Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date, the pathogenesis of systemic lupus erythematosus (SLE) remains unclear. By critically analyzing clinical facts and laboratory data, a hypothesis is proposed: drug-induced lupus erythematosus (DILE) is linked to a deficiency in Coenzyme A (CoA) that is secondary to a deficiency in pantothenic acid. This hypothesis is used to explain the high incidence of SLE in females, the role of sex hormones in this disease and the mechanism underlying a flare. The actions of anti-malarials and steroids are also discussed. The protean clinical presentation of SLE is attributed to co-existing deficiencies of dietary factors in addition to pantothenic acid. Contributing factors to these deficiencies may include increased nutritional requirements resulting from gene mutations. Treatment is replacement therapy with doses of pantothenic acid that is hundreds of times higher than that of the Dietary Reference Intake (DRI) and other vitamins. Using this method, 12 SLE females were studied with promising results.
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PMID:Systemic lupus erythematosus: a combined deficiency disease. 1514 49