Pediatric Malabsorption Syndromes Follow-up

Updated: Oct 06, 2017
  • Author: Stefano Guandalini, MD, AGAF; Chief Editor: Carmen Cuffari, MD  more...
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Further Outpatient Care

Strict follow-up monitoring with the primary care pediatrician is necessary to reevaluate diet therapy efficacy and compliance.


Further Inpatient Care

If a patient with a malabsorption syndrome shows any symptoms of dehydration or malnutrition, admit the patient to a medical care facility and immediately initiate treatment with parenteral fluid and nutrition supplements.

Treatment for severe acquired carbohydrate malabsorption requires admission to a medical care facility for enteral nutrition with a low-carbohydrate formula and administration of parenteral dextrose.



The availability of sensitive and specific serological testing for celiac disease, namely the antitissue transglutaminase and the newer antideamidated gliadin peptides antibodies, allows the screening of first-degree relatives of patients, in whom the prevalence of celiac disease is higher. [20]

Asymptomatic subjects with positive results and celiac disease that is eventually confirmed by biopsy findings can then initiate a gluten-free diet, thus preventing all malabsorptive symptoms.



Mucosal atrophy caused by infectious gastroenteritis, food-sensitivity enteropathies, or malnutrition can result in an 80% reduction of intestinal surface area. Once the causative agent is removed, the repair of the small bowel is usually rapid (4-6 days). In some patients, repair may be slow, and after 2 months, the villi surface area is 63% normal and the microvillous surface area is only 38% normal.

Some malabsorption syndromes are transient, whereas others simply require a change in diet. Most disorders that cause secondary malabsorption are progressive and, because of systemic complications, result in a limited lifespan in patients. For example, patients with abetalipoproteinemia can die in early adulthood because of cardiac abnormalities, whereas patients with severe autoimmune enteropathies or microvillus inclusion disease have a very poor prognosis without intestinal transplantation.

Outcome in patients with short gut syndrome varies. The long-term prognosis depends primarily on the amount of time parenteral nutrition is required. The complications of parenteral nutrition and the lack of trophic stimulation of intestinal mucosal growth impede recovery. Delayed intestinal autonomy depends on the characteristics of the residual intestine length, presence of the ileocecal valve and colon, and motor function. Bacterial overgrowth compromises intestinal adaptation and increases the risk of liver disorders.