"Newborn screening for biotinidase deficiency in Brazil: biochemical and molecular characterizations". Brazilian Journal of Medical and Biological Research. 37 (3): 295–9. doi:10.1590/S0100-879X2004000300001. PMID 15060693. Weber, Peter; Scholl, Sabine; Baumgartner, E Regula (2007). "Outcome in patients with profound biotinidase deficiency: relevance of newborn screening". Developmental Medicine & Child Neurology. 46 (7): 481–4. doi:10.1111/j.1469-8749.2004.tb00509.x. PMID 15230462. Wolf, Barry (2003). "Biotinidase deficiency: New directions and practical concerns". Current Treatment Options in Neurology. 5 (4): 321–8. doi:10.1007/s11940-003-0038-4. PMID 12791199. S2CID 25158348. External links
OMIM entries on Biotinidasa deficiency

 This article incorporates public domain material from Genetics Home Reference. United States National Library of Medicine.
Meconium peritonitis refers to rupture of the bowel prior to birth, resulting in fetal stool (meconium) escaping into the surrounding space (peritoneum) leading to inflammation (peritonitis). Despite the bowel rupture, many infants born after meconium peritonitis in utero have normal bowels and have no further issues. Infants with cystic fibrosis are at increased risk for meconium peritonitis. Signs and symptoms
Diagnosis
Twenty percent of infants born with meconium peritonitis will have vomiting and dilated bowels on x-rays which necessitates surgery. Meconium peritonitis is sometimes diagnosed on prenatal ultrasound where it appears as calcifications  within the peritoneum. Treatment
Adhesiolysis
partial resection of pseudocyst
covering enterostomy. History
Meconium peritonitis was first described in 1838 by Carl von Rokitansky. References


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