Place of lactase deficiency in the pathogenesis of rotavirus infection and possibilities of its correction
DOI:
https://doi.org/10.14739/2310-1210.2014.4.27378Keywords:
Rotavirus Infections, Lactase Deficiency, Infants, Breast Feeding, LactaseAbstract
Rotavirus infection is one of the causes of the lactase deficiency. The pathogenesis of the lactase deficiency in this disease has been actively studied recently. But the dynamic changes of clinical and laboratory signs of the lactase deficiency in early age children on the background of rotavirus infection and methods of their correction are still not well investigated.
The aim of research: tо enhance the effectiveness of treatment of rotavirus infection in early age children through the study of clinical and laboratory parameters of lactase deficiency gravity and development of the method of its correction.
Materials and methods: the research bases on the results of examination of 40 children aged 1 to 18 months suffered with rotavirus infection, who were breastfed. 20 of them had been accepted basic and symptomatic therapy and were in the first group of observation. The second group consisted of another 20 at the same age patients with rotavirus infection, received drug lactase along with this therapy. All the children of the investigation groups had Benedict test (determining the content of carbohydrates in the faeces ) and pH-metry faeces and clinical, biochemical, immunochromatographic and bacteriological tests.
Results: The most part of children had increased levels of carbohydrates in faeces on the day of hospitalization due the clinical manifestations of the disaccharidase deficiency (osmotic diarrhoea, flatulence, intestinal colic): on the day of hospitalization Benedict test result was 0,6±0,3%; increased to 1,0±0,3% on the third day and remained at the same level (0,9± 0,3%) on the fifth day of the observation.
Strongly acidic faeces pH (5,3±0,2)was recorded on the day of hospitalization in absolute majority of patients (80% - 16 children). On the third day of the disease this rate was 5,3±0,2 and was strongly acidic in 75%, and only on the fifth day of the rotavirus infection there were observed the raising of the acidity of faeces to 5,6±0,3.
The analysis of clinical and laboratory parameters of lactase deficiency in patients suffered with rotavirus depending on the type of treatment (with and without drug lactase) pointed to some differences between groups of observation. The duration of diarrhea in children from the second group was significantly lower (5,5±1,0 days) than the duration of the first patient group (7,7±1,2 days, p<0.05) as the duration of flatulence and rumbling gut 3,2±0,9 and 3,5±1 compared with 4,7±1,6 and 4,6±1,0 respectively (p<0.05).
The levels of carbohydrates in the feces of children from the first and second groups were not statistically different with each other on the first day (0,6±0,3% and 0,7±0,4%, respectively) and on the third day of hospital stay (1,0±0,3% and 0,9±0,3% respectively). However, the indicators of the Benedict test had been decreased almost two times (0,5±0,1%) in children from the second group on the fifth day of treatment compared with patients of the first group (0,9±0,3%, p<0.05).
Children of both groups had strongly acidic pH of the faeces (less than 5.5) on the day of hospitalization. There was a normalization of this indicator in 65% (13) patients of the second group and only in 35% (7 children) of the first group. On the fifth day of the observation 95% and 80% of children, respectively, had a normal acidity of the faeces (5,5-6,9).
Conclusion: all infants, who were breastfed, on the background of rotavirus infection had clinical and laboratory signs of the secondary lactase deficiency of varying severity: diarrhea, flatulence, decreased pH of feces to 5,3±0,2, increased level of carbohydrates in the faeces to 1,0±0,1%. The additional purpose of the lactase in the therapy of rotavirus infection helps to reduce the manifestations of secondary lactase deficiency. The rapid acceleration of the leveling of diarrhea syndrome and flatulence occurs by the normalization of samples acidity and by reducing of the level of carbohydrates in the faeces (on the fifth day of illness).
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