This is a rare, autosomal recessive cause of congenital diarrheal.
Types:
- Early onset (95%): since birth
- Late onset (5%): 1-3 months
Pathophysiology:
Management:
- Unusual parenteral hydration & electrolyte (sodium, potasium, chloride, acetate) needs due to high stool losses.
- Progressive cholestasis often worse than other PN dependent conditions. Case reports suggestive that it is responsive to intavenous omega-3 therapy.
- Monitor urine electrolytes frequently.
- Often require intravenous iron due poor enteral absorption.
- Anecdotally, diarrhea may improve with antibiotic treatment for altered microbiota.
- Extra-intestinal manifestations of MVID:
- Gallbladder
- Lung
- Pancreas (insulin resistance)
- Learning difficuties, autism
- Renal (Fanconi's, hematuria)
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Gonzales E, Taylor SA, Davit-Spraul A, Thébaut A, Thomassin N, Guettier C, Whitington PF, Jacquemin E. MYO5B mutations cause cholestasis with normal serum gamma-glutamyl transferase activity in children without microvillous inclusion disease. Hepatology. 2017 Jan;65(1):164-173. doi: 10.1002/hep.28779. Epub 2016 Oct 5. PubMed PMID: 27532546.
Fuchs J, Fallon EM, Gura KM, Puder M. Use of an omega-3 fatty acid-based emulsion in the treatment of parenteral nutrition-induced cholestasis in patients with microvillous inclusion disease. J Pediatr Surg. 2011 Dec;46(12):2376-82. doi: 10.1016/j.jpedsurg.2011.09.061. Review. PubMed PMID: 22152886.
Halac U, Lacaille F, Joly F, Hugot JP, Talbotec C, Colomb V, Ruemmele FM, Goulet O. Microvillous inclusion disease: how to improve the prognosis of a severe congenital enterocyte disorder. J Pediatr Gastroenterol Nutr. 2011 Apr;52(4):460-5. doi: 10.1097/MPG.0b013e3181fb4559. PubMed PMID: 21407114.