It is thought that<unk><unk>  is the result of<unk>  malabsorption caused by low levels of small intestinal<unk> .<unk>  is metabolized by the intestinal<unk>  to galactose and glucose in villous enterocytes. In the colon, unabsorbed<unk>  is converted to hydrogen and short chain fatty acids such as acetate, butyrate and propionate by intestinal bacteria and creates symtoms of<unk><unk> .<unk><unk>  is inherited in an autosomal recessive pattern. Acquired primary<unk>  deficiency is associated with a CC genotype at -13.9 kb upstream of the<unk>  gene. On gross and microscopic pathology, there are no characteristic findings of<unk><unk> .
Lactose intolerance pathophysiology
Galactosemia pathophysiology
Zollinger-Ellison syndrome pathophysiology
Short bowel syndrome pathophysiology
Hirschsprung's disease pathophysiology
Tropical sprue risk factors
Ileus pathophysiology
Pyloric stenosis pathophysiology