Therefore, all patients receiving TPN must also receive biotin at the recommended daily dose, especially if TPN therapy is expected to last more than 1 week. All hospital pharmacies currently include biotin in TPN preparations. Protein deficiency: A shortage of proteins involved in biotin homeostasis can cause biotin deficiency. The main problems involved in biotin homeostasis are HCS, BTD (biotinidase deficiency) and SMVT
Anticonvulsant therapy: Prolonged use of certain drugs (especially highly common prescription anti-seizure medications such as phenytoin, primidone, and carbamazepine), may lead to biotin deficiency; however, valproic acid therapy is less likely to cause this condition. Some anticonvulsants (antiepileptic drugs) inhibit biotin transport across the intestinal mucosa. Evidence suggests that these anticonvulsants accelerate biotin catabolism, which means that its necessary for people to take supplemental biotin, in addition to the usual minimum daily requirements, if theyre treated with anticonvulsant medication(s) that have been linked to biotin deficiency. Severe malnourishment
Prolonged oral antibiotic therapy: Prolonged use of oral antibiotics has been associated with biotin deficiency. Alterations in the intestinal flora caused by the prolonged administration of antibiotics are presumed to be the basis for biotin deficiency. Genetic mutation: Mikati et al. (2006) reported a case of partial biotinidase deficiency (plasma biotinidase level of 1.3 nm/min/mL) in a 7-month-old boy. The boy presented with perinatal distress followed by developmental delay, hypotonia, seizures, and infantile spasms without alopecia or dermatitis. The childs neurologic symptoms abated following biotin supplementation and antiepileptic drug therapy.
PMID 12706308. Thompson, J, Manore M, Sheeshka J (2010). "Nutrients involved in energy metabolism and blood health". In Bennett G, Swieg C,  et al. (eds.). Nutrition: A functional Approach. Toronto: Pearson Canada. p. 353. ISBN 9780321740212. Velázquez A (1997). "Biotin deficiency in protein-energy malnutrition: implications for nutritional homeostasis and individuality". Nutrition. 13 (11–12): 991–2. doi:10.1016/S0899-9007(97)00345-6. PMID 9433719. Weber P, Scholl S, Baumgartner ER (July 2004). "Outcome in patients with profound biotinidase deficiency: relevance of newborn screening". Dev Med Child Neurol. 46 (7): 481–4. doi:10.1111/j.1469-8749.2004.tb00509.x. PMID 15230462. Welling DB (August 2007). "Long-term follow-up of hearing loss in biotinidase deficiency". J. Child Neurol. 22 (8): 1055. doi:10.1177/0883073807305789. PMID 17761663. S2CID 39911504. Wiznitzer M, Bangert BA (July 2003). "Biotinidase deficiency: clinical and MRI findings consistent with myelopathy". Pediatr. Neurol. 29 (1): 56–8. doi:10.1016/S0887-8994(03)00042-0. PMID 13679123. Wolf B (2001). "Disorders of biotin metabolism". In Scriver CR, Beaudet AL,  et al. (eds.). The metabolic & molecular bases of inherited disease. New York: McGraw-Hill. pp. 3935–62. ISBN 978-0-07-913035-8. External links

GeneReviews/NCBI/NIH/UW entry on Biotinidase deficiency
OMIM entries on Biotinidasa deficiency