Search

Urinary tract infection (UTI) is a common and important clinical problem in all age groups. Diagnosis of UTI without localization is not difficult, while the differential diagnosis of UTI is complicated by the lack of specific criteria for pyelonephritis and cystitis. The presence of certain clinical symptoms in combination with a positive bacteriological examination of urine does not allow us to reliably determine the localization of the inflammatory process in the urinary system, which is important due to the different approaches to the treatment of pyelonephritis and cystitis. The review considers in detail the data of studies demonstrating insufficient sensitivity and specificity of the accepted markers of urinary tract infection. Studies have found that ESR and CRP cannot act as specific markers for UTI, especially in children with fever. It has been shown that the procalcitonin test can be considered as such a marker, however, a limited number of studies and a noticeable heterogeneity between studies do not allow us to state this fact definitely. In this regard, it is necessary to search for modern, more accurate biomarkers, that allow differentiating pyelonephritis and cystitis at the earliest stages. The article presents data of modern studies, demonstrating the role of cytokines as biomarkers of UTI, showing their role in differentiating UTI of the lower and upper parts. In addition, the potential role of antimicrobial peptides as diagnostic markers of UTI is considered.

Introduction. Vitamin deficiency states are found in 50–80% of pregnant women. Vitamin D deficiency is hazardous because it significantly increases the risk of complications during pregnancy, childbirth, as well as its effect on the child’s condition. Aim. To analyse the relationships between vitamin D status and levels of pro-inflammatory cytokines (IL-1β, IL-6) in children born to mothers with endocrine pathology.Materials and methods. Clinical-anthropometric and laboratory examination included 218 newborns: 98 (45.0%) infants of obese mothers, 32 (14.7%) infants of gestational diabetic mothers with underlying obesity, 22 (10.1%) infants of gestational diabetic mothers, 31 (14.2%) infants of mothers with type I diabetes mellitus and 35 (16.0%) infants of mothers without obesity and signs of impaired glucose tolerance.Results. Severe calcidiol deficiency is more often recorded in infants born to mothers with obesity, gestational diabetes mellitus and type I diabetes mellitus than in infants born to mothers without endocrine pathology. Serum IL-1β level was 2.6 times higher in newborns born to mothers with obesity than in the newborns from the control group — 14.6 (4.7; 36.5) and 5.6 (1.5; 13. 8) pg/ml, respectively (p = 0.04), 2.8 times higher in those born to women with gestational diabetes mellitus with underlying obesity —15.7 (6.5; 54.3) pg/ml (p = 0.02), 4.5 times higher in those born to mothers with gestational diabetes — 25.4 (5.0; 40.5) pg/ml (p = 0.035), and 6.1 times higher in those born to mothers with type I diabetes — 34.3 (3.8; 61.3) pg/ml (p = 0.01). Newborns born to mothers with type 1 diabetes mellitus had a higher serum IL-6 level as compared to the control group — 48.2 (21.3; 75.6) and 20.2 (5.1; 53.2) pg/ml (p = 0.006).Conclusion. Overweight and impaired glucose tolerance in the mother negatively affect the vitamin D sufficiency status, and if a fetus experiences vitamin D deficiency, provoke excessive production of pro-inflammatory cytokines in newborns.

Introduction. Inadequate vitamin D supply worldwide is a public health problem. Low vitamin D levels during pregnancy can lead to abnormal placentation, placental insufficiency and abnormal fetal development, which contributes to poor health after birth.Objective of the study is to analyze the vitamin D status of premature infants born in the south of Russia.Materials and methods. A total of 141 premature infants were examined. Extremely low birth weight was found in 19 (13.4%) newborns, very low birth weight in 35 (24.8%), and low birth weight in 75 (53.2%).Results and discussion. Premature infants had vitamin D deficiency in the majority of cases (51%), with a median of 16.9 [11.7; 22.9] ng/mL. Correlation analysis demonstrated a positive association between 25(OH)D levels and body weight in very low birth weight infants (r = 0.34, p = 0.043). Serum vitamin D concentrations were 1.6 times lower in infants whose mothers did not receive multivitamins than in those whose mothers received multivitamins, 13.8 [9.7; 20.9] and 21.6 [16.9; 28.6] ng/mL, respectively (p = 0.001). Infants with an Apgar score of 7-10 had higher vitamin D levels, 17.8 [11.9; 22.7] ng/mL, than infants with severe asphyxia, 13.8 [9.9; 16.8] ng/mL (p = 0.036). Premature infants with congenital infection had lower 25(OH)D levels than infants without an infectious process, 15.6 [10.8; 22.9] and 18.4 [14.2; 22.7] ng/mL, respectively. Children with an infectious process that subsequently ended in death had lower 25(OH)D levels than children without an infectious process (p = 0.001). Children with cerebral ischemia had lower 25(OH)D concentrations than children without cerebral ischemia (p = 0.001).Conclusions. Premature infants born in the south of Russia have vitamin D deficiency in more than half of the cases. Administration of preparations containing cholecalciferol reduces the proportion of newborns with severe vitamin D deficiency, but does not ensure optimal serum levels. Initially low levels of 25(OH)D can be considered as an unfavorable prognostic sign against the background of the development of congenital infection.

This review presents information on the prevalence, pathogenesis, clinical manifestations, diagnosis and treatment of Duhring’s dermatitis herpetiformis. Although the disease was first clinically described in 1884 by the American dermatologist L.A. Duhring, the study of its pathogenesis and the search for prognostic markers of its occurrence continue. Against the background of a significant expansion of ideas about gluten-dependent diseases and conditions, views on the mechanisms of autoimmune skin damage in dermatitis herpetiformis are detailed. A strong association with hereditary predisposition through the major human leukocyte histocompatibility complex (HLA) DQ2 and DQ8, and a role of epidermal transglutaminase as a major autoantigen in dermatitis herpetiformis are shown. The hypotheses explaining the decline in the incidence of dermatitis herpetiformis in recent decades against the background of increased and more effective serological screening and the resulting earlier diagnosis of celiac disease are commented on. A typical clinical picture of dermatitis herpetiformis, in which erythematous papules, plaques, vesicles are seen, usually clustered on the flexural surfaces of the extremities. Secondary elements are erosions, excoriations and crusts due to rupture of blisters and due to scratching caused by intense itching. A generally favourable prognosis for life and disease is shown with a gluten-free diet and the use of dapsone, glucocorticoids and, if these are ineffective, immunosuppressants. The authors describe a clinical case of the disease in an adolescent girl with a typical clinical history and characteristic rashes on the extensor surfaces of the limbs. The authors show that drug therapy without a gluten-free diet cannot be considered effective, and that the diet for dermatitis herpetiformis, like that for celiac disease, is lifelong. The growing understanding of gluten-associated pathology, which includes dermatitis herpetiformis, in recent decades has led to an intensive search for diagnostic and prognostic markers, as well as the development of ways to correct this group of diseases, including those not related to the lifelong elimination of cereal prolamines.