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When lactose intolerance is due to secondary lactase deficiency, treatment of the underlying disease may allow lactase activity to return to normal levels. [6] In people with celiac disease, lactose intolerance normally reverts or improves several months after starting a gluten-free diet, but temporary dietary restriction of lactose may be needed.
Some affected children are better able to tolerate glucose and galactose as they get older. [citation needed] Small amounts of glucose in the urine (mild glucosuria) may occur intermittently in this disorder. Affected individuals may also develop kidney stones or more widespread deposits of calcium within the kidneys. [citation needed]
It is an autosomal recessive metabolic disorder that can cause liver disease and death if untreated. Treatment of galactosemia is most successful if initiated early and includes dietary restriction of lactose intake. Because early intervention is key, galactosemia is included in newborn screening programs in many areas.
Hereditary fructose intolerance (HFI) results in poor feeding, failure to thrive, chronic liver disease and chronic kidney disease, and death. HFI is caused by a deficiency of fructose 1,6-biphosphate aldolase in the liver, kidney cortex and small intestine. Infants and adults are asymptomatic unless they ingest fructose or sucrose. [citation ...
Galactosemia is sometimes confused with lactose intolerance, but galactosemia is a more serious condition. Lactose intolerant individuals have an acquired or inherited shortage of the enzyme lactase, and experience abdominal pains after ingesting dairy products, but no long-term effects. In contrast, a galactosemic individual who consumes ...
Based on histologic findings the differential diagnosis of pediatric autoimmune enteropathy is graft-versus-host disease, Crohn's disease, and food sensitivity enteropathies such as celiac disease and lactose intolerance. [6] Lactose intolerance should be excluded in infants with intractable diarrhea. Like autoimmune enteropathy, lactose ...
The development of early cataracts in homozygous affected infants is fully preventable through early diagnosis and treatment with a galactose-restricted diet. Some studies have suggested that, depending on milk consumption later in life, heterozygous carriers of galactokinase deficiency may be prone to presenile cataracts at 20–50 years of age.
enzyme deficiencies or mucosal abnormality, as in food allergy and food intolerance, e.g. celiac disease (gluten intolerance), lactose intolerance (intolerance to milk sugar, common in non-Europeans), and fructose malabsorption. pernicious anemia, or impaired bowel function due to the inability to absorb vitamin B 12,