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.
NBTE usually occurs during a hypercoagulable state such as system-wide bacterial infection, or pregnancy, though it is also sometimes seen in patients with venous catheters. NBTE may also occur in patients with cancers, particularly mucinous adenocarcinoma where Trousseau syndrome can be encountered. Typically NBTE does not cause many problems on its own, but parts of the vegetations may break off and embolize to the heart or brain, or they may serve as a focus where bacteria can lodge, thus causing infective endocarditis.Another form of sterile endocarditis is termed Libman–Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes. Like NBTE, Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations. These immune complexes precipitate an inflammation reaction, which helps to differentiate it from NBTE. Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium. References
Further reading
Meine TJ, Nettles RE, Anderson DJ, Cabell CH, Corey GR, Sexton DJ, Wang A (2001). "Cardiac conduction abnormalities in endocarditis defined by the Duke criteria". American Heart Journal. 142 (2): 280–285. doi:10.1067/mhj.2001.116964. PMID 11479467. Tissières P, Gervaix A, Beghetti M, Jaeggi ET (2003). "Value and limitations of the von Reyn, Duke, and modified Duke criteria for the diagnosis of infective endocarditis in children". Pediatrics. 112 (6 Pt 1): e467–e471. doi:10.1542/peds.112.6.e467. PMID 14654647. External links

Endocarditis at Curlie