Научная статья на тему 'THE VALUE OF LABORATORY INDICATORS ESTIMATION IN PATIENTS WITH METABOLICALLY HEALTHY OBESITY: ANALYSIS OF A CLINICAL CASE WITH LITERATURE REVIEW'

THE VALUE OF LABORATORY INDICATORS ESTIMATION IN PATIENTS WITH METABOLICALLY HEALTHY OBESITY: ANALYSIS OF A CLINICAL CASE WITH LITERATURE REVIEW Текст научной статьи по специальности «Клиническая медицина»

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Ключевые слова
metabolically healthy obesity / metabolically unhealthy obesity / metabolic syndrome / laboratory indicators / метаболічно здорове ожиріння / метаболічно нездорове ожиріння / метаболічний синдром / лабораторні показники

Аннотация научной статьи по клинической медицине, автор научной работы — Holubkina Yevheniia, Skokova Nataliia, Tykhonova Tetiana

Introduction. Obesity currently is a relevant issue of modern medicine due to its global prevalence, heterogeneity of clinical and laboratory manifestations, as well as the association with various comorbid conditions. Depending on the metabolic status, metabolically unhealthy obesity (MUO) and metabolically healthy obesity (MHO) are distinguished. MUO is defined with the presence of criteria for metabolic syndrome (MS) and is associated with an increased risk of cardiovascular and metabolic complications. MHO is characterized by a «metabolically healthy» profile, but the probability of a favorable course of the disease is controversial; many studies indicate the instability of the MHO phenotype and the possibility of further development of MUO. The aim of study: to analyze the features of laboratory indicators associated with MHO and determine the risk factors for the MUO development on the example of a clinical case. Materials and methods. A clinical case of 24 year old female patient diagnosed with alimentary-constitutional obesity class III. Objectively: height – 174 cm, weight – 124.7 kg, body mass index (BMI) – 41.21 kg/m2, waist circumference – 107 cm, hips circumference – 144 cm; white striae on the abdomen; excessive subcutaneous fat stores, mostly distributed in the abdomen, thighs; blood pressure (BP) – 125/80 mm Hg. Investigation data: hyperleptinemia – 86.82 ng/ml, increased level of HOMA index – 4.6, hyperuricemia – 6.8 mg/dl, vitamin D deficiency – 9.19 ng/ml; lipid profile, fasting plasma glucose, glycated haemoglobin (HbA1c), thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), anti-thyroid peroxidase (anti-TPO) antibodies, cortisol, blood electrolytes, liver function tests – within normal limits. Electrocardiography (ECG), ultrasound of the heart and abdominal organs – without pathology. Results. Normal indicators of lipid metabolism, blood glucose and BP measurement in our patient are characteristic for MHO. However, the combination of hyperleptinemia with insulin resistance, hyperuricemia and vitamin D3 deficiency indicate metabolic and hormonal imbalance and are considered as a risk factors for the development of MS and the further transition of MHO to MUO. Conclusion. MHO should be considered as a transient state, the management of such patients requires careful laboratory monitoring with early detection of metabolic disorders and its adequate and timely correction.

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ЗНАЧЕННЯ ОЦІНКИ ЛАБОРАТОРНИХ ПОКАЗНИКІВ У ПАЦІЄНТІВ З МЕТАБОЛІЧНО ЗДОРОВИМ ОЖИРІННЯМ: АНАЛІЗ КЛІНИЧНОГО ВИПАДКУ З ОГЛЯДОМ ЛІТЕРАТУРИ

Вступ. В даний час ожиріння є актуальною проблемою сучасної медицини, що пов’язано з його глобальної поширеністю, гетерогенністю клінічних та лабораторних проявів, а також асоціацією з різними коморбідних станами. Залежно від метаболічного статусу розрізняють метаболічно нездорове ожиріння (MНЗО) та метаболічно здорове ожиріння (MЗO). MНЗО визначається за наявності критеріїв метаболічного синдрому (МС) і асоціюється з підвищеним ризиком виникнення кардіоваскулярних і метаболічних ускладнень. МЗО характеризується «метаболічно здоровим» профілем, однак питання щодо сприятливого перебігу захворювання є суперечливим; багато досліджень свідчать про нестійкість фенотипу МЗО та можливість розвитку МНЗО у подальшому. Мета дослідження: проаналізувати особливості лабораторних параметрів, пов’язаних з МЗО, та визначити фактори ризику розвитку МНЗО на прикладі клінічного випадку. Матеріали та методи. Клінічний випадок пацієнтки 24 років з діагнозом аліментарно-конституціонального ожиріння III ступеня. Об’єктивно: зріст – 174 см, вага – 124,7 кг, індекс маси тіла (ІМТ) – 41,21 кг/м2, обхват талії – 107 см, обхват стегон – 144 см. Об’єктивно: на шкірі живота – білі стрії; підшкірно-жирова клітковина розвинена надмірно, більш виражена в області живота, спини, стегон; АТ – 125/80 мм рт. ст. Лабораторні дані: гіперлептинемія – 86,82 нг/мл, підвищений рівень індексу HOMA – 4,6, гіперурикемія – 6,8 мг/дл, дефіцит вітаміну D – 9,19; ліпідний профіль, глюкоза в плазмі крові натще, глікований гемоглобін (HbA1c), тиреотропний гормон (ТТГ), трийодтиронін (Т3), тироксин (Т4), антитіла до тиреопероксидази (антиТРО), кортизол, електроліти крові, печінкові проби – у межах норми. Електрокардіографія (ЕКГ), ультразвукове дослідження серця та органів черевної порожнини – без патології. Результати. Нормальні показники ліпідного обміну, глюкози крові та вимірювання артеріального тиску у нашої пацієнтки характерні для МЗО. Однак поєднання гіперлептинемії з інсулінорезистентністю, гіперурикемією та дефіцитом вітаміну D свідчить про метаболічний та гормональний дисбаланс і розглядається як фактор ризику розвитку МС та подальшого переходу МЗО до МНЗО. Висновок. МЗО слід розглядати як перехідний динамічний стан, ведення таких пацієнтів вимагає ретельного лабораторного моніторингу з раннім виявленням метаболічних порушень та їх адекватною і своєчасною корекцією.

Текст научной работы на тему «THE VALUE OF LABORATORY INDICATORS ESTIMATION IN PATIENTS WITH METABOLICALLY HEALTHY OBESITY: ANALYSIS OF A CLINICAL CASE WITH LITERATURE REVIEW»

Clinical case

UDC 616-036.12: 616-036.15: 616-079.3: 616-092.12: 616-43 DOI: 10.26565/2313-6693-2022-44-09

THE VALUE OF LABORATORY INDICATORS ESTIMATION IN

PATIENTS WITH METABOLICALLY HEALTHY OBESITY: ANALYSIS OF A CLINICAL CASE WITH LITERATURE REVIEW

Holubkina Yevheniia B CD, Skokova Nataliia CD,E, Tykhonova Tetiana A,D,F

A - research concept and design; B - collection and/or assembly of data; C - data analysis and interpretation; D -writing the article; E - critical revision of the article; F - final approval of the article

Introduction. Obesity currently is a relevant issue of modern medicine due to its global prevalence, heterogeneity of clinical and laboratory manifestations, as well as the association with various comorbid conditions. Depending on the metabolic status, metabolically unhealthy obesity (MUO) and metabolically healthy obesity (MHO) are distinguished. MUO is defined with the presence of criteria for metabolic syndrome (MS) and is associated with an increased risk of cardiovascular and metabolic complications. MHO is characterized by a «metabolically healthy» profile, but the probability of a favorable course of the disease is controversial; many studies indicate the instability of the MHO phenotype and the possibility of further development of MUO.

The aim of study: to analyze the features of laboratory indicators associated with MHO and determine the risk factors for the MUO development on the example of a clinical case.

Materials and methods. A clinical case of 24 year old female patient diagnosed with alimentary-constitutional obesity class III. Objectively: height - 174 cm, weight - 124.7 kg, body mass index (BMI) -41.21 kg/m2, waist circumference - 107 cm, hips circumference - 144 cm; white striae on the abdomen; excessive subcutaneous fat stores, mostly distributed in the abdomen, thighs; blood pressure (BP) -125/80 mm Hg. Investigation data: hyperleptinemia - 86.82 ng/ml, increased level of HOMA index - 4.6, hyperuricemia - 6.8 mg/dl, vitamin D deficiency - 9.19 ng/ml; lipid profile, fasting plasma glucose, glycated haemoglobin (HbA1c), thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), antithyroid peroxidase (anti-TPO) antibodies, cortisol, blood electrolytes, liver function tests - within normal limits. Electrocardiography (ECG), ultrasound of the heart and abdominal organs - without pathology.

Results. Normal indicators of lipid metabolism, blood glucose and BP measurement in our patient are characteristic for MHO. However, the combination of hyperleptinemia with insulin resistance, hyperuricemia and vitamin D3 deficiency indicate metabolic and hormonal imbalance and are considered as a risk factors for the development of MS and the further transition of MHO to MUO.

Conclusion. MHO should be considered as a transient state, the management of such patients requires careful laboratory monitoring with early detection of metabolic disorders and its adequate and timely correction.

KEY WORDS: metabolically healthy obesity, metabolically unhealthy obesity, metabolic syndrome, laboratory indicators

INFORMATION ABOUT AUTHORS

Holubkina Yevheniia, MD, assistant of the Department of Internal Medicine of V. N. Karazin Kharkiv National University, 6, Svobody sq., Kharkiv, Ukraine, 61022; e-mail: eugenia.golubkina@karazin.ua, ORCID ID: https://orcid.org/0000-0002-2587-8894

Skokova Nataliia, MD, assistant of the Department of Internal Medicine of V. N. Karazin Kharkiv National University, 6, Svobody sq., Kharkiv, Ukraine, 61022; e-mail: nataliaskokova@karazin.ua, ORCID ID: http://orcid.org/0000-0003-0499-712X

Tykhonova Tetiana, MD, PhD, Professor, Head of the Department of Internal Medicine, V. N. Karazin Kharkiv National University, 6, Svobody sq., Kharkov, Ukraine, 61022; e-mail: tmtykhonova@karazin.ua, ORCID ID: https://orcid.org/0000-0001-9196-9113

Для цитування:

Holubkina Ye, Skokova N, Tykhonova T. THE VALUE OF LABORATORY INDICATORS ESTIMATION IN PATIENTS WITH METABOLICALLY HEALTHY OBESITY: ANALYSIS OF A CLINICAL CASE WITH LITERATURE REVIEW. Вюник Харювського национального ушверситету ÍMern В. Н. Каразша. Серш «Медицина». 2022: 44; С. 119-126. DOI: 10.26565/2313-6693-2022-44-09

© Holubkina Ye., Skokova N., Tykhonova T., 2022

INTRODUCTION

Obesity is a chronic multifactorial disease characterized by the formation of abnormal or excessive body fat stores that can be harmful to health. Obesity is diagnosed when the body mass index (BMI) is > 30.0 kg/m2, overweight corresponds to a BMI in the range of 25.029.9 kg/m2 [1, 2]. The problem of obesity has remained relevant for many years, which is primarily due to the steady increase in its prevalence. According to the WHO (World Health Organization), between 1975 and 2016, the number of people suffering from obesity worldwide had more than tripled [1]. According to the results of the STEPS study conducted in Ukraine in 2019, obesity was detected in 24.8 %, and overweight - in 59 % of the adult population [3].

Another feature of obesity is the heterogeneity of its clinical manifestations and the relationship with diseases of various organs and systems: cardiovascular, endocrine, musculoskeletal, digestive, etc. The association of obesity with comorbid conditions leads to the appearance of dangerous complications, deterioration in the quality of life and increased levels of disability in patients. Obesity is a significant risk factor for the development of cardiovascular diseases (arterial hypertension, ischemic heart disease, etc.) and metabolic pathological conditions (impaired glucose tolerance, type 2 diabetes mellitus, hyperuricemia, etc.) [1, 2, 4, 5, 6]. Also, patients with obesity have a higher mortality rate compared with normal body weight persons [7].

Depending on the metabolic status of patients, several phenotypes of obesity are distinguished. The combination of obesity, arterial hypertension, impaired glucose tolerance and atherogenic dyslipidemia refers to metabolic syndrome (MS) or metabolically unhealthy obesity (MUO) [8]. According to the criteria of the International Diabetes Federation (IDF), MS is defined in the presence of: increased waist circumference (WC) > 94 cm in men and > 80 cm in women; increased triglyceride (TG) levels > 150 mg/dL (1.7 mmol/L); decreased high density lipoprotein (HDL) levels < 40 mg/dL (1.03 mmol/L) in men and < 50 mg/dL (1.29 mmol/L) in women; increased fasting plasma glucose > 100 mg/dL (5.6 mmol/L); increased blood pressure (BP) either systolic

> 130 mm Hg or diastolic > 85 mm Hg. The presence of 3 positive criteria indicates MS [9].

Patients without evidence of MS are categorized in a group of metabolically healthy obesity (MHO), the main feature of which is complete or partial absence of MS criteria [8, 10]. This phenotype of obesity was defined in 1982 by researchers Andreas and Sims [11]. The prevalence of MHO is quite variable and often depends on the severity of the selected criteria (complete or partial absence of MS components) [12]. Thus, according to the results of The BioSHaRE-EU Healthy Obese Project, using data from 10 different studies in 7 European countries (n = 163.517), the prevalence of MHO varies from 7 % to 28 % [12]. Of great interest to researchers is the study of pathogenetic conditions for the formation of a «healthy metabolic» profile in MHO, as well as the assessment of its stability over time. Pathogenetic features of MHO include first of all structural ones, such as smaller size of adipocytes compared to MUO, as well as the predominance of subcutaneous fat over visceral and ectopic [8]. Another factor determining the MHO phenotype is a low level of inflammatory markers: C-reactive protein (CRP), tumor necrosis factor alpha, and interleukin IL-6 [8, 11, 13, 14, 15]. Patients with MHO are usually characterized with higher level of physical activity than patients with MUO [8]. Assessment of risk of cardiovascular and metabolic diseases development remains the relevant issue in the study of MHO. Despite controversial debates over prognosis of patients with MHO, numerous studies show that MHO often has a transient character with the subsequent occurrence of metabolic disorders and the development of MUO, which characterizes the clinical significance of MHO [13, 16, 17].

Determination of metabolic laboratory indicators is an important factor in differentiating various phenotypic forms of obesity and predicting the occurrence of possible complications and comorbid conditions associated with it at the preclinical stage. Therefore, the management of patients with MHO requires careful laboratory monitoring in order to prevent the development of MS and its complications.

The aim of this article is to study the characteristics of laboratory parameters in patients with MHO and to determine the risk

factors for the development of MUO on the example of a clinical case.

MATERIALS AND METHOD

A 24-year-old female patient complains of excessive body mass. She was first diagnosed with obesity grade II at the age of 13 (BMI = 36.5 kg/m2). Subsequently the patient's weight progressively increased, she did not consult an endocrinologist in following years, periodically consulted a nutritionist, didn't follow the recommendations. The patient maintained an average level of physical activity (morning routine, jogging) with her weight remaining at the level of 110-112 kg, however, since 2019 the level of her physical activity has significantly decreased as a result of the change in the mode of work (online work from home). In January 2020, due to a progressive increase in body weight (from 115 to 124 kg), she began to follow a diet, increased physical activity and over the next 3 months she lost 5 kg. Subsequently adherence to diet and physical activity decreased; at the time of examination, he does not adhere to diet and sports.

Objectively: the general condition is satisfactory; height - 174 cm, weight - 124.7 kg, BMI - 41.21, WC - 107 cm, hips circumference - 144 cm, waist-hip ratio - 0.74. The skin is pale pink and clean, turgor is preserved. In the abdomen, white striae are present. Visible mucous membranes are clean. Subcutaneous fat is developed excessively, more pronounced in the abdomen, back, thighs. There is no visible edema. Examination of the musculoskeletal system revealed no pathological changes. The thyroid gland is not palpable. Percussion over the lungs revealed clear pulmonary sound, auscultation - vesicular breathing, RR-19/min. On heart auscultation -the sounds are rhythmic, slightly muffled, HR is equal to pulse - 75 beats/min, BP on both arms - 125/80 mm Hg. The abdomen is soft, painless on palpation. The liver is at the edge of the costal arch, painless. The spleen is not palpable. The tapping symptom is negative on both sides. Urination, defecation - without pathological changes.

Questionnaire data: the survey was carried out using the questionnaire of the level of physical activity ODA 23+: low physical activity was recorded. We also analyzed the data of the food diary, which was filled in by the patient during 2 working days and 2 days off, taking into account the type of food, size of

the portion, method of food preparation, the frequency and the conditions of food intake. The dietary assessment showed low consumption of fruits and vegetables along with increased consumption of fast food, red meet and sweet drinks by the patient. The patient also smokes (1 pack of cigarettes per day).

Laboratory investigations data: general blood and urine analysis, CRP, TSH, T3, T4, anti-TPO antibodies, cortisol, blood electrolytes, alanine transaminase (ALT), aspartate transaminase (AST), lipid profile, fasting plasma glucose, glycated hemoglobin -within normal limits. Was detected: hyperleptinemia - 86.82 ng/ml (N - 3.711.1 ng/ml), an increase in the HOMA index -4.6 (N < 2.77), hyperuricemia - 6.8 mg/dL (N -2.4-5.7 mmol/l), vitamin D deficiency (25 (OH) D) - 9.19 ng/ml (N > 30 ng/ml). Instrumental investigations data: ECG, ultrasound of the heart and abdominal organs, computed tomography (CT) scan of the brain -without pathology.

Diagnosis: alimentary-constitutional obesity class III.

Treatment. Lifestyle modification: diet with restriction of saturated fats, fast-digesting carbohydrates, foods rich in purines; food intake 5-6 times a day in small portions, reducing the daily calorie content by 5001000 kcal, taking into account the patient's energy consumption; increased physical activity through aerobic exercise (walking at least 10,000 steps per day); smoking cessation counseling. Metformin - 1000 mg 1 time/day for 6 months under the control of ALT levels. Cholecalciferol 20,000 IU weekly under the control of vitamin D3.

DISCUSSION

A feature of this case is the development of moderate insulin resistance (IR) in a patient with gynoid obesity in the absence of disorders of carbohydrate and lipid metabolism. However, in the absence of any complaints, hyperuricemia was detected, as well as hyperleptinemia and a decreased level of serum vitamin D. This indicates the relativity of metabolic intactness of the gynoid type of obesity, including MHO.

The stability of indicators of metabolic health in patients with MHO causes conflicting opinions among researchers. However, most authors agree that MHO is a dynamic transient state with the possibility of the development of

metabolic abnormalities and the transition to MUO [13, 16, 17]. According to the research, the factors contributing to the transformation of MHO into MUO are defined as: an increase in BMI, WC, waist-hip ratio, a decrease in HDL levels and the female sex of patients [18, 19]. From the history of our patient, it is known that her BMI has been progressively increasing since puberty, but a significant increase has been noted in the last 3 years. On the contrary, physical activity decreased during this period; the lack of systematic adherence to the diet and the presence of bad habits (smoking) were also noted. Lifestyle modification is one of the key

Compliance of the indicators of our

approaches in the treatment of obesity and plays an important role in the prevention of comorbid conditions associated with obesity, in particular the components of MS. Thus, the results of studies by Chang Hee Jung, Woo Je Lee et al. demonstrate that diet correction, a high level of physical activity, as well as bad habits cessation are protective factors that prevent the development of metabolic disorders in patients with MHO [13].

The data of anthropometric, laboratory studies and the results of BP measurement in our patient correspond to the MHO according to the IDF criteria (see Table 1).

Table 1.

tient with the criteria for MS (IDF).

Laboratory indicators MS criteria (IDF) Patient data

Triglycerides >150 mg/dL (1.69 mmol / L) 1.33 mmol / L

HDL cholesterol <40 mg/dL (1.0 mmol / L) in men and <50 mg/dL (1.29 mmol / L) in women 1,35 mmol / L

Fasting plasma glucose >100 mg/dL (5.6 mmol / L) 5,03 mmol / L

Systolic blood pressure > 130 mm Hg 125 mm Hg

Diastolic blood pressure >85 mm Hg 80 mm Hg

Waist circumference > 94 cm for men, > 80 cm for women 107 cm

However, there were detected increased laboratory parameters of HOMA index - 4.6 (N < 2.77) and the serum uric acid - 6.8 mg/dL (N - 2.4-5.7 mg/dL), which indicate metabolic and hormonal imbalance. The results of numerous studies prove that IR is often combined with arterial hypertension, hypertriglyceridemia, hypercholesterolemia and hyperglycemia [9, 20]. Also strong relationship between the components of MS and hyperuricemia was established: high level of serum uric acid correlates with dyslipidemia, and especially with hypertriglyceridemia, IR and hyperglycemia [21]. Therefore, from our point of view, the presence of IR and hyperuricemia in patients with MHO should be considered as preclinical manifestations of metabolic disorders - risk factors for the development of MS and further transition of MHO to MUO.

As already noted, the laboratory test results of our patient demonstrate the presence of significant hyperleptinemia (86.82 ng/ml) and vitamin D deficiency (9.19 ng/ml). Hyperlep-tinemia is one of the key mechanisms determining the pathogenesis of obesity, which is confirmed by many studies [22, 23, 24, 25,

26, 27, 28]. Leptin is a regulator of hunger-satiety mechanisms, and normally its production leads to a decrease in appetite, activation of the sympathetic nervous system and an increase in energy expenditure, which contributes to the maintenance of normal body weight. Obesity is characterized by hyperleptinemia, but with the lack of positive effects of leptin, which is considered as a manifestation of a decreased sensitivity of tissue receptors to leptin - leptin resistance (LR) [22, 26]. Researchers emphasize the important role of leptin as a biomarker of cardiometabolic disorders. It has been proven that hyperleptinemia is associated with cardiovascular diseases (myocardial infarction, coronary artery disease, hypertension, etc.), which is primarily associated with the effect of leptin on the vascular wall, the development of hypertrophy and vascular remodeling [22, 24, 25]. Data obtained by Ifeyinwa Osegbe et al. confirm the relationship between hyperlepti-nemia and metabolic disorders: they studied the levels of hyperleptinemia and IR in obese non-diabetic women (n = 80) and found that the level of leptin increased depending on the BMI;

in the group of patients with morbid obesity (BMI > 40 kg / m2), the indicators of hyperleptinemia ranged within 50.1 ng / ml (SD = 1.8). At the same time, a positive correlation was found between the levels of serum leptin and IR, especially pronounced in morbid obesity [23]. Similar results were obtained in other studies [28, 29]. The study of leptin concentration in different phenotypes of obesity proves that the level of hyperleptinemia in patients with MHO is significantly lower than in patients with metabolic obesity [25, 27, 28]. Also, patients with MUO were found to have higher indices of insulin resistance (HOMA index) and leptin resistance (serum leptin and free leptin index) compared with MHO [30]. Therefore, a significant increase in the level of leptin in MHO patients, as in our clinical case, can be associated with leptin resistance and should be considered as an unfavorable factor in the development of cardiometabolic disorders.

An equally important deviation of laboratory parameters in patients with obesity is vitamin D deficiency, which is confirmed by research data [15, 31, 32, 33, 34]. The inhibitory role of vitamin D in relation to excessive accumulation of fat stores, adipocyte hypertrophy, and the development of inflammation has been proven [15, 33]. Also, according to the authors, there is an inverse correlation between the level of vitamin D and BMI [35, 36]. For example, the results of a large-scale meta-analysis conducted by Karani S. Vimaleswaran et all., using data from 21 studies (n = 42.024) showed that a 1 kg/m2 increase in BMI was associated with a 1.15 % decrease in serum 25 (OH) D [36]. The results of another research aimed at studying the level of vitamin D in patients with different BMIs (n = 2126) indicated that in the group of patients with BMI > 30 kg / m2, the level of 25 (OH) D3 was 20 % lower than normal, and in the group of patients with morbid obesity

REFERENCES

severe deficit of 25 (OH) D3 was found [35]. It has been established that vitamin D deficiency is associated with MS and its components: IR, impaired glucose tolerance and type 2 diabetes mellitus, as well as dyslipidemia [15, 37, 38, 39]. It has also been found that vitamin D levels < 50 nmol/L (< 20 ng/ml) are associated with an increased risk of cardiometabolic mortality [40]. Interesting data was obtained in study of vitamin D concentration in MHO patients: according to authors patients with MHO have a higher level of vitamin D concentration than patients with MUO, which also indicates the protective role of vitamin D in relation to the development of metabolic disorders [15]. In this regard, promising scientific direction is the study of effect of vitamin D supplementation on the prevention of MS and correction of already existing metabolic disorders in obesity.

Thus, despite the fact that MHO is characterized by lower levels of leptinemia and vitamin D concentration in comparison with MUO, patients with morbid obesity, as in our clinical case, have an increased risk for the development of leptin resistance and vitamin D deficiency, which in turn are closely related with MS.

CONCLUSIONS

According to the IDF criteria, our clinical case meets the MHO definition. However, the combination of hyperleptinemia with insulin resistance, hyperuricemia, and vitamin D deficiency indicate metabolic and hormonal imbalance and are risk factors for the development of MS and further transformation of the MHO into MUO. Thus, MHO should be considered as a transient dynamic state, and the management of such patients requires careful laboratory monitoring with early detection of metabolic disorders and its adequate and timely correction.

1. WHO. Obesity and overweight [document on the Internet]. World Health Organisation; 2021 [cited 2021 September 15]. Available from: http://www.who.int/mediacentre/factsheets/fs311/en/.

2. Fadeenko GD, Maslyaeva LV. Ozhirenie kak problema klinicheskoy meditsinyi. Liky Ukrainy. 2009; 6 (132): 31-7 [In Russian].

3. Doslidzhennia STEPS: poshyrenist faktoriv ryzyku neinfektsiinykh zakhvoriuvan v Ukraini u 2019 rotsi. Kopenhahen, Yevropeiske rehionalne biuro VOOZ. 2020. [In Ukrainian] Available from: https://apps.who.int/iris/bitstream/handle/10665/336643/WHO-EURO-2020-1468-41218-56061-ukr.pdf

4. Durrer Schutz D, Busetto L, Dicker D, Farpour-Lambert N, et al. European Practical and Patient-Centred Guidelines for Adult Obesity Management in Primary Care. Obes Facts 2019; 12: 40-66. DOI: https://doi.org/10.1159/000496183.

5. Garvey WT, Mechanick JI, Brett EM, et al. American association of clinical endocrinologists and american college of endocrinology comprehensive clinical practice guidelines for medical care of patients with obesity. Endocr Pract. 2016; 22 (3): 1-203. DOI: https://doi.org/i0.4i58/EPi6i365.GL.

6. Purnell JQ. Definitions, Classification, and Epidemiology of Obesity. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. 2018 [cited 2021 Sep 15]. Available from: https://www.ncbi.nlm. nih. gov/books/NBK279 i 67/.

7. Flegal KM, Kit BK, Orpana H, Graubard BI. Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. JAMA. 2013; 309 (i): 71-82. DOI: https://doi.org/i0.i00i/jama.20i2.ii3905.

8. Romantsova TI, Ostrovskaya EV, Metabolicheski zdorovoe ozhirenie: definitsii, protektivnyie faktoryi, klinicheskaya znachimost. Almanah klinicheskoy meditsinyi [serial online]. 2015. 13 (21): 75-87. [In Russian] Available from: https://www.almclinmed.ru/jour/article/view/73/74.

9. Alberti KG, Eckel RH, Grundy SM, et al. International Diabetes Federation Task Force on Epidemiology and Prevention; Hational Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; International Association for the Study of Obesity. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009; 120 (16): 1640-5. DOI: https://doi.org/i0. i 161/CIRCULATIONAHA. 109.192644

10. Muñoz-Garach A, Cornejo-Pareja I, Tinahones FJ. Does Metabolically Healthy Obesity Exist? Nutrients. 2016; 8 (6): 320. DOI: https://doi.org/10.3390/nu8060320.

11. Brandäo I, Martins MJ, Monteiro R. Metabolically Healthy Obesity-Heterogeneity in Definitions and Unconventional Factors. Metabolites. 2020; 10 (2): 48. DOI: https://doi.org/10.3390/metabo10020048.

12. van Vliet-Ostaptchouk JV, Nuotio M-L, Slagter SN, et al.The prevalence of metabolic syndrome and metabolically healthy obesity in Europe: a collaborative analysis of ten large cohort studies. BMC Endocrine Disorders. 2014; 14 (1): 9. DOI: https://doi.org/10.1186/1472-6823-14-9.

13. Jung CH, Lee WJ, Song KH. Metabolically healthy obesity: a friend or foe? Korean J Intern Med. 2017; 32 (4): 611-621. DOI: https://doi.org/10.3904/kjim.2016.259.

14. Karelis AD, Rabasa-Lhoret R. Obesity: Can inflammatory status define metabolic health? Nat Rev Endocrinol. 2013 Dec; 9 (12): 694-5. DOI: https://doi.org/10.1038/nrendo.2013.198.

15. Esteghamati A, Aryan Z, Esteghamati A, Nakhjavani M. Differences in vitamin D concentration between metabolically healthy and unhealthy obese adults: associations with inflammatory and cardiometabolic markers in 4391 subjects. Diabetes Metab. 2014; 40 (5): 347-55. DOI: https://doi.org/10.1016/j.diabet.2014.02.007.

16. Tremmel M, Lyssenko V, Zöller B et al. Characteristics and prognosis of healthy severe obesity (HSO) subjects - The Malmo Preventive Project. Obesity Medicine. 2018; 11: 6-12. DOI: https://doi.org/10.1016/j.obmed.2018.06.005.

17. Soriguer F, Gutiérrez-Repiso C, Rubio-Martín E, et al. Metabolically healthy but obese, a matter of time? Findings from the prospective Pizarra study. J Clin Endocrinol Metab. 2013; 98 (6): 2318-25. DOI: https://doi.org/10.1210/jc.2012-4253.

18. Hwang YC, Hayashi T, Fujimoto WY, et al. Visceral abdominal fat accumulation predicts the conversion of metabolically healthy obese subjects to an unhealthy phenotype. Int J Obes 2015; 39: 1365-1370. DOI: https://doi.org/10.1038/ijo.2015.75.

19. Schröder H, Ramos R, Baena-Díez JM, Mendez MA, Canal DJ, Fíto M, Sala J, Elosua R. Determinants of the transition from a cardiometabolic normal to abnormal overweight/obese phenotype in a Spanish population. Eur J Nutr. 2014; 53 (6): 1345-53. DOI: https://doi.org/10.1007/s00394-013-0635-2.

20. Uchamprina VA., Romantsova TI. Kalashnikova MF. Metabolicheskiy sindrom: argumentyi «za» i «protiv». Ozhirenie i metabolizm. 2012; (9) 2: 17-27. [In Russian] DOI: https://doi.org/10.14341/omet2012217-27

21. Zagayko A L., Bryuhanova TA., Shkapo AI. Giperurikemiya kak element patogeneza metabolicheskogo sindroma. Ukrainian biopharmaceutical journal. 2015; 1 (36): 47-51. [In Russian] Available from: http://nbuv.gov.ua/UJRN/ubfj_2015_1_12

22. Gruzdeva O, Borodkina D, Uchasova E, Dyleva Y, Barbarash O. Leptin resistance: underlying mechanisms and diagnosis. Diabetes Metab Syndr Obes. 2019; 12:191-198. DOI: https://doi.org/10.2147/DMSO.S182406

23. Osegbe I, Okpara H, Azinge E. Relationship between serum leptin and insulin resistance among obese Nigerian women. AnnAfrMed. 2016; 15 (1): 14-19. DOI: https://doi.org/10.4103/1596-3519.158524

24. Ghantous CM, Azrak Z, Hanache S, Abou-Kheir W, Zeidan A. Differential Role of Leptin and Adiponectin in Cardiovascular System. Int J Endocrinol. 2015; 2015: 534320. DOI: https://doi.org/10.1155/2015/534320

25. Jamar G, Caranti DA, de Cassia Cesar H, Masquio DCL, Bandoni DH, Pisani LP. Leptin as a cardiovascular risk marker in metabolically healthy obese: Hyperleptinemia in metabolically healthy obese. Appetite. 2017; 108: 477-482. DOI: https://doi.org/10.1016/j.appet.2016.11.013

26. Duque AP, Rodrigues Junior LF, Mediano MFF, Tibiriga E, De Lorenzo A. Emerging concepts in metabolically healthy obesity. Am J Cardiovasc Dis. 2020; 10 (2): 48-61. Available from: https://www.ncbi.nlm. nih. gov/pmc/articles/PMC7364278/

27. ChangCS, LuYJ, ChangHH et al. Role of adiponectin gene variants, adipokines and hydrometry-based percent body fat in metabolically healthy and abnormal obesity. Obes Res ClinPract. 2018; 12 (2): 49-61. DOI: https://doi.org/10.1016Zj.orcp.2016.05.003

28. Zak KP, Mankovskiy BN, Melnichenko SV et al. Immunitet u bolnyih saharnyim diabetom 2 tipa s soputstvuyuschim metabolicheskim sindromom/ ozhireniem. Soobschenie 2. Rol adipotsitokinov (interleykina-6, faktora nekrozaopuholey alfa, leptina i adiponektina). Endokrynolohiia. 2013; 18 (2): 2632. [In Russian] Available from: https://endokrynologia.com.ua/index.php/journal/article/view/387

29. Suslyk HI. Hiperleptynemiia ta stan insulinovoi rezystentnosti u khvorykh na tsukrovyi diabet 2-ho typu z ozhyrinniam. Klinichna endokrynolohiia ta endokrynna khirurhiia. 2012; 2 (39): 309-16. [In Ukrainian] DOI: https://doi.org/10.24026/1818-1384.2(39).2012.82296.

30. Ott AV, Chumakova GA, Veselovskaya NG. Znachenie leptinorezistentnosti v razvitii razlichnyih metabolicheskih fenotipov ozhireniya. Rossiyskiy kardiologicheskiy zhurnal. 2016; (4): 14-18. [In Russian] Available from: https://russjcardiol.elpub.ru/jour/article/view/676/628

31. Pereira-Santos M, Costa PR, Assis AM, Santos CA, Santos DB. Obesity and vitamin D deficiency: a systematic review and meta-analysis. ObesRev. 2015; 16 (4): 341-9. DOI: https://doi.org/10.1111/obr. 12239

32. Fiamenghi VI, Mello ED. Vitamin D deficiency in children and adolescents with obesity: a meta-analysis. J Pediatr (Rio J). 2021; 97 (3): 273-279. DOI: https://doi.org/10.1016/jjped.2020.08.006

33. Ding C, Gao D, Wilding J, Trayhurn P, Bing C. Vitamin D signalling in adipose tissue. Br J Nutr. 2012; 108 (11): 1915-1923. DOI: https://doi.org/10.1017/S0007114512003285

34. Duan L, Han L, Liu Q, Zhao Y, Wang L, Wang Y. Effects of Vitamin D Supplementation on General and Central Obesity: Results from 20 Randomized Controlled Trials Involving Apparently Healthy Populations. Ann NutrMetab. 2020; 76 (3): 153-164. DOI: https://doi.org/10.1159/000507418

35. Lagunova Z, Porojnicu AC, Lindberg F, Hexeberg S, Moan J. The dependency of vitamin D status on body mass index, gender, age and season. Anticancer Res. 2009; 29 (9): 3713-20. Available from: https://pubmed. ncbi.nlm. nih. gov/19667169/

36. Vimaleswaran KS, Berry DJ, Lu C et al. Causal Relationship between Obesity and Vitamin D Status: BiDirectional Mendelian Randomization Analysis of Multiple Cohorts. PLoSMed. 2013. 10(2): 1001383. DOI: https://doi.org/10.1371/journal.pmed.1001383

37. García-Bailo B, Da Costa LA, Arora P, Karmali M, El-Sohemy A, Badawi A. Plasma vitamin D and biomarkers of cardiometabolic disease risk in adult Canadians, 2007-2009. Prev Chronic Dis. 2013; 10. DOI: https://doi.org/10.5888/pcd10.120230.

Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682811/

38. Khan H, Kunutsor S, Franco OH, Chowdhury R. Vitamin D, type 2 diabetes and other metabolic outcomes: a systematic review and meta-analysis of prospective studies. Proc Nutr Soc. 2013. 72: 89-97. DOI: https://doi.org/10.1017/S0029665112002765.

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39. Huang CY, Chang HH, Lu CW, Tseng FY, Lee LT, Huang KC. Vitamin D status and risk of metabolic syndrome among non-diabetic young adults. Clin Nutr. 2015; 34 (3): 484-9. DOI: https://doi.org/10.1016/j.clnu.2014.05.010.

40. Al-Khalidi B, Kimball SM, Kuk JL, Ardern CI. Metabolically healthy obesity, vitamin D, and all-cause and cardiometabolic mortality risk in NHANES III. Clin Nutr. 2019; 38 (2): 820-828. DOI: https://doi.org/10.1016/j.clnu.2018.02.025.

ЗНАЧЕННЯ ОЦ1НКИ ЛАБОРАТОРНИХ ПОКАЗНИК1В У ПАЩСНТ1В З МЕТАБОЛ1ЧНО ЗДОРОВИМ ОЖИР1ННЯМ: АНАЛ1З КЛ1НИЧНОГО ВИПАДКУ З ОГЛЯДОМ Л1ТЕРАТУРИ

Голубкта €. О., Скокова Н. I., Тихонова Т. М.

A - концепця та дизайн дослвдження; B - 36ip даних; C - анал1з та штерпретащя даних; D - написання статп; E - редагування статп; F - остаточне затвердження статт

Вступ. В даний час ожиршня е актуальною проблемою сучасно! медицини, що пов'язано з його глобально! поширешстю, гетерогеннiстю клiнiчних та лабораторних проявiв, а також асощащею з рiзними коморбiдних станами. Залежно ввд метаболiчного статусу розрiзняють метаболiчно нездорове ожирiння (МНЗО) та метаболiчно здорове ожирiння (M3O). МНЗО визначаеться за наявносп критерпв метаболiчного синдрому (МС) i асоцiюеться з шдвищеним ризиком виникнення кардiоваскулярних i метаболiчних ускладнень. МЗО характеризуеться «метаболiчно здоровим» профiлем, однак питання щодо сприятливого перебiгу захворювання е суперечливим; багато дослщжень свiдчать про нестiйкiсть фенотипу МЗО та можливють розвитку МНЗО у подальшому.

Мета дослiдження: проаналiзувати особливостi лабораторних параметрiв, пов'язаних з МЗО, та визначити фактори ризику розвитку МНЗО на приклащ клшчного випадку.

Матер1али та методи. Кттчний випадок пацiентки 24 рок1в з дiагнозом алiментарно-конституцiонального ожирiння III ступеня. Об'ективно: зрiст - 174 см, вага - 124,7 кг, iндекс маси тша (1МТ) - 41,21 кг/м2, обхват тали - 107 см, обхват стегон - 144 см. Об'ективно: на шкiрi живота - бш стрп; пiдшкiрно-жирова клiтковина розвинена надмiрно, бiльш виражена в областi живота, спини, стегон; АТ - 125/80 мм рт. ст. Лабораторш дат: гiперлептинемiя - 86,82 нг/мл, тдвищений рiвень шдексу HOMA - 4,6, гiперурикемiя - 6,8 мг/дл, дефщит вiтамiну D - 9,19; лшвдний профiль, глюкоза в плазмi кровi натще, глжований гемоглобiн (HbA1c), тиреотропний гормон (ТТГ), трийодтиронш (Т3), тироксин (Т4), антитша до тиреопероксидази (антиТРО), кортизол, електролгги кровi, печiнковi проби - у межах норми. Електрокардiографiя (ЕКГ), ультразвукове дослiдження серця та органiв черевно! порожнини - без патологи.

Результати. Нормальш показники лiпiдного обмiну, глюкози кровi та вимiрювання артерiального тиску у нашо! пацiентки характернi для МЗО. Однак поеднання гшерлептинемп з шсулшорезистентшстю, гiперурикемiею та дефiцитом впамшу D свiдчить про метаболiчний та гормональний дисбаланс i розглядаеться як фактор ризику розвитку МС та подальшого переходу МЗО до МНЗО.

Висновок. МЗО слщ розглядати як перех1дний динашчний стан, ведення таких пацiентiв вимагае ретельного лабораторного монiторингу з раншм виявленням метаболiчних порушень та !х адекватною i своечасною корекцiею.

КЛЮЧОВ1 СЛОВА, метаболiчно здорове ожирiння, метаболiчно нездорове ожирiння, метаболiчний синдром, лабораторш показники

1НФОРМАЦ1Я ПРО АВТОР1В

Голубкша бвгешя Олександр1вна, асистент кафедри внутршньо! медицини, Харкгвський нацюнальний унiверситет iменi В. Н. Каразгна, майдан Свободи, 6, Харкгв, Укра!на, 61022; е-mail: eugenia.golubkina@karazin.ua, ORCID ID: https://orcid.org/0000-0002-2587-8894

Скокова Натал1я 1гор1вна, асистент кафедри внутршньо! медицини, Харювський нацiональний унiверситет iменi В. Н. Каразiна, майдан Свободи, 6, Харкгв, Укра!на, 61022; е-mail: nataliaskokova@karazin.ua, ORCID ID: http://orcid.org/0000-0003-0499-712X

Тихонова Тетяна Михайл1вна, д.мед.н., професор, зав. кафедри внутршньо! медицини, Харкiвський нацюнальний унiверситет iменi В. Н. Каразгна, майдан Свободи, 6, Харкгв, Украша, 61022; е-mail: tmtykhonova@karazin.ua, ORCID ID: https://orcid.org/0000-0001-9196-9113

For citation:

Голубкша СО, Скокова HI, Тихонова ТМ. ЗНАЧЕННЯ ОЦ1НКИ ЛАБОРАТОРНИХ ПОКАЗНИК1В У ПАЩеНПВ З МЕТАБОЛ1ЧНО ЗДОРОВИМ ОЖИР1ННЯМ: АНАЛ1З КЛ1НИЧНОГО ВИПАДКУ З ОГЛЯДОМ Л1ТЕРАТУРИ The Journal of V. N. Karazin Kharkiv National University. Series «Medicine». 2022: 44; 119-126. DOI: 10.26565/2313-6693-2022-44-09

Conflicts of interest: author has no conflict of interest to declare. KoH^mKm mmepecie: eidcymmu.

OmpuMano npuuHxmo do dpyKy Received Accepted

: 09.03.2022 : 15.04.2022 : 03.09.2022 : 04.15.2022

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