Hypertransaminasemia is a common extra-intestinal manifestation of celiac disease. Aim. To analyze the frequency of hypertransaminasemia, clinical and anamnestic, serological and morphological picture in children in the active period of celiac disease. Materials and methods. The study included 272 children with celiac disease aged from 8 months to 17 years. The patients were divided into two groups: the first children with hypertransaminasemia, the second without hypertransaminasemia. Results. Hypertransaminasemia was detected in 55.9% of children with celiac disease. The age of manifestation of the disease in the first group was 1.0 [0.5; 2.0] years, in the second group 1.9 [0.5; 4.0] years (p=0.0004). Children of the first group were diagnosed at 2.5 [1.7; 4.9] years, the second group at 4.9 [3.0; 10.8] years (p0.001). The duration of the latency period in children of the first and second groups was 1.4 [0.6; 3.1] years and 2.4 [0.9; 4.3] years, respectively (p=0.002). The average values of IgA anti-tTG antibodies in children of the analyzed groups did not differ, and the indicators of IgG anti-tTG antibodies in the first group were 1.6 (p=0.04) times higher. The level of EMA in children with hypertransaminasemia was 2 times higher than in children without hypertransaminasemia. Conclusion. Hypertransaminasemia is more often detected in young children with early manifestation of the disease, increases with the deepening of atrophy in the mucous membrane of the small intestine. Higher titers of celiac-specific antibodies were detected in children with hypertransaminasemia.

Celiac disease (CD) is characterized by the formation of an anemic syndrome whose etiopathogenesis if of a multifactorial origin. The main types of anemias in children with celiac disease are iron deficiency anemia (IDA) and anemia of inflammation, also called anemia of chronic disease (ACD). This bibliographical review presents current information on the iron metabolism, morphological changes in the epithelium of the intestinal mucosa in celiac disease leading to the development of iron deficiency, pathogenesis of ACD formation in celiac disease, as well as the diagnosis of IDA and ACD in celiac disease.

Aim. To increase detection frequency and reduce the risk of celiac disease complications based on a comprehensive analysis of patterns of iron deficiency states in the active period of celiac disease in children. Materials and methods. 228 children diagnosed with celiac disease, aged 8 months to 18 years, were enrolled. Forms of iron deficiency (ID) were determined according to the complete blood count. Results. The median age of onset was 1.0 [0.6; 2.6] years in children without ID; 1.0 [0.5; 2.1] years in the latent iron deficiency (LID) group and 1.2 [0.5; 3.0] years in children with iron deficiency anemia (IDA). The median age at diagnosis of celiac disease in the analyzed groups was years, respectively. Gastrointestinal symptoms of celiac disease were more common in children with IDA, who were diagnosed with total villous atrophy of the small intestinal mucosa (SIM) in 82.1% of cases, which was 5 times higher than in children with LID (p=0.001) and 2.5 times higher than in children without IDS (p=0.001). Conclusion. Iron deficiency states in the active period of celiac disease have been diagnosed in 73.3% of patients, with the highest incidence observed in infants and older children.

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.