This article presents the results of a study reflecting the history of the Department and Clinic of Pediatric Diseases of the Dagestan Medical Institute during the Great Patriotic War of 1941–1945. Professor P.D. Davydov work in Dagestan and his role in creating children healthcare was examined based on archival documents, literature, and periodicals for the first time introduced in scholarly discourse. Special attention was paid to educational process organization at the Department of Pediatric Diseases at the Dagestan Medical Institute during the war. The authors devoted considerable attention to scientific research conducted by P.D. Davydov, specifically focusing on the results of the fight against dysentery, which were reflected in his doctoral dissertation, defended in 1944. The article also examines public health education and the activities of the Dagestan Society of Pediatricians.

Hypokalemic periodic paralysis is a rare genetic pathology characterized by spontaneous muscle weakness up to paralysis along with hypokalemia. The disease development is associated with changes in the CACNA1S, SCN4A, KCNJ2, and KCNJ18 genes regulating ion channels functioning in skeletal muscle cells. This article discusses features of etiology, clinical signs, and treatment methods for hypokalemic periodic paralysis, as well as issues of differential diagnosis with other types of periodic paralysis. Variants of prevention of muscle weakness episodes to improve patients’ quality of life are also covered.

Background. Autoimmune gastritis (AIG) is a chronic immune-mediated disease that primarily affects the cells of the gastric mucosa and fundus, characterized by the development of two main types of autoantibodies: antibodies to gastric parietal cells and antibodies to intrinsic factor. The characteristics of the manifestation and diagnosis of AIG in children are currently not defined worldwide.

Case description. A 13-year-old girl complains of intermittent abdominal pain. She is being monitored at her community hospital for recurrent iron deficiency anemia. A blood test revealed an increase in the level of antibodies to deamidated gliadin peptides of the IgG class — 26.0 U/ml, antibodies to gliadin of the IgG class — 72.0 U/ml, antibodies to gliadin of the IgA class — 38.0 U/ml. She was referred to the Children’s Endoscopy Center of the N.F. Filatov Children’s City Hospital of the Moscow Health Department to rule out celiac disease. An esophagogastroduodenoscopy was performed, and pseudopyloric metaplasia of the gastric mucosa was suspected. This was confirmed histologically, and AIG was suspected. Subsequently, IgG antibodies to gastric parietal cells (> 100.0 U/ml) were detected, and the child was finally diagnosed with AIG. The girl’s twin sister, who had similar complaints, was then examined. According to the research conducted, she also had verified AIG.

Conclusion. In children, AIG often occurs with latent clinical symptoms, which leads to the diagnosis being established only years after the onset of the disease. Early diagnosis of AIG is of particular importance, since this pathology can lead to the development of serious complications, including adenocarcinoma, neuroendocrine tumors of the stomach, atrophy of the mucous membrane, pernicious anemia, etc. In this regard, a comprehensive approach and vigilance are necessary when examining patients with risk factors (iron deficiency anemia, pernicious anemia, autoimmune thyroid diseases, type 1 diabetes mellitus, celiac disease, vitiligo, Addison’s disease). Currently, endoscopic examination with biopsy is one of the leading diagnostic methods.

Background. Blaschkolinear Acquired Inflammatory Skin Eruption (BLAISE) is a rare condition observed in variety of acquired benign diseases. There are no effective management approaches for patients with BLAISE.

Case description. Female patient, 17 years old. She suffers from atopic dermatitis from the age of 9. She was admitted to the dermatology department due to previous therapy inefficacy. The examination has revealed typical rashes along the Blashko lines along with atopic dermatitis signs. Considering severe and continuously recurrent course of the underlying disease, the patient was administered with interleukin (IL) 4/13 inhibitor dupilumab, 600 mg, followed by 300 mg once per 2 weeks. Both atopic dermatitis and BLAISE have regressed during this therapy.

Conclusion. Association of atopic dermatitis and BLAISE may demonstrate torpid course with topical and systemic glucocorticoids administration. Dupilumab, IL-4/13 inhibitor, may be an acceptable therapeutic option in patients with severe atopic dermatitis and comorbid BLAISE.

Background. Diagnosis of mild forms of mucopolysaccharidosis (MPS) causes significant difficulties, and its untimely recognition delays pathogenetic therapy initiation.

Case description. Girl Ya., was consulted by neurologist at the age of 6 months due to delayed motor development. Umbilical hernia was diagnosed at the age of 1 year, appearance of fine motor disorders, adenoid hypertrophy and hearing impairment were noted at the age of 3 years, elbow and knee stiffness, gait disturbance, fatigue, exertional dyspnea, and corneal opacity — at 4 years, myelopathy of cervical spinal cord with flail hands paraparesis, external hydrocephalus, flexion elbow contractures, varus feet deformity, and bilateral tubotitis were diagnosed in the hospital at the age of 5. She was examined by a geneticist for а first at the age of 8, disease from the MPS group was suspected. Decreasein arylsulfatase B activity (1.8 nM/mg/h) (reference values 42.8–129.8 nM/mg/h) and dermatan sulfate excretion were revealed, thus, MPS, type VI was suspected. Full sequencing of the ARSB gene was performed, no pathogenic or probably pathogenic variants were revealed. Arylsulfatase activity was within the reference values during the next analysis, however dramatic decrease in a-L-iduronidase activity was detected — up to 0.001 μM/L/h (reference values 1–25 μM/L/h). Pathogenic variant c.208C> T (p.Gln70*) was revealed in exon 2 of the IDUA gene, as well as variant of unknown clinical value c.1505G> C (p.Arg502Pro) in exon 10, both in a heterozygous state. The patient was diagnosed with mucopolysaccharidosis, type I (Scheie syndrome). Pathogenetic (enzyme replacement) therapy was initiated, its results were followed-up until the age of 17 years old.

Conclusion. Early diagnosis of MPS is crucial for timely pathogenetic treatment initiation, as it can significantly improve the prognosis for mild forms of the disease.

Congenital clubfoot is one of the most common musculoskeletal disorders in children. Timely diagnosis and early management via Ponseti method allow to achieve good and excellent results in 98% of all cases. Neonatologists and pediatricians frequently encounter children with this condition in their outpatient practices. Parents of these children often ask questions about congenital clubfoot management to nonspecialized doctor. This article provides detailed description of clinical examination of a child with congenital clubfoot, features of Ponseti method treatment process, challenges patients and their parents face during treatment, and answers to frequently asked questions during outpatient visits.