Introduction. In patients with thermal injury, changes in microcirculation and liver dysfunction lead to impaired detoxification of ammonia, resulting in its accumulation in the body. This develops hyperammonemia, which exacerbates the phenomena of encephalopathy. To date, questions remain regarding the application of hypoammonemic therapy in burn patients and its impact on disease outcomes.Aim: To assess the severity of hepatic encephalopathy, the level of ammonia in capillary blood, and its reduction against the backdrop of therapy in patients with thermal injury.Materials and methods. The study selectively included a group of 29 patients with severe burn injury (IF more than 145 units) who were treated in the intensive care unit, and a group with mild burn injury (IF no more than 90 units) of 15 patients who were in the hospital ward. The severity of hepatic encephalopathy was determined using the West Haven scale. The level of ammonia in the serum was investigated by microdiffusion method using the portable express analyzer PocketChemTM BA PA-4140. For the correction of hyperammonemia, ornithine was intravenously administered via an infusion pump at a dose of 80 g/day for 10 days. All statistical calculations were performed using the software SPSS v27 (Statistical Package for the Social Sciences).Results. According to the Frank index, patients with burn injury were divided into 3 subgroups (1-3), the lesion depth ranged from 31 units to 91 units or more. High levels of ammonia in the blood were recorded in all three subgroups, and with a Franck index of 91 units. and higher than 285 mmol/l in more than half of the patients. There was a direct relationship between the Franck index and the level of ammonia in patients with burn injury (p=0.01). The higher the Franc Index, the higher the level of ammonia in the blood plasma. This trend can be traced both before the start of treatment (rs1=0.971, rs2=0.996) and after the start of treatment (rs1=0.898, rs2=0.948) in both groups of patients. On the 2-3 day of combined treatment with the inclusion of ornithine, a decrease in ammonia in the blood by 20-30 % of the baseline level was noted in all study groups (p <0.001). The level of ammonia after treatment decreased significantly in all 44 patients (p <0.001).Conclusions. Hepatic dysfunction is one of the manifestations of the systemic response to thermal injury. Therefore, disruption of ammonia utilization processes can have an adverse effect on the overall clinical picture. The presence of liver dysfunction, high levels of ammonia and, as a result, the development of hepatic encephalopathy aggravate the course of burn disease, which significantly complicates the provision of care to this category of patients.
Hyperuricemia is a significant and independent risk factor for cardiovascular diseases. In recent years, scientists have been paying attention to the gut microbiota and its impact on various processes in the human body. Currently, there is evidence of the important role of the microbiota in the pathogenesis of hyperuricemia. An increase in the number of pathogenic microflora contributes to chronic inflammation and an increase in uric acid levels through the mechanisms of purine metabolism. The purpose of this review is to analyze and systematize current data on the impact of the intestinal microbiota on the pathogenesis of hyperuricemia and cardiovascular risk. The article discusses promising methods for correcting hyperuricemia, such as lifestyle modification, fecal microbiota transplantation, probiotics, and postbiotics. The review highlights the need for further research on the microbiota as a key factor in the pathogenesis of hyperuricemia and the development of new and innovative therapeutic strategies.
Thallium compounds are extremely toxic. Their mechanisms of toxicity are associated with reduced activity of enzymes involved in glucose metabolism and impaired synthesis of high-energy compounds. Symptoms of thallium intoxication appear 3-4 hours after its ingestion in the form of dyspeptic phenomena. Within 2-5 days, symptoms of nervous system damage appear in the form of sensory polyneuropathy with neuropathic pain syndrome. After 2-3 weeks, dermatological complications develop: alopecia, anhidrosis, glossitis. The antidote is potassium hexacyanoferrate.Clinical case. A 38-year-old woman was admitted to the hospital with subacute sensorimotor polyneuropathy, hepatitis, and alopecia. Laboratory tests showed a slight increase in liver enzyme levels and a tendency towards decreased blood potassium levels. Stimulatory electroneuromyography revealed sensorimotor polyneuropathy of the axonal type. Given the multisystem involvement, a differential diagnosis was conducted between autoimmune diseases and acute intoxication. A blood test for markers of systemic connective tissue diseases was negative. Toxicological analysis of serum and urine revealed a sharp increase in thallium levels. Administration of potassium hexacyanoferrate yielded a positive result. A follow-up examination of the patient one year later showed complete resolution of motor and sensory symptoms and regrowth of hair.Thallium intoxications are currently extremely rare and present challenges for timely diagnosis. In cases of toxic polyneuropathies, differential diagnosis should include intoxication with other heavy metals (lead, mercury, cadmium) as well as autoimmune processes. Timely administration of the antidote facilitates the elimination of thallium compounds from the body and yields a pronounced positive clinical effect.
The article is devoted to the analysis of the therapeutic potential of mesenchymal stem cells obtained from adipose tissue in the treatment of diabetes mellitus types 1 and 2 and their complications. Brief information on the prevalence of the disease is provided, the main existing approaches to the treatment of diabetes mellitus aimed at maintaining normal glucose and glycated hemoglobin levels are considered, the use of mesenchymal stem cells obtained from adipose tissue is based. The main disadvantage of insulin therapy is the impossibility of imitation the physiological regulation of the glycemic profile and completely eliminating vascular complications in patients. This fact became the reason for searching for more advanced techniques using the regenerative potential of mesenchymal stem cells obtained from adipose tissue. The morphological and immunohistochemical features of these cells are described; a wide range of growth factors and signaling molecules determining their immunomodulatory, antioxidant and antiapoptotic properties is characterized. The paracrine effect of mesenchymal stem cells obtained from adipose tissue can be used in transplantation of pancreatic islets to increase their survival. The ability to preserve the residual mass of the patient’s β-cells, as well as to supply their number by differentiating into insulin-producing cells determines the use of these cells in the treatment of type 1 diabetes mellitus. At the same time, a positive effect on the mechanisms of insulin resistance, stimulation of glycogenesis and regulation of the glycemic profile characterizes the demand for them in the treatment of type 2 diabetes mellitus. Pluripotency and plasticity of mesenchymal stem cells obtained from adipose tissue allow their use in the treatment of diabetic complications: trophic ulcers, diabetic retinopathy and nephropathy. The state of clinical trials aimed at obtaining evidence-based data on the efficacy and safety of mesenchymal stem cells obtained from adipose tissue in the treatment of types 1 and 2 diabetes mellitus is discussed.
Background: To identify independent clinical and laboratory predictors of 28-day mortality in patients with liver cirrhosis.Materials and Methods: A prospective cohort study included 137 patients with liver cirrhosis (decompensated cirrhosis without ACLF, n=72; with ACLF, n=65). Univariate and multivariate Cox regression analysis was used to identify independent predictors of 28-day mortality. Three models were built and compared: a comprehensive model (all significant variables), a basic clinical model (CLIF-C OFs, SpO₂/FiO₂, pneumonia, ACLF stages), and an extended laboratory model (basic model + lactate, ammonia, C-reactive protein).Results: In the univariate analysis, significant predictors of mortality were the severity according to the CLIF-C OFs score, ACLF grades 2 and 3, the presence of pneumonia and urinary tract infection (UTI), elevated levels of lactate, ammonia, C-reactive protein (CRP) and transaminases, as well as decreased SpO₂/FiO₂. In all multivariate models, the following remained independent predictors of an unfavorable outcome: CLIF-C OFs score, ACLF grades 2 and 3, presence of pneumonia, UTI, elevated levels of lactate, ammonia, CRP, and decreased SpO₂/FiO₂.Conclusion: The short-term prognosis in liver cirrhosis is determined by the severity of organ failure, infectious complications, and markers of metabolic stress and inflammation. A comprehensive approach using the CLIF-C OFs score and monitoring lactate, ammonia, and CRP is necessary for risk stratification, which will allow for optimized patient management.
Abramov-Fiedler myocarditis (idiopathic giant cell myocarditis) represents one of the most malignant forms of non-rheumatic inflammatory heart disease. It is typically diagnosed in young and middle-aged patients and is characterized by rapidly progressive heart failure, life-threatening arrhythmias, and thromboembolic complications. The present clinical observation is of particular interest due to the development of Abramov-Fiedler myocarditis in an elderly patient, which is uncommon for this condition. An 80-year-old male was admitted with a clinical picture of ST-segment elevation acute coronary syndrome. On admission, he presented with severe retrosternal chest pain, hypotension, dyspnea, and signs of acute left ventricular failure. Laboratory tests revealed markedly elevated troponin and cytolytic enzymes. Electrocardiography demonstrated ST-segment elevation in the inferolateral wall of the left ventricle, while coronary angiography showed only a 30 % stenosis of the right coronary artery with preserved coronary flow. Despite intensive therapy, the patient developed cardiogenic shock and died on the second day of illness. Post-mortem examination revealed extensive myocardial inflammatory lesions with dystrophic and necrotic changes of cardiomyocytes, massive mixed-cell infiltration, and the presence of multinucleated giant cells. Immunohistochemical staining using CD68 antibodies confirmed the macrophage origin of the infiltrating elements, consistent with the diagnosis of giant cell myocarditis. This clinical case highlights the diagnostic challenges of atypical Abramov–Fiedler myocarditis in elderly patients, where the presentation may closely mimic acute coronary syndrome. The findings emphasize the importance of maintaining clinical vigilance for inflammatory myocardial diseases in older individuals and underscore the decisive role of morphological and immunohistochemical confirmation in establishing the diagnosis.
The improvement of diagnostic methods and the possibilities of modern medicine lead to a deeper study of autoimmune pathology. In clinical practice, cases of a combined course of two or more immunological diseases have become increasingly common, which is called the term “overlap-syndrome” or “crossroads syndrome”. There is still no data on the specific causes of the overlap-syndrome, among the most likely versions is a combination of genetic changes, including the diversity of human leukocyte antigen (HLA) alleles, with external trigger factors. The features of this syndrome are the difficulties of differential diagnostic search due to the variety of symptoms. Untimely verification of the diagnosis leads to a late appointment of treatment and a less favorable long-term prognosis. In clinical practice, a combination of systemic scleroderma or systemic lupus erythematosus with rheumatoid arthritis is most common. This article provides an example of the overlap-syndrome in a 69–year-old patient with three autoimmune pathologies — systemic scleroderma, CABG, and primary biliary cholangitis with multiple organ damage (lungs, skin, gastrointestinal tract, salivary glands, blood vessels, and nervous system). The patient had a long history of Raynaud’s syndrome, as well as primary biliary cholangitis. Two years before the treatment, the patient was diagnosed with Sjogren’s syndrome, and in 2025, a limited form of systemic scleroderma. Thus, during her lifetime, the patient developed 3 autoimmune pathologies included in the overlap-syndrome. Specialists should pay increased attention to patients with a long history of rheumatological disease in order to detect other autoimmune pathologies in a timely manner and initiate timely treatment to prevent the development of complications.
COVID-19 is associated with a high risk of thrombotic complications, which determine the severity and outcome of the disease. Identifying key predictors of adverse outcomes among hemostatic system parameters remains an important task. Aime. To assess the significance of hemostatic system parameters as predictors of adverse outcomes in patients with COVID-19. Materials and methods. A single-center retrospective cohort study was conducted, including 9256 patients with confirmed COVID-19. Depending on the outcome (adverse/favorable), patients were divided into groups. Upon admission, coagulogram parameters (APTT, prothrombin index, thrombin time, fibrinogen, D-dimer, antithrombin III) were assessed using an ACL TOP 750 analyzer. Statistical analysis was performed using the Mann-Whitney U test. For the description of quantitative indicators, the median, the 25th and 75th percentiles were used. Results. Statistically significant differences were recorded in patients with adverse outcome compared to survivors: a significant increase in D-dimer level (median 464.5 [Q25–Q75: 245.0–1120.0] ng/mL vs. 198.0 [110.0–350.0] ng/mL; p<0.0001) and fibrinogen (5.62 [4.70–6.80] g/L vs. 5.03 [4.30–5.90] g/L; p<0.0001), a decrease in antithrombin III activity (81.0 % [73.0–89.0] vs. 99.0 % [90.0– 108.0]; p=0.0001) and prothrombin index (83.0 % [77.0–90.0] vs. 93.0 % [88.0–98.0]; p<0.0001), as well as a prolongation of thrombin time (15.4 s [14.5–16.5] vs. 14.9 s [14.2–15.8]; p=0.0001). The APTT parameter did not differ significantly between the groups (p=0.95). Conclusion. Patients with adverse COVID-19 outcomes exhibited marked hypercoagulation with signs of consumption coagulopathy, characterized by a sharp increase in D-dimer and fibrinogen against a background of decreased antithrombin III and prothrombin index. Monitoring these parameters, especially D-dimer and antithrombin III, has high prognostic value for risk stratification and timely therapy adjustment.
Objective. To identify clinical, laboratory and instrumental predictors of 12-month mortality in patients after PE and to develop a prognostic model. Material and methods. This retrospective study included 150 patients discharged after an episode of PE (2021–2024). The diagnosis was confirmed predominantly by CT pulmonary angiography. Demographic, clinical, laboratory and echocardiographic parameters were assessed. The primary endpoint was death within 12 months after PE (excluding in-hospital and early mortality within 30 days). Univariable and multivariable logistic regression were used to identify independent predictors. Model discrimination was evaluated using the AUC, and calibration using the Hosmer–Lemeshow test and a calibration plot; internal validation was performed by bootstrap resampling. Results. During follow-up, 20 patients (13.3 %) died. Three independent predictors of 12-month mortality were included in the multivariable model: hemoglobin level, estimated glomerular filtration rate (eGFR) and left ventricular ejection fraction (LVEF). The model demonstrated high discriminatory ability (AUC 0.906; 95 % CI 0.852–0.960; p <0.001) and good calibration (χ²=4.009; p=0.856). At the probability threshold p=0.08, sensitivity of the model was 100 % and specificity 69.2 %. The Mezo score showed higher AUC values compared with sPESI, ICOPER, GPS and the Yamaki scores. Conclusion. The Mezo score, based on hemoglobin level, eGFR and LVEF, provides high accuracy in predicting 12-month mortality in patients after PE and, after external validation, may be used for early risk stratification.
A review of modern Russian and foreign literature on the problem of impaired coronary blood flow reserve as a manifestation of microvascular dysfunction has been conducted. When searching for information on this issue, materials from the following databases were used: RSCI, Best Evidence, Scopus, Elsevier, PubMed, Clinical Evidence, Cochrane Library. Violation of the coronary blood flow reserve is an important manifestation of microvascular dysfunction and a key diagnostic criterion for microvascular angina. The evaluation of this indicator has high prognostic and therapeutic significance. Given the heterogeneity of pathogenesis, further research is needed for a personalized approach to the treatment of patients with microvascular angina.
Timely recognition and treatment of pulmonary arterial hypertension, a dangerous complication of systemic connective tissue diseases, is extremely important, as these patients have a poor prognosis.In this article, cardiologists present a clinical case of a diagnostic search for the cause of severe pulmonary arterial hypertension of high functional class and pericardial effusion in a 60-year-old female patient with suspected Sjögren’s syndrome. An assessment of the clinical status and autoimmune markers was performed, echocardiography, computed tomography and magnetic resonance imaging, coronary angiography and right heart catheterization, ophthalmological testing, as well as biopsy, ultrasound examination and salivary gland scintigraphy were performed. Subsequently, Raynaud’s syndrome and scleredema, as well as specific immunological disorders, were verified, which made it possible to diagnose a limited form of systemic scleroderma, prescribe immunosuppressive therapy, and establish the secondary nature of Sjögren’s syndrome.The diagnostic results, supported by the opinions of the supervising doctors, can be discussed by the medical community and are of practical use for cardiologists, who rarely encounter rheumatological diseases in their routine practice.
Heart failure (HF) remains one of the leading causes of morbidity and mortality among patients with HIV infection. Over the past decades, the phenotypes of HF in this population have shifted substantially: while heart failure with reduced ejection fraction (HFrEF) was historically predominant, heart failure with preserved ejection fraction (HFpEF) has emerged as an increasingly important clinical manifestation. The pathogenesis of these conditions is multifactorial, driven by virus-related mechanisms, chronic inflammation, immune dysregulation, cardiometabolic disturbances, and adverse effects of antiretroviral therapy (ART). HFrEF in HIV-infected individuals is primarily associated with chronic inflammation, monocyte– macrophage activation, accelerated atherosclerosis, ischemic heart disease, and pathological myocardial remodeling. By contrast, HFpEF is linked to systemic metabolic abnormalities such as obesity, insulin resistance, dyslipidemia, gut barrier dysfunction, and adipose tissue dysregulation, ultimately leading to the cardiometabolic HF phenotype. A central role in this process is played by metabolic inflammation and the impact of ART (including integrase inhibitors, nucleoside and non-nucleoside reverse transcriptase inhibitors). Understanding the immune and metabolic mechanisms of HIVassociated HF opens new opportunities for therapeutic development. Promising approaches include immunomodulation, metabolic correction, and the use of statins, SGLT2 inhibitors, and GLP-1 receptor agonists. Future studies focusing on patient stratification and clinical outcomes are essential for optimizing the management of this complex patient group
Objective. We aimed to study the parameters of arterial stiffness and its variability during 24-hour monitoring in relation to the clinical and endoscopic activity of ulcerative colitis. Materials and methods. This cross-sectional retrospective study involved 100 patients with ulcerative colitis (mean age 40 [33; 49] years, 38 (38 %) men, disease duration >1 year, without concomitant cardiovascular diseases or metabolic disorders) and 50 healthy control subjects. Arterial stiffness parameters were assessed via 24-hour ambulatory blood pressure monitoring with Vasotens technology. Based on disease activity patients were divided into 3 groups: Group 1 included 30 patients in clinical and endoscopic remission; Group 2 consisted of 22 patients in clinical remission with endoscopic activity; Group 3 included 48 patients with both clinical and endoscopic exacerbation. Statistical analysis was performed using the software package “IBM SPSS Statistics Version 25.0”. Results. Increased arterial stiffness (aortic pulse wave velocity (PWVао) >10 m/s) was detected in 67 (67 %) of ulcerative colitis patients, which was significantly higher than in the control group (OR = 4.74; p<0.001). The most pronounced alterations were observed in the group with clinical-endoscopic exacerbation, which showed increased aortic pulse wave velocity at systolic blood pressure (SBP)=100 mmHg and heart rate (HR)=60 bpm (PWVао 100-60) (p=0.003), augmentation index adjusted for HR=75 bpm (AIx75) (p<0.001), and PWVао variability (p=0.002). In endoscopically active disease without clinical symptoms, AIx75, PWVао100-60, and variability of the rate of increase in blood pressure in the aorta (dP/dt var.) were significantly higher compared to controls. Logistic regression analysis identified age >40 years (p=0.001; 95 % CI: 2.045 to 15.309), disease activity of ulcerative colitis (p=0.025; 95 % CI: 1.151 to 8.200), and a positive family history of cardiovascular disease (p=0.033; 95 % CI: 1.131 to 17.312) as independent predictors of increased arterial stiffness in patients with ulcerative colitis. The prediction model demonstrated good performance: аrea under the ROC curve (AUC) = 0.76 ± 0.051 (95 % CI: 0.66–0.86), sensitivity 0.851, specificity 0.638, and accuracy 0.747 (p <0.001) and can be implemented in practice for the early identification of patients with high cardiovascular risk. Conclusion. Patients with ulcerative colitis exhibit a significant increase in arterial stiffness, which correlates with the degree of inflammatory activity. Endoscopic activity, even in the absence of clinical symptoms, is associated with adverse vascular changes. The developed predictive model, based on three clinical criteria (age >40 years, active ulcerative colitis, and positive family history), could be implemented clinically for the early identification of high cardiovascular risk in this patient population.
Non-invasive vagus nerve stimulation (nVNS) is a promising treatment showing positive results for a wide range of diseases and is currently under active investigation. Surface electrodes are used to stimulate the cervical or auricular branch of the vagus nerve. The growing interest in nVNS is driven by its simplicity, accessibility, safety, and good tolerability. However, to date, this method has not been widely adopted in Russia. This review covers the main stimulation parameters for auricular and cervical vagus nerve targets and the clinical evidence supporting nVNS use in managing headache, tinnitus, sleep disorders, and anxiety. We discuss FDA guidance on cervical VNS for headache and the research gaps that need to be filled to advance the evidence for nVNS in various conditions. We emphasize the necessity and prospects for a domestic (Russian) peripheral vagus nerve stimulation device, which would promote wider clinical integration and data collection on outpatient use.
Pure adenocarcinoma is a somatic-type malignancy that comes from a germ cell tumor and is extremely rare but has been reported. It is usually seen as sarcoma, and less often as carcinoma. This rare phenomenon is generally attributed to the development of a teratomatous component. In most cases, the diagnosis remains straightforward due to the mixing of different germ cell tumor parts and the existence of germ cell neoplasia in situ (GCNIS). But, there are some rare instances where metastatic carcinoma to the testis could be something more. This case presentation discusses a 35-year-old man who had a testicular tumor of adenocarcinoma with enteric features, which looked like metastatic colorectal carcinoma. GCNIS was found in the background testicular tissue, and fluorescence in situ hybridization for chromosome 12p abnormalities showed the presence of i(12p) in the testicular adenocarcinoma, which supports a shared germ cell origin. After the retroperitoneal lymph node dissection, it was found that there were metastatic deposits made up of mucinous adenocarcinoma. Extensive clinical workup helped exclude metastasis from another primary, particularly the GI tract. Our report indicates that adenocarcinoma of intestinal type in an orchiectomy specimen, although usually strongly suggestive of metastasis from a gastrointestinal tract primary, maybe a primary testicular neoplasm of germ cell tumor origin. The patient was treated with radial orchidectomy with retroperitoneal metastasectomy followed by somatic-type malignant histology-directed chemotherapy for colorectal adenocarcinoma. The patient remained in complete remission for a 3.5-years follow-up period.
The article presents the current state and problems of clinical diagnostics of undifferentiated connective tissue dysplasia based on the determination of external phenotypic features, while postulating the primacy of clinical diagnostics of this condition. The terms applied to this problem are considered — phenotypic feature, stigma, minor developmental anomaly, congenital malformation. An original concept of the dysplastic process is introduced to describe the global in the population and private for a specific patient dynamic of the course of the state of altered metabolism of connective tissue, which is determined by the interaction of hereditary and behavioral factors, environmental conditions and the natural process of growth and aging of the organism. An original classification of external phenotypic features by categories of belonging to the organ system, determination method, influence on the clinical picture, potential dynamics of the feature, frequency of occurrence, relation to ontogenesis, dysplastic process and the affected element of connective tissue is given as the basis for pathogenetic analysis of their diagnostic significance. As an example of the application of this approach, minor developmental anomalies are analyzed, anamnestic (impaired hemostasis, traumatic episodes), subjective (variants of pain syndrome), bone (dolichostenomelia, osteochondral dysplasia, limitation of elbow joint extension) and skin external phenotypic signs, for each of which the methods of determination are specified and possible limitations in real clinical practice are indicated. For skin signs, a grouping is carried out in relation to the main properties of the skin determined by a specific structural element of connective tissue. For the sign of increased extensibility, an alternative method of determination by a stretching maneuver on a plane between two standard strokes is proposed.
We presented a clinical case of diagnosing eosinophilic esophagitis in a patient suffering from severe asthma for a long time and receiving therapy with genetically engineered biological drugs: Dupilumab. Difficulties in diagnosis are associated, on the one hand, with the need for histological verification of the diagnosis, and on the other hand, with the heterogeneity of the manifestations of the disease. The frequent coexistence of EoE and other allergic diseases emphasizes the unity of pathogenetic pathways united by mucosal immune reactions. Our clinical case demonstrates the possibility of diagnosing EoE in the absence of characteristic complaints and endoscopic picture in a patient with polyvalent allergies and a long history of severe asthma. Timely use of effective therapy helps prevent remodeling of the esophageal wall with the development of strictures, which can significantly worsen the patient’s quality of life.
For many decades, cardiovascular diseases have been the leading cause of death worldwide. There is evidence that the total number of cardiovascular diseases has doubled over the past 30 years, and the number of deaths from them has steadily increased by 65 % over the same time. At the same time, the increasing prevalence of arterial hypertension as the most important risk factor for cardiovascular diseases is a global problem for world health. In this situation, the issue of antihypertensive therapy and its quality is relevant. There is still a need for further research into new classes of antihypertensive drugs. The article briefly discusses the evolution of views on the pathogenesis of arterial hypertension, the gradual introduction of drugs that lower blood pressure into widespread clinical practice. The article also presents new groups of drugs and the latest trends in the treatment of arterial hypertension.
Still’s disease (SD) is a rare chronic autoinflammatory disease manifested by the development of high peak fever, joint involvement (arthralgias and arthritis), and the appearance of a salmon-colored maculopapular rash. The 2024 EULAR guidelines unified the diagnostic criteria for Still’s disease including fever ≥39°C (102.2°F), recurrent erythematous rash, musculoskeletal involvement, neutrophilic leukocytosis, and elevated CRP and ferritin. If S100 or interleukin (IL)18 levels can be determined, their elevated values will point in favor of SD. Also, treatment strategy have been modified with the administration of biologics of IL-1 or IL-6 inhibitors if glucocorticoids (GCs) are ineffective, and the use of methotrexate (MTX) is considered if biologic therapy cannot be initiated.This case report focuses on the situation of timely diagnosis of SD and resistance to standard therapy with GCs (including pulse therapy) and MTX. Due to insufficient availability of biologics, based on the existing experience of colchicine prescription in SD in the scientific literature, the patient’s therapy was modified with the addition of colchicine at a dose of 1 mg orally per day, after the administration of which regression of clinical manifestations and normalization of acute-phase markers were noted.This clinical experience demonstrates the feasibility of colchicine administration as an alternative to biologics to reduce disease activity if SD is refractory to GC and MTX therapy.
