Deficiency barbiturates

Acute intermittent porphyria is a dominantly inherited partial deficiency of porphobilinogen deaminase, and causes axonal polyneuropathy. Acute intermittent porphyria is caused by partial deficiency of porphobilinogen deaminase, an enzyme required for heme biosynthesis. Patients may present with acute abdominal pain, rapidly progressive sensorimotor axonal polyneuropathy or psychosis, and have elevated concentrations of the heme precursor 8-amino-levulinic acid in their urine. Symptoms may be precipitated by treatment with barbiturates or other drugs and are suppressed by treatment with hematin [59]. 

Measurements in vivo, such as barbiturate sleeping times, are in agreement with these findings, sleeping times being longer in protein-deficient animals. Toxicity may also be influenced by such factors as a low-protein diet. For example, the hepa to toxicity of carbon tetrachloride is markedly less in protein-deficient rats than in normal animals, and this correlates with the reduced ability to metabolize the hepato toxin in the protein-deficient animals. 

HA, mild pain Action Nonnarco tic analgesic w/ barbiturate Dose 1—2 tabs or caps PO q4-6h PRN i in renal/hepatic impair 4 g/24 h APAP max Caution [C, D, +] Alcoholic liver Dz Contra G6PD deficiency Disp Caps, Liq, tabs SE Drowsiness, dizziness, hangover effect Interactions T Effects OF benzodiazepines, opiate analgesics, sedatives/hypnotics, EtOH, methylphenidate hydrochloride i effects OF MAOIs, TCAs, corticosteroids, theophylline, OCPs, BBs, doxycycline EMS See Acetaminophen may impair coordination, monitor for depression concurrent EtOH use T CNS depression butalbital is habit forming... 

M.I.R. (1985) Interactions of Barbiturates and a Choline Deficient Diet in Promotion of Liver Carcinogenesis. This Volume. 

Barbiturates, Choline-Deficient Diet, and Liver Cancer 329... 

Tuberculous patients lacking in liver N-acetyl transferase who are treated with isoniazid are likely to develop polyneuritis (39). An enzyme abnormality is also responsible for the precipitation of acute intermittent porphyria by the barbiturate drugs (40). Likewise, the rare hereditary resistance to coumarin anticoagulant drugs is thought to be due to an enzyme deficiency (41). 

Most interactions of trimethoprim and co-trimoxazole with other drugs are due to fohc acid antagonism. This may be more pronounced with co-trimoxazole than with either drug alone. Such interactions have previously been suspected with anticonvulsants, such as barbiturates, phe-nytoin, and primidone, which themselves produce folic acid deficiency and megaloblastic anemia (88). In order to circumvent the risk of folate deficiency, folic acid or folinic acid can be given. There is some concern that folate replacement may antagonize the desired antimicrobial effect, particularly in some protozoal parasites, but this concern has been debated (89). 

Lack of sufficient vitamin D causes faulty bone mineralization as previously described. The symptoms of vitamin D deficiency are the same as for calcium deficiency—tingling, muscle spasms, and numbness. Using mineral oil, barbiturates, or cholestyramine, or abusing alcohol can cause vitamin D deficiency. So can fiver or kidney disorders, or certain bowel prob-... 

Neuropsychiatric, neuromuscular, autonomic dysfunction, and intense abdominal pain characterize AIP. In the liver, this enzyme deficiency results in the increased inducibility of abnormal heme intermediates by certain drugs. Drugs and agents known to induce hepatic cytochrome P450 enzymes or to increase hepatic heme mrnover are theoretically capable of precipitating porphyria. Barbiturates, estrogens, alcohol, and heavy metals such as lead have been documented to induce porphyria in genetically susceptible people. ... 

Measurements in vivo, such as barbiturate sleeping times, are in agreement with these findings, sleeping times being longer in protein-deficient animals. Toxicity may also be influenced by such factors as a... 

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