| 摘要 |
Treatment or prophylaxis of depressed or inadequate intracellular pyridoxal phosphate levels in a human or animal patient resulting from a condition, wherein the pyridoxihe (PN)-pyridoxal phosphate (PLP) pathway is disturbed or insufficient, either by chemical factors as occur in physiological shock myocardial, infarction, release of polyamines or toxins by cell death or microbes, vitamin B6 antagonistic drugs; or by enzymatic insufficiencies inherent in the cells of a patient caused by genetic lack of oxidase or genetic oxidase polymorphism; cellular immaturity of premature infants; in conditions involving anemia, destruction of erythrocytes (e.g. malaria, biliary fever). The deficiencies are counteracted by the administration of pyridoxal or a precursor of pyridoxal which in vivo, once it has entered the bloodstream, is rapidly converted into pyridoxal without the intervention of oxidase or oxygen, optionally and preferably without the intervention of kinase.
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