УДК 616.24:612.1]-06

Leptin, a hormone produced by white adipose tissue and recognised as an inflammatory biomarker, has an undefined role in the progression of chronic obstructive pulmonary disease (COPD). Objective — to evaluate the leptin level and its correlations with the levels of clinical, functional and anamnestic indicators in COPD patients.
Materials and methods. This study employed a case-control design involving 42 patients experiencing acute exacerbation of COPD and 20 control subjects. The patients were examined according to the standard protocol. Additionally, the examination included ultrasonic scanning of the abdominal cavity, evaluation of the serum leptin level, scoring of the anxiety and depression and quality of life.
Results and discussion. It was revealed that hyperleptinemia in the patients with acute exacerbation of COPD occurred significantly more frequently than in the healthy persons ((73.8 ± 6.8) vs (40.0 ± 11.0) %; р < 0.05). Besides, the COPD patients manifested increased leptin levels much more frequently than normal levels ((73.8 ± 6.8) vs (26.2 ± 6.8) %; р < 0.01). Hyperleptinemia was found to co-occur with severe COPD 
cases belonging to E clinical group ((51.6 ± 9.0) vs (18.2 ± 11.6) % in group with normal leptin level; р < 0.05). Kendall correlation analysis established that elevated circulating leptin levels were associated with an increased body mass index ( = 0.3; р = 0.02), female gender ( = 0.3; р = 0.01), non-smoking history ( = – 0.2; р = 0.03), stronger manifestation of such symptoms as shortness of breath ( = 0.3; р=0.01), disturbed home ( = 0.3; р = 0.002) and out-of-home activities ( = 0.3; р = 0.02) and lack of energy ( = 0.3; р = 0.01). It also correlated with increased severity of pulmonary insufficiency ( = 0.3; р = 0.003) and decreased forced vital capacity (= – 0.2; р = 0.04), elevated systolic blood pressure ( = 0.2; р = 0.02), elevated cholesterol ( = 0.3; р = 0.01) and -lipoproteins levels ( = 0.2; р = 0.04), pronounced depression ( = 0.3; р = 0.002) and lowered quality of life ( = 0.3; р = 0.01).
Сonclusions. COPD patients with elevated leptin levels manifest not only with an increased body weight, but also with arterial hypertension, disturbed lipid metabolism, more pronounced pulmonary insufficiency, depressive disorders and lowered life quality with more severe subjective respiratory symptoms.
Keywords. Chronic obstructive pulmonary disease, leptin, hyperleptinemia

УДК 616.002.5-021.3-053.8-035.7

Objective — to study the frequency and causes of diagnostic errors in primary pulmonary tuberculosis (PrPTB) in adults.
Materials and methods. The frequency and causes of diagnostic errors in verifying PrPTB in adults were studied by analyzing thpathomorphosis aspect of a specific process. Sectional material from 200 adult deaths due to primary forms of tuberculosis (PrFTB) over a period of 45 years (1974—2020) was analyzed. The study period was divided into three periods: the first period spanned from 1974 to 1988, during which three 
antimycobacterial drugs (isoniazid, streptomycin, and PASC) were used; the second period ranged from 1989 to 2005, during which rifampicin, ethambutol, and pyrazinamide were added to the treatment regimen; and the third period covered from 2005 to 2020, during which aminoglycosides, fluoroquinolones, linezolid, and other antimycobacterial drugs were widely utilized.
Results and discussion. Studies conducted on clinical and pathological material from 200 deaths related to primary forms of tuberculosis (PrFTB) over the last 45 years (1974—2020) based on data from prosectures in Lviv indicate a significant decrease in the number of deaths from primary pulmonary tuberculosis (PrPTB) among the adult population. This decline is attributed to the widespread adoption of modern antimycobacterial therapy for patients with pulmonary tuberculosis (PTB). The predominant clinico-pathological form of PrPTB is tuberculosis of the intrathoracic lymph nodes (TBILN), which manifests with various progression variants. Complications of a specific nature (such as miliary TB, TB meningitis, and TB sepsis) prevail among the direct causes of death. However, diagnosing PrPTB in adults poses significant challenges in modern conditions, with an increasing frequency of underdiagnosis over the years. Diagnostic errors most commonly occur in general diagnostic hospitals during the verification of TBILN and its complications in patients over 30 years old.
Conclusions. The frequency of underdiagnosing PrPTB has increased due to its atypical course, likely resulting from the pathomorphosis of a specific process. The discrepancy between clinical and pathoanatomical diagnoses, attributable to the unique clinical course of PrPTB, was observed in 7.3 % of cases in the first period, 27.2 % in the second, and 40.0 % in the third. Several factors contribute to the underdiagnosis of PrPTB, including short-term hospital stays, the atypical course of PrPTB due to the pathomorphosis of a specific process, inadequate patient examination, the lack of urgency for phthisiological evaluation in general medical institutions and incorrect interpretation of clinical, radiological and laboratory data.
Keywords Primary tuberculosis in adults, diagnosis, errors