Exacerbation of isoniazid induced peripheral neuropathy by pyridoxine.

Nisar, Mohamed; Watkin, Simon; Bucknall, R C; Agnew, R. A. L.

doi:10.1136/thx.45.5.419

Cited by 24 publications

(7 citation statements)

References 4 publications

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“…It can easily be trans formed into half-life t 1/2 according to: t 1/2 = In2/K [36]. The slow elimination of PLP in its ß-Phase explains its accumula tion in the human organism and its potential chronic toxicity [18][19][20].…”

Section: Pharmacokinetics In Blood Plasma After Oral or Intravenous Vmentioning

confidence: 99%

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Pharmacokinetics of vitamin B6 supplements in humans.

Zempleni

1995

Journal of the American College of Nutrition

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The use of vitamin B6 supplements is widespread today. Doses used are often elevated far above the physiological range and reach levels up to 600-fold higher than recommended dietary allowances for healthy people. While the toxic effects caused by chronic high doses of vitamin B6 have been described earlier, pharmacokinetic data on vitamin B6 supplements are rare. This article reviews the pharmacokinetic data of vitamin B6 from human subjects.

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Section: Pharmacokinetics In Blood Plasma After Oral or Intravenous Vmentioning

confidence: 99%

“…Availability of such data is even more desirable, as toxic effects (ataxia, severe sensory-nervous-sys tem dysfunction) have been described for chronic high-dosed consumption of vitamin B 6 [18]. Such side-effects were ob served when consuming doses of 150-200 mg/day for several weeks [19,20].…”

Section: Introductionmentioning

confidence: 96%

Pharmacokinetics of vitamin B6 supplements in humans.

Zempleni

1995

Journal of the American College of Nutrition

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“…Parry and Bredesen (1985) subsequently reported that as little as 200 mg of pyridoxine per day could induce this syndrome. It has been successfully reproduced in both acutely and chronically treated dogs (oral dosages of 50-300 mg kg À1 day À1 for up to 112 days) (Hoover et al, 1981;Krinke et al, 1980;Montpetit et al, 1988;Schaeppi and Krinke, 1982) as well as rats (Bowe and Veale, 1988;Krinke and Fitzgerald, 1988;Krinke et al, 1985;Nisar et al, 1990;Windebank et al, 1985;Xu et al, 1989), and appears to be secondary to a reversible sensory nerve axonopathy at low and intermediate doses and an irreversible sensory ganglion neuropathy at high doses (Krinke et al, 1980(Krinke et al, , 1985Phillips et al, 1978;Schaeppi and Krinke, 1982;Windebank et al, 1985). In rat studies, three intraperitoneal dosing regimens were generally employed, as follows: short term/high dose 1200 mg kg À1 day À1 for 1-15 days (Krinke and Fitzgerald, 1988;Xu et al, 1989); intermediate dosing, 600 mg kg À1 day for 1-15 days (Krinke et al, 1985;Xu et al, 1989); long term/low dose, 100-300 mg kg À1 day À1 for up to 12 weeks (Krinke and Fitzgerald, 1988;Windebank et al, 1985;Xu et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Pyridoxine-induced toxicity in rats: a stereological quantification of the sensory neuropathy

Perry

Weerasuriya

Mouton

et al. 2004

Experimental Neurology

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Excess ingestion of pyridoxine (vitamin B6) causes a severe sensory neuropathy in humans. The mechanism of action has not been fully elucidated, and studies of pyridoxine neuropathy in experimental animals have yielded disparate results. Pyridoxine intoxication appears to produce a neuropathy characterized by necrosis of dorsal root ganglion (DRG) sensory neurons and degeneration of peripheral and central sensory projections, with large diameter neurons being particularly affected. The major determinants affecting the severity of the pyridoxine neuropathy appear to be duration and dose of pyridoxine administration, differential neuronal vulnerability, and species susceptibility. The present study used design-based stereological techniques in conjunction with electrophysiological measures to quantify the morphological and physiological changes that occur in the DRG and the distal myelinated axons of the sciatic nerve following pyridoxine intoxication. This combined stereological and electrophysiological method demonstrates a general approach that could be used for assessing the correlation between pathophysiological and functional parameters in animal models of toxic neuropathy.

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“…Patients who develop polyneuritis should be treated with 100-200 mg/day of pyridoxine. (3,5,27,28) • Clinical hepatitis: Recent studies have…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Drogas antituberculose: interações medicamentosas, efeitos adversos e utilização em situações especiais - parte 1: fármacos de primeira linha

et al. 2010

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The main objectives of tuberculosis therapy are to cure the patients and to minimize the possibility of transmission of the bacillus to healthy subjects. Adverse effects of antituberculosis drugs or drug interactions (among antituberculosis drugs or between antituberculosis drugs and other drugs) can make it necessary to modify or discontinue treatment. We briefly review the new guidelines for the pharmacological treatment of tuberculosis, introduced by the Brazilian National Ministry of Health in 2009, and describe the general mechanism of action, absorption, metabolization, and excretion of the first-line drugs used in the basic regimen. We describe adverse drug reactions and interactions (with other drugs, food, and antacids), as well as the most appropriate approach to special situations, such as pregnancy, breastfeeding, liver failure, and kidney failure. We also describe the mechanisms by which the interactions among the antituberculosis drugs used in the basic regimen can cause druginduced hepatitis, and we discuss the alternatives in this situation.Keywords: Tuberculosis; Drug interactions; Antibiotics, antitubercular; Pharmacologic actions; Drug toxicity; Drug-induced liver injury. ResumoOs objetivos principais do tratamento da tuberculose são curar o paciente e minimizar a possibilidade de transmissão do bacilo para indivíduos saudáveis. Reações adversas ou interações das drogas antituberculose entre si e com outros fármacos podem causar modificação ou descontinuação da terapêutica. Revisamos sucintamente o novo tratamento farmacológico da tuberculose introduzido pelo Ministério da Saúde do Brasil em 2009 e mostramos os mecanismos gerais de ação, absorção, metabolização e excreção dos medicamentos utilizados no esquema básico. Descrevemos as reações adversas e as interações (com medicamentos, alimentos e antiácidos) assim como a abordagem mais adequada para situações especiais, como gravidez, amamentação, insuficiência hepática e renal. Também descrevemos os mecanismos pelos quais as interações das drogas antituberculose do esquema básico podem causar hepatite medicamentosa e as possíveis alternativas nessa situação.Descritores: Tuberculose; Interações de medicamentos; Antibióticos antituberculose; Ações farmacológicas; Toxicidade de drogas; Doença hepática induzida por drogas.

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Exacerbation of isoniazid induced peripheral neuropathy by pyridoxine.

Abstract: Mycobacterium kansasii was isolated from an area of cavitating pneumonia in a man with rheumatoid arthritis.

Cited by 24 publications

References 4 publications

Pharmacokinetics of vitamin B6 supplements in humans.

Pharmacokinetics of vitamin B6 supplements in humans.

Pyridoxine-induced toxicity in rats: a stereological quantification of the sensory neuropathy

Drogas antituberculose: interações medicamentosas, efeitos adversos e utilização em situações especiais - parte 1: fármacos de primeira linha

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