see

Depending on the value of this indicator, 4 degrees of obesity are distinguished: the 1st degree of obesity corresponds to an excess of ideal body weight by 15-29%, the 2nd degree - by 30-49%, the 3rd - by 50-99%, 4- I am more than 100%.

Currently, the most widely used indicator of the degree of obesity is the body mass index (BMI), or Quetelet index:

BMI \u003d Body weight (kg) / height (m 2).

It is believed that for people aged 20-55 years who have a height close to the average (men - 168-188 cm, women - 154-174 cm), BMI quite accurately reflects the situation. Most studies on the relationship of body weight with morbidity and mortality confirm that the maximum allowable body weight corresponds to a BMI of 25 kg/m 2 .

Classification of excess mbody scores in adults depending on BMI (WHO report, 1998)

Measurement of the circumference of the waist and hips. Of great clinical importance is not only the severity of obesity, but also the distribution of fat. It must be determined primarily in patients with average overweight, since this does not take into account BMI. It is believed that the risk of complications in obesity to a greater extent depends not on excess body weight, but on the localization of adipose tissue deposits. The amount of visceral fat can be measured using MRI. However, a simpler and more accurate measure of fat distribution is the waist-to-hip ratio (WHT).

Measurement of WTP is important in determining body fat deposition, which is of particular importance in assessing the risk of morbidity. Depending on the distribution of fat, two types of obesity are distinguished: android and ganoid. android, or apple-shaped obesity is called the distribution of fat around the waist. The deposition of fat around the buttocks and thighs is known as hypoid, or obesity in the form of a pear. In the case of android fat distribution, the likelihood of morbidity and mortality is higher than in the ganoid type. With the deposition of the bulk of fat on the trunk and in the abdominal cavity, the likelihood of complications associated with obesity (hypertension, ischemic disease heart disease, type 2 diabetes). It is believed that normally in women the OTB does not exceed 0.8, and in men - 1, the excess of these parameters is associated with metabolic disorders. If the waist circumference in men reaches 102 cm, and in women - 88 cm, in this case there is a serious risk of increasing the risk of morbidity and weight loss should be recommended (Table 40.3).

Definition of overweight and obesity by waist circumference (cm)

Obesity Treatment:

Basic treatments for overweight and obesity

• These include adherence to a diet with a high content of fiber, vitamins and other biologically active components(cereals and whole grains, vegetables, fruits, nuts, herbs, etc.) and limiting the intake of easily digestible carbohydrates (sugar, sweets, pastries, bakery and pasta products from high-grade flour), as well as physical exercises.
• General approach for drug treatment obesity is to test all known drugs for the treatment of obesity. For this purpose, drugs are used to treat obesity.
• If the result of drug treatment is insignificant or absent, then it is necessary to stop such treatment.

Then the question of surgical treatment is considered. Liposuction - as an operation during which fat cells are sucked off, is currently used not to combat obesity, but only for cosmetic correction of local small fat deposits. Although the amount of fat and body weight after liposuction may decrease, but, according to a recent study by British doctors, such an operation is useless for health. Apparently, not subcutaneous, but visceral fat, located in the omentum, as well as around internal organs located in the abdominal cavity. Previously, isolated attempts were made to do liposuction for weight loss (the so-called megaliposuction with the removal of up to 10 kg of fat), but at present it is abandoned as an extremely harmful and dangerous procedure, inevitably giving a lot of serious complications and leading to gross cosmetic problems in the form of uneven body surface .

Diets often increase obesity. The reason is that a rigid diet (dramatic reduction in calorie intake) can help you lose weight quickly, but after stopping the diet, appetite increases, food digestibility improves, and weight gain is greater than before the diet. If an obese person tries to lose weight again with a strict diet, each time losing weight becomes more difficult, and gaining weight becomes easier, and the weight gained increases each time. Therefore, diets focused on quick results (lose as much weight as possible in a short time) are a harmful and dangerous practice. In addition, many weight loss products contain diuretics and laxatives, resulting in water loss rather than fat loss. Loss of water is useless to fight obesity, it is harmful to health, and weight is restored after stopping the diet.

Moreover, according to a study by American psychologist Tracey Mann and her colleagues, diets are generally useless as a means of combating obesity.

However, it should be noted that without adequate control of the calorie content of food and taking into account the adequacy of the amount of incoming calories to physical activity, successful treatment of obesity is impossible. For successful weight loss, the WHO recommends calculating habitual calorie intake and then reducing calories by 500 kcal each month until reaching a figure 300-500 kcal below adequate energy intake. For persons not engaged in active physical labor, this value is 1500-2000 kcal.

Surgery morbid obesity

Long-term studies have shown that surgery (bariatric surgery) has the maximum effect in the treatment of obesity. Only surgical treatment makes it possible to solve this problem definitively. Currently, the world uses mainly two types of surgery for obesity. In the USA and Canada, gastric bypass is used in the form of Roux-en-Y gastric bypass (90% of all operations). It makes it possible to get rid of 70-80% of excess weight. In Europe and Australia, adjustable gastric banding dominates (90% of all operations), which makes it possible to get rid of 50-60% of excess weight.

Currently, all bariatric operations are performed laparoscopically (that is, without incision, through punctures) under the control of a miniature optical system.

Operative treatment of obesity has strict indications, it is not intended for those who believe that they are simply overweight. It is believed that indications for surgical treatment of obesity occur with a BMI above 40. However, if the patient has problems such as type 2 diabetes, hypertension, varicose veins and problems with the joints of the legs, indications already arise with a BMI of 35. Recently, studies have appeared in the international literature that have studied the effectiveness of gastric banding in patients with a BMI of 30 or more.

Obesity Prevention:

Prevention of obesity is to eliminate hypodynamia and rational nutrition. Children need to follow the rules of feeding and regularly monitor the physical development of the child by systematically measuring height and body weight (especially with a constitutional predisposition to obesity). Early detection and treatment of diseases accompanied by hypothalamic and endocrine obesity is important.

Currently, the terms "obesity in children" and "overweight" are used equally often in pediatrics, with the term "overweight" being more preferable.

Obesity (lat. adipositas, alimentary obesity) - a chronic eating disorder characterized by excessive accumulation of adipose tissue in the body.

ICD-10 codes

• E65-E68. Obesity and other types of overnutrition.
• E66. Obesity.
• E66.0. Obesity due to excess intake of energy resources.
• E66.8. Other forms of obesity.
• E66.9. Obesity, unspecified.
• E68. Consequences of overnutrition.

Epidemiology of childhood obesity

In economically developed countries, including Russia, 16% of children are already obese and 31% are at risk for the formation of this pathology, which occurs more often in girls than in boys.

According to the WHO Regional Office for Europe (2007), over the past twenty years, the prevalence of obesity has increased 3 times, reaching epidemic proportions. According to epidemiological studies, in the presence of obesity in the father, the probability of its development in children is 50%, in the presence of this pathology in the mother - 60%, and in the presence of both parents - 80%.

The causes of the obesity epidemic are considered to be a change in the composition of the diet (increased consumption of energy-rich foods), eating habits (eating in fast foods, frequent use of ready-made breakfast cereals), insufficient consumption of fruits and vegetables, and a sharp decrease in physical activity.

What causes obesity in children?

In the vast majority of children, obesity is not associated with hereditary or endocrine diseases, although the role of hereditary predisposition to obesity is considered established. The leading role in the formation of a positive energy balance is played by genetically determined features of metabolism and the structure of adipose tissue:

• increased number of adipocytes and their accelerated differentiation from fibroblasts;
• congenital increased activity of lipogenesis enzymes and reduced - lipolysis;
• increased intensity of fat formation from glucose;
• reduced formation of leptin in adipocytes or a defect in leptin receptors.

The pathogenesis of obesity

One of the main pathogenetic mechanisms for the development of obesity in children is an energy imbalance: energy consumption exceeds energy consumption. As it is currently established, the pathogenesis of obesity is based not only on energy, but also on nutrient imbalance. Obesity in children progresses if the body is not able to ensure the oxidation of incoming fat.

Obesity in children: types

Obesity in children currently does not have a generally accepted classification. In adults, the diagnosis of obesity is based on the calculation of BMI [the ratio of body weight (in kilograms) to a person's height (in meters) squared]. BMI can overestimate the obesity of trained athletes or muscular children, however, BMI calculation is the most reliable and reliable method for determining overweight. Other methods for assessing obesity are also used, but they are either very expensive (ultrasound, CT, MRI, x-ray absorptiometry), or require special equipment (caliper), or are poorly reproduced (measurement of waist and hips), or do not have standards for childhood(bioelectric impedance analysis).

How to recognize obesity in children?

Obesity in children is not associated with specific changes in outcomes general analysis blood and urinalysis. A biochemical blood test detects:

• increased levels of cholesterol, triglycerides, low-density lipoproteins, free fatty acids;
• decrease in the content of high density lipoproteins;
• acidosis;
• hyperinsulinemic type of glycemic curve.

Obesity screening

Systematic (once a quarter) monitoring of weight and growth indicators with the determination of BMI, as well as blood pressure.

Treatment of obesity in children

Obesity in children should be treated with the following goals - to achieve an energy balance between energy intake and energy expenditure. The criterion for the effectiveness of the treatment of obesity in children is weight loss. Necessary condition diet therapy in all age groups - calculation of nutrition in terms of proteins, fats, carbohydrates, as well as calories with a comparison of actual and recommended consumption.

Chronic, lifelong, multifactorial, genetically determined, life-threatening disease caused by the accumulation of excess body fat, leading to serious medical, psychosocial, physical and economic consequences.

The role of obesity in the development of cancer of the mammary glands, uterus, prostate, and colon is known. Obesity is accompanied by a decrease in physical and mental performance up to complete disability, deprives patients of the opportunity to lead a normal life, leads to social disadaptation and the development of depressive conditions in them.

ICD-10 CODES

E66.0. Obesity due to excess intake of energy resources.
E66.1. Obesity due to medication.
E66.2. Extreme obesity accompanied by alveolar hypoventilation.
E66.8. Other forms of obesity.
E66.9. Obesity, unspecified.

obesity surgery, or bariatric surgery(from Greek baros - heavy, fat, weighty) - a relatively young field of surgical gastroenterology, the subject of which is morbid(morbid) obesity, ie. clinical manifestations of the disease.

Obesity related diseases

Obesity is the most important cause of the development of arterial hypertension, sleep apnea syndrome, type 2 diabetes mellitus, diseases of the joints, spine, veins of the lower extremities, digestive tract, sexual disorders, infertility, as well as a complex of metabolic disorders, united by the concept "metabolic syndrome"(syndrome-X, insulin resistance syndrome).

The development of the metabolic syndrome, described in 1988 by G. Riven, is based on abdominal obesity and the state of insulin resistance that develops against this background, which in turn determines the development of type 2 diabetes mellitus, arterial hypertension, atherogenic dyslipidemia, coagulopathy, urinary metabolism disorders. acids, etc. An inevitable consequence of this complex and interrelated complex of disorders is the development of atherosclerosis and cardiovascular diseases(the main cause of death in the population).

Epidemiology

At the end of the 20th century, the WHO described obesity as a non-communicable epidemic.

In industrialized countries, morbid obesity affects from 2 to 6% of the population, which is 1,700,000 people on the planet; Two-thirds of the US population is overweight, with one in five adults and one in seven teenagers being morbidly obese. The cause of death of more than 700,000 people in the US and 1,000,000 people in Europe every year is obesity. In the structure of European mortality, 13% of cases are associated with obesity.

Over the past 20 years in Europe, the incidence of obesity has tripled, and now about half of adults and one in five children are overweight. Compared with the situation in 1970, the incidence of obesity among children has increased 10 times.

obesity classification

The main criterion for determining the stage of obesity, as well as approaches to its treatment (Table 70-1), is the body mass index (BMI), determined by the formula:

BMI = weight (kg) / height 2 (m 2).

Table 70-1. Classification and principles of treatment of obesity

Body mass index, kg / m 2	State characteristic	Treatment
18-25	normal body weight	Not required
25-30	Overweight	Self-restriction in food, increased physical activity
30-35	Obesity I degree (initial)	Conservative treatment, including medication, in case of ineffectiveness - installation of an intragastric balloon
35-40	Obesity II degree (expressed)	Conservative treatment, installation of a balloon, in the presence of concomitant diseases - surgical intervention
40-50	Obesity III degree (morbid)	If conservative measures fail, surgery is performed.
Over 50	Obesity IV degree (superobesity)	Surgery; a significant proportion of patients require preoperative preparation

Principles of obesity treatment

Medical treatment of obesity

On early stages the development of obesity (with a BMI up to 35 kg / m 2) are used conservative methods treatment(diet therapy, psychotherapy, prescribing exercise, drug treatment), but they do not always restrain the progression of the disease and provide a stable result.

Principles rational nutrition and diet therapy for obesity are well defined, but most patients are unable to radically change their lifestyle:

• lifelong introduction of strict self-restrictions in food;
• systematic control of the energy content of the diet;
• increase in physical activity.

With the progression of obesity, secondary hormonal and metabolic disorders develop (hyperinsulinemia, hyperleptinemia, hyperglycemia, dyslipidemia), resulting in a constantly increasing need for food and fluids. All this, combined with a progressive decrease in physical activity, determines an uncontrolled, avalanche-like increase in body weight at the stage of morbid obesity.

Treating obesity as a lifelong disease involves a dual challenge:effective and clinically significant weight loss at the first stage and maintaining the result throughout life, which is the most difficult. Previously, it was shown that with obesity with a BMI of more than 35-40 kg/m 2 conservative methods of treatment are ineffective in the long term: 90-95% of patients restore body weight to the previous level within the first year.

Surgery

Surgical interventions on the digestive tract for obesity have been known since the early 1950s.

In order to reduce body weight in 1953, V. Henriksson (Sweden) conducted two patients large area resection small intestine .

Due to the irreversible nature of the changes in the intestinal tract, this operation has not gained popularity. In the 1960s and 1970s it was common jejunoileoshunt surgery. Due to a sharp decrease in the absorptive surface of the small intestine after surgery, a significant steady loss of body weight was observed, and an effective correction of hypercholesterolemia was also noted. At the same time, the study of long-term results showed that they were achieved at the cost of severe water and electrolyte imbalance, hypoproteinemia, liver failure, nephrolithiasis, and polyarthralgia due to anaerobic bypass enteritis in the small intestine excluded from the passage. Currently, jejunoileoshunting is used extremely rarely.

As a historically passed stage, various modifications should be considered horizontal gastroplasty that were popular in the 1980s. Their essence was reduced to a transverse (horizontal) stitching of the stomach with the help of a stapler, leaving a narrow exit from its small part to the large one. Due to the insufficient and unstable effect, as well as due to the relatively high frequency of late complications and reoperations, the number of supporters of vertical gastroplasty and non-adjustable gastric banding has significantly decreased over time.

Yu.I. Yashkov