Echinococcosis or hidatid disease is a parasitic illness which is caused by the most common pathogens Echinococcus granulosus, E. multilocularis and E. oligarthrus. When the agent gets into the organism, it penetrates the organ and forms a cyst. Cysts are located more often (75%) in the liver where they exist without any clinical manifestation. They can be located in other internal organs: lungs, the heart and others. The localization of cysts in several organs simultaneously is a very rare case. The article aims to demonstrate a patient who had a combined echinococcosis of the lungs, heart and liver.

Invasive aspergillosis is a disease that occurs mostly in people with a compromised immune system. The most important pathogen is Aspergillus fumigatus (it accounts for about 90% of the patients). The risk group includes patients who have primary and secondary immunodeficiencies, people receiving immunosuppressive therapy, cancer patients, etc. However, the incidence of this disease among COVID-19 (COronaVIrus Disease 2019) patients have been reported recently. The aim of our work is to present a patient with invasive aspergillosis after COVID-19 who was not in a standard risk group and did not receive immunosuppressive therapy. Conclusion. Patients who had COVID-19 are under a risk of developing invasive pulmonary aspergillosis. Therefore, it is important to exclude this disease in a patient with prolonged pneumonia that does not respond to standard therapy.

Among the most dangerous causes of mortality worldwide, coronary artery disease (CAD) remains the leading cause. Despite the fact that atherosclerosis of the coronary arteries is the main cause of the development of coronary artery disease, clinicians are increasingly identifying myocardial ischemia without coronary obstruction. Myocardial ischemia with non-obstructive coronary arteries (INOCA) is characterized by clinical signs of myocardial infarction (MI) with evidence of coronary artery stenosis on angiography of less than 50%. In recent years, significant advances have been made in understanding the pathophysiological changes that underlie this condition, but the predictors of development of this condition remain unclear. And a diagnosis of INOCA remains a difficult task for the clinician to this day. Determining the mechanism of INOCA and excluding other possible causes of elevated cardiac troponin is important for the development of secondary prevention measures aimed at improving the prognosis of patients after acute myocardial infarction (AMI). A history of disease and use of invasive and noninvasive imaging should lead to the identification of possible vasospastic or microvascular causes of INOCA and their differentiation from myocardial injury caused by other diseases. Compared with patients with AMI due to obstructive coronary artery disease (CAD), patients with INOCA are more often women and tend to have fewer traditional cardiovascular disease (CVD) risk factors.The aim of this article was to review the literature and evaluate the clinical features, ethiology, diagnosis, treatment, and prognosis of INOCA. This review summarizes the current knowledge of INOCA in the areas of epidemiology, pathophysiology and treatment, with an emphasis on modern diagnostic tools for this disease.

Introduction: Langerhans cell histiocytosis (LCH) is a rare clonal myeloid disorder characterized by tissue infiltration with pathological antigen-presenting cells morphologically and phenotypically similar to Langerhans cells. Activating mutations in the MAPK/ERK signaling pathway play a key role in the pathogenesis of LCH. The aim of this study was to characterize the morphological and molecular features of the neoplastic process. Materials and Methods: This study presents a clinical case of a 34-year-old patient with a rare mixed form of LCH combined with Erdheim-Chester disease (ECD), involving multiple organs including kidneys, skin, bones, ENT organs, eyes, and the central nervous system. The patient also had diabetes insipidus, chronic external otitis, and presumptive hereditary forms of anemia and hemochromatosis. A comprehensive histopathological evaluation was performed, including histochemical, immunohistochemical, and immunofluorescent analyses, alongside molecular genetic testing using whole exome sequencing (WES) of blood and skin samples. The patient demonstrated a partial clinical and laboratory response to targeted therapy with trametinib and desmopressin. Results: Comparison of WES data from blood and skin revealed 71,953 shared variants consistent with likely germline changes, as well as 3,081 unique somatic variants in skin and 2,633 unique variants in blood. Low-level mosaic BRAF V600E mutation (VAF = 1%) was detected in the skin, alongside pathogenic germline variants in the STEAP3 (c.523-2A>T, NM_182915.3) and SLC40A1 (c.332T>A, p.Met111Lys, NM_014585.6) genes. Immunofluorescence analysis of the trephine biopsy revealed diverse cellular populations, including sparse tryptase-positive mast cells, which showed minimal contact with each other or other labeled cells. The populations of Vimentin⁺CD11b^–CD34⁺ and Vimentin⁺CD11b⁺CD34^– cells (excluding endothelial cells) accounted for median values of 0.68% and 7.78%, respectively, of the total Vimentin⁺ cells. Regarding CD68 and S100 expression, CD68⁺ cells predominated (median = 55.61%), S100⁺ cells constituted a median of 43.02%, whereas CD68⁺S100⁺ cells were the rarest (median = 2.174%), reflecting the transition of Langerhans cells to LCH cells, encompassing up to 4.81% of the cellular population. This hybrid microenvironment paralleled the patient’s systemic inflammatory activity (elevated acute-phase reactants), multi-organ involvement, and renal interstitial fibrosis/tubular atrophy with reduced kidney function, without serological or histological evidence of vasculitis. Conclusion: This case illustrates the histological heterogeneity and hybrid pathology of mixed histiocytosis, where canonical dendritic LCH cells coexist with macrophage-rich ECD-like stroma. An integrated approach involving a multidisciplinary clinical team, thorough molecular genetic testing, and the application of targeted therapy is essential for improving prognosis and quality of life in young patients.

Hemorrhagic fever with renal syndrome (HFRS) is an acute infectious disease of viral etiology, the main complication of which is severe kidney damage. The disease is characterized by a cyclic course, there are 4 periods (febrile, oliguric, polyuric, recollection). In Russia, the disease occurs almost everywhere, but endemic areas are the Far East, the Urals, and the Volga region. In the pathogenesis of the disease, the greatest significance is the development of vascular endothelial damage, where virus reproduction occurs, leading to increased permeability of the vascular wall with the development of hemorrhagic syndrome, edema. In addition, hemorrhages are promoted by a decrease in coagulation factors, as well as platelets. Cases of mild course of this disease in patients carrying the human leukocyte antigen (HLA)-B27 allele have been described in the literature. The aim of our article is to demonstrate a clinical case of mild course of HFRS in a patient with spondyloarthritis associated with HLA-B27. The patient presented with prolonged subfebrileitis as well as inguinal lymphadenopathy. The disease proceeded without kidney damage, development of hemorrhagic syndrome, which are characteristic manifestations of HFRS. Detected IgG and IgM to hantaviruses (causative agents of HFRS) confirmed the diagnosis. The patient had spondyloarthritis associated with HLA-B27, which, according to the literature, can make the clinical picture less vivid, which is observed in our case. Pathogenetic treatment with glucocorticoids resulted in regression of complaints and improvement of the patient’s condition. This article will be useful for specialists of different profiles, as the clinical picture of HFRS has many nonspecific symptoms that can be considered as manifestations of various diseases.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease of unknown etiology, most commonly occurring in the elderly. The main factors leading to the development of IPF are environmental factors, viruses, and genetic predisposition. The «gold standard» for diagnosis is high-resolution computed tomography. Antifibrotic drugs such as nintedanib and pirfenidone are used as pathogenetic therapy. The aim was to present a patient with a long history of dyspnea and heart failure, in whom the diagnosis of IPF was established only upon hospitalization due to worsening dyspnea. High-resolution computed tomography revealed a characteristic pattern of “honeycomb lung”. Conclusion . The article demonstrates the difficulties in diagnosing IPF in old age associated with polymorbidity (chronic obstructive pulmonary disease, chronic heart failure), which leads to a late start of specific therapy.