Anticonvulsive therapy, long-term

Associated with Fat malabsorption Long-term antibiotic fllerapy Breast-fed newborns Infrmt whose mother was taking anticonvulsant therapy during pr nancy Associated with Diet deficient in citrus fruit, green vegetables... 

Choice of a Mood Stabilizer. With the advance of atypical antipsychotics and an ever-expanding list of anticonvulsants, the number of medications reported to treat acute mania and hypomania continues to grow. In fact, all of the atypical antipsychotics, olanzapine, quetiapine, risperidone, ziprasidone, and aripiprazole have FDA approval for the treatment of acute mania. Long-term protection against future episodes of illness has also been demonstrated with several of these agents, which can influence the choice of initial therapy. 

Benzodiazepines are the drugs of choice for status epilepticus (see above) however, development of tolerance renders them less suitable for long-term therapy. Clonazepam is used for myoclonic and atonic seizures. Clobazam, a 1,5-benzodiazepine exhibiting an increased anticonvulsant/seda-tive activity ratio, has a similar range of clinical uses. Personality changes and paradoxical excitement are potential side effects. 

Long-term anticonvulsive therapy with diphenylhydantoin or phenobarbital is known to cause osteomalacia by influencing calcium metabolism (24,25). Alteration in the metabolism of vitamin D, presumably secondary to induction of hepatic microsomal enzymes, leads to the calcium and bone abnormalities (26). Patients on anticonvulsive therapy with phenytoin exhibit a decrease in serum 25-hydroxyvitamin D (27). Adequate dietary amounts of vitamin precursors or microsomal enzyme stimulators might prevent these effects of long-term therapy. 

Bray GP, Harrison PM, O Grady JG, et al. Long-term anticonvulsant therapy worsens outcome in paracetamol-induced fulminant hepatic failure. Hum Exp Toxicol 1992 11 265-270. 

It is not surprising that infant L. suffered diffuse encephalopathy (brain disorder), a cerebral infarction, and seizures during the neonatal period (Yager, 2002). Both asphyxia and hypoglycemia are injurious to the brain. The treatment for seizures consists of providing normal metabolic substrates (e.g., glucose) and appropriate anticonvulsant therapy (phenobarbital), as was done in the present case. The long-term treatment for the child s developmental disabilities is complex and involves the skills of many members of the health care team. 

Osteomalacia and rickets have been reported with long-term anticonvulsant therapy additional risk factors for these conditions (e.g., poor sunlight exposure) increases risk... 

Hoikka V, Savolainen K, Alhava M, Sivenius J, Karjalainen P, Repo A. Osteomalacia in institutionalised epileptic patients on long term anticonvulsant therapy. Arch Dis Child 1981 56 446. 

Feldkamp J, Becker A, Witte OW, Scharff D, Scherbaum WA. Long-term anticonvulsant therapy leads to low bone mineral density—evidence for direct drug effects of phenytoin and carbamazepine on human osteoblast-hke cells. Exp Clin Endocrinol Diabetes 2000 108(l) 37-43. 

The duration of action of rocuronium can be reduced during long-term therapy with anticonvulsants (42). In one study the mean times to recovery of twitch height to 25% of baseline after rocuronium 0.6 mg/kg were 21 minutes in patients taking either carbamazepine or phe-nytoin versus 45 minutes in controls (43). It was suggested that the dose of rocuronium should be increased in patients taking antiepileptic drugs. 

Most patients who ingest these mushrooms require no treatment other than observation. In recent, accidental ingestions, activated charcoal may be administered, although the efficacy of this treatment is unknown. In severe cases, when seizures occur, benzodiazepine therapy may be required. Long-term anticonvulsant therapy should not be required because the effects of the mushroom are short-lived. All other treatment is supportive and symptomatic in nature. Atropine should not be administered because these mushrooms, despite their name, contain only trace to no amounts of muscarine or other cholinergic substances. 

Richens and Rowe (R16) found that the rise in serum alkaline phosphatase in patients receiving anticonvulsants was due to elevation of the hepatic as well as the bone isoenzyme. It was subsequently reported that significant elevations in hepatic enzymes other than alkaline phosphatase occur in patients on long-term anticonvulsant therapy (All, R27) and that the rise in the hepatic isoenzyme of serum alkaline phosphatase precedes the rise in circulating skeletal enzyme (H3). 

C37. Crosley, C. J., Chee, C., and Berman, P. H., Rickets associated with long-term anticonvulsant therapy in a pediatric outpatient population. Pediatrics 56, 52-57... 

L14. Lifshitz, F., and Maclaren, N. F., Vitamin D-dependent rickets in institutionalized, mentally retarded children receiving long-term anticonvulsant therapy. I. A survey of 285 patients. J. Pediatr. 83, 612-620 (1973). 

Kodama, S., Tanaka, K., Konishi, H., Momota, K., Nakasako, H., Nakayama, S., Yagi, J., and Koderazawa, K. (1989) Supplementary thyroxine therapy in patients with hypothyroidism induced by long-term anticonvulsant therapy. Acta Paediatr. Jpn. 31, 555-562. 

B. Adverse effects of chronic valproic acid therapy include hepatic failure (high-risk patients are less than 2 years of age, receiving multiple anticonvulsants, or have other long-term neurologic complications) and weight gain. Hepatitis is not dose related and Is not usually seen after an acute overdose. Pancreatitis is usually considered a non-dose-related effect. Alopecia, red cell aplasia, thrombocytopenia, and neutropenia have been associated with both acute and chronic valproic acid intoxication. 

Matsuda I, Takekoshi Y, ShidaN, FujiedaK, Nagai B, Arashima S, Anakura M, Oka Y. Renal tubular acidosis and skeletal deminei zation in patients on long-term anticonvulsant therapy. 

Maclaren N, Lifshitz F. Vitamin D-dependency rickets in institutionalized, mentally retarded children on long term anticonvulsant therapy. II. The response to 25-hydro> cholecalciferol and to vitamin D2. PecSatrRes( 973) 7, 914-22. 

The anticonvulsants primidone and carbamazepine inhibit biotin uptake into brush-border membrane vesicles from human intestine (Zempleni et al. 2009). Long-term therapy with anticonvulsants increases both biotin catabolism and urinary excretion of 3-hydroxyisovaleric acid. These eifects might be due to displacement of biotin from biotinidase by anticonvulsants, thereby aifecting plasma transport, renal handling or cellular uptake of biotin. 

Mock, D.M., and Dyken, M.E., 1997. Biotin catabolism is accelerated in adults receiving long-term therapy with anticonvulsants. Neurology. 49 1444-1447. 

Mock, D.M., Mock, N.I., Nelson, R.P., and Lombard, K.A., 1998. Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. Journal of Pediatric Gastroenterology and Nutrition. 26 245-250. 

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