Aim. To evaluate the course of chronic obstructive pulmonary disease (COPD) in patients who had SARS-CoV-2 infection of various severity.

Design. Three-centre cross-sectional study under the STROBE standard (STrengthening the Reporting of OBservational studies in Epidemiology).

 Materials and methods. We conducted a complete medical examination of 46 patients with COPD who had COVID-19 during the past year: without viral damage to pulmonary tissue (CT 0, n = 18), with viral damage to pulmonary tissue of max. 50 % (CT 1–2, n = 24) and with viral damage to pulmonary tissue of at least 50 % (CT 3–4, n = 4).

Examinations included analysis of clinical information, laboratory and functional tests, as well as assessment of physical and emotional condition of patients using questionnaires and scales.

Results. After the novel coronavirus infection (NCI), 69.6 % of patients developed COPD complications, 26.1 % of patients presented with COPD symptoms for the first time, which required medical assistance. Disease exacerbation was observed approximately 24 weeks after COVID-19. Post-COVID-19 patients required intensification of baseline therapy. COPD patients who had NCI with viral pulmonary involvement had elevated D-dimer levels; CT 3–4 group also had significant impairment of diffusive capacity of lungs. Patients with pulmonary involvement, corresponding to CT 3–4, had statistically higher (p < 0.001) risk of reduction in the quality of life and aggravated anxiety and depression.

Conclusion. In post-COVID-19 period, patients with COPD are at high risk of disease exacerbation requiring review of outpatient COPD baseline therapy in post-COVID-19-patients. COPD patients who had mild SARS-CoV-2 require long-term monitoring of their coagulation profile and diffusive capacity of lungs and are recommended long-term psychological support.

Aim. Using a specialized fatigue rating scale, to identify risk factors for fatigue syndrome formation in patients hospitalized for COVID-19-induced lung damage at different follow-up periods — at long-COVID and post-COVID.

Design. A retrospective observational study.

Materials and methods. The study included 100 patients — 60 women and 40 men aged 25 to 84 years, Me — 58 (50–64) years, who underwent hospitalization for lung lesions caused by PCR-confirmed COVID-19 infection. Fatigue was detected in 66% of them. Patients were divided into long-COVID (up to 12 weeks) and post-COVID (more than 12 weeks) groups according to the time period after hospital discharge. Fatigue was assessed using the validated Fatigue Assessment Scale (FAS). With a score of 21 or more, fatigue was considered clinically significant. Key inflammatory markers (ferritin, C-reactive protein, neutrophil-lymphocyte ratio, erythrocyte sedimentation rate) and various medical interventions (vaccination, transfer to the intensive care unit, use of etiotropic and anticoagulant therapy at the outpatient stage) were considered as possible predictors of fatigue, the data on which were taken from medical records.

Results. Key inflammatory markers associated with the severity of acute COVID-19 have different prognostic value in the assessment of fatigue. A statistically significant association was found between fatigue syndrome as assessed by FAS and neutrophil-lymphocyte ratio at hospital admission (p = 0.042), erythrocyte sedimentation rate at discharge (p = 0.013), ferritin level at discharge (p = 0.021), whereas a similar association between FAS score and CRP level was not found either at hospital admission (p = 0.775) or at hospital discharge (p = 0.272). Various medical interventions were also associated with the formation of fatigue syndrome. Patients who underwent hospitalization in the intensive care unit were significantly more likely to report fatigue syndrome (p = 0.044, for the long-COVID period p = 0.006), the protective effect of vaccination was significant (p = 0.002, for post-COVID p = 0.009). No association was found between fatigue syndrome and outpatient use of etiotropic therapy (p = 0.459) or anticoagulants (p = 0.358).

Conclusion. Fatigue syndrome after a COVID-19 with lung lesions is associated with the features of the therapy administered and the levels of some laboratory markers during the acute phase of infection.

Aim. To study the association of serum nesfatin 1 (NF-1) levels with body mass index (BMI), body composition and rheumatic cachexia (RC).

Design. Cross-sectional comparative study.

Materials and methods. 110 patients with rheumatoid arthritis (RA) and 60 healthy controls were enrolled in our study. Standard clinical and laboratory examination was performed. NF-1 levels were determined with enzyme-linked immunosorbent assay. Each person undergone dual-energy X-ray absorptiometry with Total Body program.

Results. Serum NF-1 levels were higher in patients with RA, compared with healthy controls (50.49 ± 34.05 vs 31.61 ± 3.17 ng/ml, t = 4.28; p < 0.0001). RC was determined in 30 patients. In healthy controls, the median level of NF-1 was higher in overweight patients than with normal BMI of class 1 obesity (H = 6.0; p = 0.049). NF-1 in patients with RA correlated with lean mass in legs (separately for the left one), left half of the body, trunk and android region. Median levels of NF-1 in patients were comparable in patients with or without RC.

Conclusion. Despite we observed association between serum NF-1 levels and lean tissue mass, this neuroendocrine peptide can’t be used as a marker for RC (Z = 1.45; p = 0.147). Additional studies should be performed to clarify the mechanism of association of NF-1 with lean tissue mass, which would likely contribute to the development of a new approach to controlling this indicator.

Aim. To evaluate the pharmacokinetics of amlodipine in patients with arterial hypertension.

Design. Open cohort study.

Materials and methods. The study included 183 patients, 98 of them with uncontrolled arterial hypertension and 85 with controlled hypertension. All patients regularly took any two antihypertensive drugs (AHD) (lisinopril, amlodipine, valsartan, metoprolol) in combination with indapamide for a month. In the morning, fasting, before taking AHD and 2 hours after taking amlodipine, venous blood samples were taken from all patients to test the concentration of the analyte using high-performance liquid chromatography with tandem mass spectrometry.

Results. In terms of the main concomitant diseases, the patients of the two groups were comparable to each other. Only angina pectoris (p = 0.02) and overweight (p = 0.02) were statistically significantly more common in the pressure–controlled group, and less often — grade 2 obesity (p = 0.002) and acute cerebrovascular accident (p = 0.05). The daily dose of amlodipine in patients with controlled hypertension was significantly (13.9%) lower (p < 0.05) than in participants with uncontrolled hypertension. Both the steadystate concentration of amlodipine and the concentration 2 hours after administration in patients with uncontrolled hypertension were not statistically significantly different from those in patients with controlled hypertension (p > 0.05). In 65.6% of patients with uncontrolled and in 49.4% with controlled hypertension, the concentration of amlodipine was within the therapeutic range (p = 0.03), in 5.2% and 16.5%, respectively, it was above the therapeutic range (p = 0.016), in 29.2% and 34.1%, respectively, — below the therapeutic range (p > 0.05).

Conclusion. Conducting therapeutic drug monitoring and assessing the pharmacokinetics of amlodipine in clinical practice may be useful to improve the effectiveness and safety of therapy.

Aim: Evaluation of Rebamipide treatment efficiency for aspirin-induced gastroduodenopathy in the patients with stable coronary heart disease (CHD).

Design: Randomised controlled study.

Materials and methods: In the course of the conducted research 340 CHD patients receiving long-term acetylsalicylic acid therapy in cardioprotective doses were studied. All the patients received complete clinical laboratory examination. For CHD verification there was applied selective method of coronary angiography. Gastroduodenopathy was verified by esophagogastroduodenoscopy. In both cases frequency and structure of the aforesaid events were assessed.

For aspirin-induced gastroduodenopathy treatment there were applied either endogenic prostaglandin stimulant Rebamipide in combination with proton pump inhibitor (PPI) Pantoprazole (study group, n = 26) or Pantoprazole only (control group, n = 25). Prior to initiating therapy and on completion all the patients were taken blood samples for evaluation of prostaglandin E2 (PGE2) and proinflammatory cytokines (interleukine-1β Il-1β and interleukine-6 Il-6, TNF-α) levels in blood serum for verification of pathogenetic mechanisms in erosive or ulcer-bearing areas developing in gastrointestinal mucosa in association with long-term aspirin therapy. Соntrol group consisted of 26 CHD patients with no evidence of gastroduodenopathy. Statistical processing of the received data was conducted with the software program “Statistics 10.0”.

Results. Aspirin-induced gastroduodenopathy was identified in 51 out of 340 (15,0%) cases. According to esophagogastroduodenoscopy data, erosions of the body and antrum of stomach were prevailing (43,1%) over all the erosive damages. CHD patients before the gastroduodenopathy treatment had significantly lower PGE2 levels in comparison with control group (p < 0,01), while proinflammatory cytokines indices were higher (p < 0,001).

On the treatment completion 19 patients in the control group did not show endoscopic evidence of gastroduodenopathy, the laboratory findings tended to normalization. Gastric mucosa condition in the study group stabilized in all the cases, which was confirmed by statistically significant PGE2 level positive alterations (p < 0,001) and also cytokine profile alterations (TNF-α: p < 0,001; Il-1β and Il-6: p < 0,01).

Conclusion. The presented study demonstrates clinical features of aspirin-induced gastroduodenopathy development in the CHD patients and proposes possible ways of correction.

Aim. To summarize the currently available information on the pathophysiological mechanisms, clinical management, diagnosis and therapeutic approaches in congenital long QT syndrome.

Key points. Congenital long QT syndrome is a hereditary disease characterized by an increased ventricles repolarization time, and, consequently, a lengthening of the QT interval on the electrocardiogram. It is accompanied by fatal cardiac arrhythmias, episodes of syncope and cases of sudden cardiac death. Sixteen genes associated with hereditary long QT syndrome have been described, and genetic testing has become an integral part of the diagnosis of this pathology and risk stratification.

Conclusion. New knowledge about the structure of these proteins contributes to a deeper understanding of the problem of channelopathy, in particular, long QT syndrome, which is the most well-studied of this group of diseases. In addition, continued progress in understanding the genetic basis and mechanisms of development of long QT syndrome leads to the emergence of more effective, targeted, individualized treatment strategies for the syndrome.

Aim. To analyze current data on the incidence, risk factors, diagnostic methods and prevention of gallbladder cancer (GBC).

Key points. GBC is a malignant tumor arising from the epithelium of the gallbladder, characterized by local and vascular invasion, extensive regional lymphogenous and hematogenous metastasis. GBC is the most common malignant tumor of the biliary tract, characterized by high malignancy and low 5-year survival rate. In international recommendations, gastrointestinal tract is considered as a natural stage of the course of biliary pathology: dyskinesia — cholecystitis — cholelithiasis — GBC. Globally, the incidence of GBC varies significantly among different geographic regions, reaching 27 per 100,000 population in Chile. In Russia, according to the Federal State Statistics Service, the incidence of GBC in 2019 was 1.4 per 100 thousand among men, and 2.5 per 100 thousand among women. The incidence of GBC is associated with female gender and increasing age. In the pathogenesis of gallstones, decisive importance is attached to long-term inflammatory changes in the epithelium due to mechanical trauma to the mucous membrane of the gallbladder by stones and a probable increase in the proportion of secondary bile acids in the bile. In the diagnosis of GBC, the recommendations of the Japanese Society of Hepato-Biliary-Pancreatic Surgery, in the first step, particular importance is attached to ultrasound examination of the abdominal organs and biochemical blood test. For a more detailed study, computed tomography, magnetic resonance imaging, magnetic resonance cholangiopancreatography, endosonography, retrograde cholangiopancreatography, oral cholangioscopy and positron emission tomography are useful. Gallstone disease is one of the five most significant risk factors. The remaining 4 leading risk factors for GBC — ethnicity, genetic predisposition, lifestyle factors (excess weight) and biliary tract infections — are common risk factors for patients with cholelithiasis. The risk of developing GBC increases significantly in patients with stones larger than 2 cm and with the duration of the pathology for more than 5 years. Another significant risk factor for GBC is patients with gallbladder polyps, therefore the article presents the main recommendations of European associations for the management of patients with gallbladder polyps.

Conclusion. GBC is currently considered as a possible and natural stage in the course of cholelithiasis. The risk of developing GBC increases significantly in patients with cholelithiasis and gallbladder polyps. Considering the above, diagnosis of possible complications in elderly patients with cholecystitis and gallstone disease should include a thorough clinical, laboratory and instrumental examination. Preventive measures for people with risk factors for GBC should include optimizing diet, weight loss, and, if possible, expanding the physical activity regime. Taking ursodeoxycholic acid preparations helps reduce the content of hydrophobic bile acids in bile and reduces the likelihood of complications of biliary pathology.

Aim. To highlight the problem of pathogenesis, diagnostics and treatment of diabetes mellitus in the outcome of surgical interventions on the pancreas.

Key points. Diabetes mellitus can develop as a result of different diseases, including diseases of the exocrine part of the pancreas. Currently, the term “Diabetes of the Exocrine Pancreas” (DEP) is used. One of the causes of DEP is pancreatic surgery. Pancreatectomy is divided into two main types: total pancreatectomy and partial or pancreatic resection. Partial pancreatectomy, in turn, has two main subtypes: resection of the right half of the pancreas — pancreatoduodenal resection (PDR) and resection of the left half of the pancreas — distal resection (DR). When analyzing the literature data, it is clearly seen that the problem of metabolic outcomes of PDR and others is actively studied and is of great interest. Despite the approximately equal volume of resected tissue, diabetes mellitus occurs more often and earlier after DR, while after PDR, remission of pre-existing diabetes is possible in a significant number of patients. With regard to exocrine function, the situation is reversed — after PDR, the probability of developing exocrine pancreatic insufficiency is higher than after DR.

Conclusion. When studying the literature data, it becomes obvious that there is an urgent necessity to develop approaches to the early combination therapy in patients after pancreatic surgery with simultaneous correction of exo- and endocrine pancreatic.

management of COVID-19.

Key points. The COVID-19 poses the greatest risk to older people and patients with diabetes mellitus type 2. These categories of patients often require long-term hospitalization and intensive care, and the prognosis of the disease and the risk of life-threatening complications are much higher than the average in the population. Determining the risk factors for a severe course of COVID-19 and the mechanisms of their occurrence helps to choose the optimal treatment tactics and significantly improve the prognosis of recovery, reduce the negative consequences of the disease, the so-called post-COVID syndrome, and shorten the rehabilitation period for patients after COVID-19. One of the hypotheses explaining the increased risk of severe COVID-19 in these groups of patients is vitamin B12 deficiency. Perhaps this factor is unifying for the elderly and patients with type 2 diabetes mellitus. Thus, the question arises whether the elimination of B12 deficiency will affect mortality from COVID-19 or recovery rates. In this review, we will analize the latest evidence that shows B12 is involved in many immunological, microbiological and hematological processes that are the target of coronavirus infection.

Conclusion. Our review data confirms the hypothesis that B12 deficiency is a potential risk factor for severe COVID-19, and replacement of this deficiency by prescribing vitamin B12 therapy can be considered as adjuvant therapy and prevention of complications for these categories of patients.

Aim. Demonstration of the rare in general medical practice cause of iron deficiency anemia in a patient with acute and chronic blood loss from vascular ectasias of the gastric mucosa.

Key points. Iron deficiency anemia is one of the most common diseases in the world. The most common cause of anemia in gastroenterological practice is chronic or acute blood loss. Gastric antral vascular ectasia, or GAVE syndrome, is the cause of 4% nonvariceal bleeding from the upper gastrointestinal tract. Diagnosis of the disease requires careful endoscopic and histological examination to differentiate GAVE from similar changes (e.g. portal hypertensive gastropathy) and to choose the correct treatment ways. The presented clinical case demonstrates the difficulties of diagnosing the disease in a polymorbid patient, refractory to endoscopic treatments.

Conclusion. GAVE syndrome is a rare but clinically significant cause of bleeding from the upper gastrointestinal tract. GAVE syndrome may be asymptomatic or accompanied by a clinical picture of anemia or obvious bleeding. Endoscopic treatment using argon plasma coagulation is considered first-line therapy in patients with GAVE syndrome, but most authors confirm the high rate of recurrence of gastrointestinal bleeding after the procedure. The presented clinical case clearly demonstrates a difficult path to the diagnosis of GAVE syndrome, which was finally verified after 7 years of follow-up of a patient with severe, refractory to the therapy iron deficiency anemia, only when a typical endoscopic picture of vascular ectasias in the antrum of the stomach organized in radial bands — the “watermelon” stomach was formed.

At the same time, even the use of modern endoscopic treatment methods was not effective.

Aim. To present a clinical case of the combination of Gilbert's syndrome and primary hemochromatosis.

Key points. The article presents a clinical example demonstrating the complexity of diagnosing diseases caused by genetic polymorphism. Examination of the patient revealed impaired liver function, elevated levels of hemoglobin, serum iron, and transferrin saturation with iron, which led to suspicion of Gilbert's syndrome and primary hemochromatosis. These diagnoses were confirmed by genetic testing.

Conclusion. Diagnosis of the causes of liver damage requires first and foremost exclusion of the most likely ones, but it is important to keep in mind the possibility of continuing the search for the causes of the disease using specific diagnostic methods. 

Aim. To discuses challenges with diagnosis of primary AL-amyloidosis as exemplified by a case study; to analyse the key steps of diagnostic search of systemic amyloidosis in a female patient with a comorbidity.

Key points. In an elderly woman complaining of generalised oedema, shortness of breath, arterial hypertension, at an early stage of diagnostic search, assumptions were made that her oedema was caused by cardiac disorders and that she had congestive heart failure. Given urinary syndrome, azotemia, hypoproteinaemia diagnosed during an initial examination in a district hospital, the patient was referred to the Nephrology Department of the Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, where a comprehensive staged follow-up examination confirmed AL-amyloidosis with kidney, liver, heart involvement.

Conclusion. We have demonstrated challenges with timely diagnosis of systemic amyloidosis as exemplified by a case study in an elderly patient with a comorbidity.

Aim. To demonstrate the possibility of developing primary immunodeficiency with impaired antibody synthesis in an adult patient and discuss the algorithm for laboratory diagnostics and treatment tacticsto demonstrate the possibility of developing primar hypoimmunoglobulinemia after a course of imunosupressive therapy.

Key points. Primary immunodeficiencies are a group of diseases associated with monogenic mutations. They do not have a typical clinical picture. A clinical observation is presented, when a selective deficiency of immunoglobulin A in combination with a selective deficiency of the subclass of immunoglobulin G was detected in a patient with chronic bronchopulmonary pathology. Clinical and laboratory criteria for diagnosis and treatment tactics are discussed.

Сonclusion. Primary immunodeficiencies are often hidden by infectious masks. It is necessary to study serum immunoglobulins, with their normal levels or selective deficiency of immunoglobulin A, to additionally investigate the content of subclasses of immunoglobulin G.