Search

The article presents the review and synthesis of mo­dern data of scientific publications from the Scopus, Web of Science databases, and the register of professional scientific publications of Ukraine on the causes, consequences, and methods of correcting secondary lactase deficiency in children. The features of secondary lactase deficiency in antibiotic therapy and other pathological changes in the gastrointestinal tract that develop with the use of antibacterial drugs are described. The authors present their own data on the treatment of secondary lactase deficiency caused by antibiotic therapy in school-age children. It has been found that the use of the lactase enzyme in children with secon­dary lactase deficiency, which has developed on the background of antibiotic therapy, leads to positive dynamics of clinical manifestations already on the third day of taking the drug, and it is a more effective method of correcting these symptoms compared to only dietary recommendations and limited consumption of lactose products. The criteria proposed for prescribing a hydrogen breath test to diagnose secondary lactase deficiency developed on the background of antibiotics are as follows: the presence of clinical manifestations (diarrhea, abdominal pain, excessive gas, bloating, nausea, vomiting) that occurred during antibiotic therapy and are aggravated by the use of lactose-containing products; repeated courses of antibacterial drugs (every 3–4 months) according to the anamnesis; changes in the results of the coprogram (yellow, mushy, foamy feces with an acidic odor, the presence of mucus, fecal pH less than 5.5, a small amount of iodophilic flora); no signs of inflammatory bowel disease according to the results of the coprogram (blood, leukocytes); negative results of rapid tests for the detection of Clostridium difficile toxins A and B in the feces. The use of these criteria to diagnose secondary lactase deficiency associated with antibiotics will improve the frequency of its detection and the reasonable prescription of lactase drugs to reduce the severity of clinical manifestations of lactase deficiency and restore the functional state of the gastrointestinal tract more quickly.

AIM: To estimate the incidence of secondary lactase deficiency (SLD) in patients with postinfectious irritable bowel syndrome (PIBS) and the value of the small bowel microflora in its development and to elaborate treatment options for SLD/MATERIAL AND METHODS: One hundred and thirty-eight patients with PIBS, including 112 (81.2%) women and 26 (18.8%) men, were examined. The patients' mean age was 33.9±9.1 years. The duration of the disease was 2.6±1.4 years. Lactase deficiency (LD) was diagnosed using the color scale to test biopsy specimens from the duodenal retrobulbar region. The bacterial overgrowth syndrome (BOS) was identified by a 2-hour lactulose (20 ml) hydrogen breath test. Sixty patients with moderate SLD were randomized to 2 groups: 1) 41 patients received basic therapy (mesim forte as one tablet t.i.d., no-spa, 40 mg, t.i.d.) and combined probiotic bifiform (Ferrosan) containing Bifidobacterium longum 107, Enterococcus faecium 107 as one capsule t.i.d. for 14 days. Group 2 patients (n=19) had basic therapy in combination with placebo/RESULTS: SLD was detected in 59.4% of the patients with PIBS, including 43.5 and 15.9% with moderate and severe forms, respectively. In all cases, SLD was accompanied by BOS in the small bowel lumen, as confirmed by the results of a hydrogen breath test [101±37 ppm (a normal value of