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While the basic defect is unknown, it has been proposed that the ultrastructural lesion that characterizes MID is best explained as an example of a normal cell component assembled in an abnormal location. The microvilli appear to be assembled on the inner surface of the intracytoplasmic vesicles rather than at the apical cell surface. Furthermore, the prominent periodic acid-Schiff staining of the apical cytoplasm (rather than the brush border), the immunofluores-cent staining of specific brush border enzymes in the apical cytoplasm and the accumulation of secretory granules in the apical region of some cells all suggest that an abnormality of exocytosis exists. Brush border proteins normally reach the plasma membrane at the base of the apical microvilli. They are synthesized in the rough endoplasmic reticulum, processed and assembled as membrane proteins in the Golgi apparatus, and transported to the cell surface along a chain of connecting intracytoplasmic vesicles. However, against this theory, normal exocytosis and localization of two brush border-targeted enzymes (sucrase-isomaltase and dipeptidylpeptidase intravenous) have been demonstrated in biopsies and organ cultures from MID patients. These studies suggested that both direct and indirect constitutive pathways of exocytosis were intact in MID. It was hypothesized that there may be an as yet uncharacterized regulated pathway of exocytosis in enterocytes that is abnormal in MID. Aberrant assembly of microvilli with microvillous inclusions can be produced by agents such as colchicine and cyto-chalasin, which interfere with intracellular trafficking by disrupting microtubules and microfilaments. Analysis of brush border membrane proteins from a patient with MID showed a paucity of a myosin-like protein compared with controls, supporting the hypothesis that this may be a disease of the brush border cytoskeleton, which leads to the distinctive morphology. Empirical trials of various medical therapies, including high dose corticosteroid, pentagastrin, human colostrum, epidermal growth factor, clonidine, and somatostatin or its long acting analogue octreotide, have been reported. Of these, only somatostatin or its analogue octreotide was effective in decreasing the volume of diarrhea and preventing recurrent episodes of dehydration. However, in no instance has medical therapy prevented reliance on parenteral nutrition and intravenous fluid replacement therapy for massive, ongoing intestinal losses. Mortality is high (diarrhea persists until death in 80% of cases [5]), with death generally occurring before 18 months of age. Intestinal transplantation is the only effective treatment for MID. Oliva et al reported the first successful small intestinal transplant in a girl who was two-and-a-half years old; subsequently, Herzog et al reported a successful combined bowel-liver transplantation in a boy who was seven months old. While MID is a rare cause of diarrhea, accurate diagnosis is important because it appears to be an autosomal recessive disease with a high mortality, and genetic counselling of the child’s parents is essential. Further investigation of the pathophysiology of this condition may reveal important insights into enterocyte biology. It's time for you to solve that health problem by using an efficient drug that will not cost you a fortune either. By shopping with the Canadian Health&Care Mall whenever you need any pills, you are going to save yourself a lot of time and money that can be spent in other ways.