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.
The association of atrial fibrillation (AF) with complete atrioventricular block (CAVB) is a common clinical feature in elderly patients. It is characterized by the loss of specific symptoms of AF (palpitations, intermissions); in the first place may come CAVB symptoms: dizziness, Morgagni–Adams–Stokes (MAS) attacks. Aim. The article objective is to illustrate the dynamic changes in the course of AF with the development of CAVB on the example of a clinical case and to discuss the difficulties in timely diagnosis and therapy correction. Case presentation. A 75-year-old male was diagnosed with a rapid ventricular response form of AF. The onset of CAVB caused the transition from rapid ventricular response form of AF to slow ventricular response form, which was initially accompanied by a subjective improvement in the patient’s condition. As the disease progressed, the patient’s condition worsened due to the development of MAS attacks. The elderly patients with a permanent form of AF require constant cardiac monitoring by an experienced specialist who has appropriate vigilance in management of patients with arrhythmias, awareness about possible concomitant conduction disorders. This provides comprehensive cardiac support, including timely pacemaker implantation which gives more options for AF symptoms monitoring and heart rate control, has a positive modifying effect on drug therapy. Conclusions. Changes in the clinical picture of AF after development of CAVB can lead to late diagnosis of CAVB, inadequate therapy and untimely pacemaker implantation, as a consequence, to progression of concomitant pathology and the development of life-threatening complications, as in our clinical case.
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