Cycloserine

Brand Names: Seromycin

Clinical Names: Cycloserine

Summary

generic name: Cycloserine

trade name: Seromycin®

type of drug: Antibiotic.

used to treat: active pulmonary and extrapulmonary tuberculosis (including renal disease), usually in conjunction with other therapeutic agents; also for acute urinary tract infections caused by susceptible strains of gram-positive and gram-negative bacteria, especially Enterobacter species and E. coli.

mechanism: Cycloserine inhibits cell-wall synthesis in susceptible strains of gram-positive and gram-negative bacteria and M. tuberculosis.

overview of interactions:
• nutrient affected by drug: Vitamin B6 (Pyridoxine)



Interactions

nutrient affected by drug: Vitamin B6 (Pyridoxine)

• research: Many studies have found that cycloserine impairs availability of vitamin B6 in the body. The clinical significance of this interaction remains uncertain.

• nutritional support: An individual taking cycloserine might protect themselves against vitamin B6 depletion by supplementing their diet with 25 mg of vitamin B6 per day. Some research indicates that such nutrient support might also aid against adverse side effects of the drug.
(Goldshtein VD, et al. Probl Tuberk 1971;49(11):15-19; Haden HT. Arch Intern Med 1967 Nov;120(5):602-606; Laine-Cessac P, et al. Biochem Pharmacol 1997 Oct 15;54(8):863-870; Nair S, et al. J Clin Pharmacol 1976 Aug;16(8-9):439-443; Roe D. 1984, 288-89, 505-523.)

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Do not rely solely on the information in this article.

The information presented in Interactions is for informational and educational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, case reports, and/or traditional usage with sources as cited in each topic. The results reported may not necessarily occur in all individuals and different individuals with the same medical conditions with the same symptoms will often require differing treatments. For many of the conditions discussed, treatment with conventional medical therapies, including prescription drugs or over-the-counter medications, is also available. Consult your physician, an appropriately trained healthcare practitioner, and/or pharmacist for any health concern or medical problem before using any herbal products or nutritional supplements or before making any changes in prescribed medications and/or before attempting to independently treat a medical condition using supplements, herbs, remedies, or other forms of self-care.


References

Goldshtein VD, Fondaminskaia LD, Semenova AS. [The influence of cycloserine on the metabolism of several B complex vitamins in pulmonary tuberculosis]. Probl Tuberk 1971;49(11):15-19. [Article in Russian]

Haden HT. Pyridoxine-responsive sideroblastic anemia due to antituberculous drugs. Arch Intern Med 1967 Nov;120(5):602-606.

Laine-Cessac P, Cailleux A, Allain P. Mechanisms of the inhibition of human erythrocyte pyridoxal kinase by drugs. Biochem Pharmacol 1997 Oct 15;54(8):863-870.
Abstract: The aim of this study was to investigate the interaction between drugs chosen for their clinical neurotoxicity or chemical structure and vitamin B6 metabolism. After a preliminary screening of drugs to determine their potential inhibitory effect on erythrocyte nonpurified pyridoxal kinase (PLK) (EC 2.7.1.35), additional investigations, including kinetic studies and detection of chemical reactivity between the inhibiting drugs and pyridoxal (PL) or pyridoxal-5'-phosphate (PLP), using UV-visible spectrophotometry and mass analysis, were carried out to specify the mechanism of PLK inhibition. Depending on the results, the inhibiting drugs were divided into three groups. The first group included theophylline and progabide and inhibited PLK using either PL or pyridoxamine (PM) as substrate and thereby were true inhibitors. Moreover, they did not form covalent complexes with PL or PLP. The second group, which included cycloserine, dopamine, isoniazid, and thiamphenicol glycinate, inhibited PLK using PL, but not PM, as substrate. They were able to react with PL or PLP to form covalent complexes, and kinetic studies suggested that the observed PLK inhibition was due to these formed complexes. A third group, which consisted of levodopa, D-penicillamine, and muzolimine, inhibited PLK using PL, but not PM, as substrate. They formed, with PL or PLP, chemical derivatives that probably had no inhibitory effect on PLK. These results and the clinical consequences of such interactions are discussed and compared with results of previous studies.

Nair S, Maguire W, Baron H, Imbruce R. The effect of cycloserine on pyridoxine-dependent metabolism in tuberculosis. J Clin Pharmacol 1976 Aug;16(8-9):439-443.
Abstract: Measurements were made of urinary tryptophan metabolites of 13 tuberculosis patients in order to reveal characteristics of pyridoxine-dependent metabolism before and during cycloserine treatment. The abnormally high level of xanthurenic acid excretion in untreated patients suggests a decreased availability of pyridoxal phosphate related to the disease process. Although plasma cycloserine levels were kept high once therapy began, xanthurenic acid excretion before and after tryptophan load became progressively more normal as symptoms diminished. This observation suggests that the convulsions which may sometimes accompany cycloserine administration are not due to a direct pyridoxine antagonism by the drug. Throughout the study, no significant changes in 5-hydroxyindoleacetic acid excretion were observed. Presumably, the metabolic pathway of serotonin is unaffected by tryptophan loading, cycloserine administration, or the apparent pyridoxine depletion associated with tuberculosis.

Roe D. Risk factors in drug-induced nutritional deficiencies. In: Roe D, Campbell T, eds. Drugs and Nutrients: The Interactive Effects. New York: Marcel Decker, 1984, 288-289, 505-523.