Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well documented in the literature that patients with active sarcoidosis exhibit elevated serum ACE activity. Since both temporal arteritis and sarcoidosis represent granulomatous inflammatory conditions, this study was undertaken to determine serum ACE activity in patients with temporal arteritis as well as in a control group. The serum ACE levels in patients with temporal arteritis were significantly lower than in the controls. Hence, granulomatous inflammation in temporal arteritis seems to differ radically from the granulomatous inflammation present in sarcoidosis. Serum ACE activity was increasing during cortisone treatment of patients with temporal arteritis, but dropped again as soon as cortisone therapy was discontinued.
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PMID:[Angiotensin-converting enzyme in patients with temporal arteritis]. 299

We suggest that polymyalgia rheumatica with giant cell arteritis (PR-GCA) is an arachidonic acid metabolites mediated disease which can be diagnosed more accurately and monitored more precisely for therapeutic benefits by the serial determinations of the major urinary prostaglandin F, serum urinary lysozymes, serum acid phosphatase, and serum angiotensin converting enzyme rather than by the erythrocyte sedimentation rate, and, when necessary by temporal artery biopsy. The pathogenetic role proposed for prostaglandins (PG) and, even more precisely perhaps, the leukotrienes in this disease is consistent with the several published clinical observations that non-steroidal anti-inflammatory drug treatment produces in some cases a therapeutic paradox of symptomatic relief with concurrent, if clinically silent, progression of the arteritis, even to blindness. Furthermore, the impressive response of PR-GCA to low maintenance dose steroid therapy, a clinical conundrum for decades, is rationally explained on the basis of depressed or obstructed PG metabolism early on in the metabolic cascade. These views warrant clinical evaluation, confirmation or correction in whole or in part, and may increase our understanding of PR-GCA.
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PMID:Polymyalgia rheumatica and giant cell arteritis--rational diagnosis and treatment predicated and disordered prostaglandin metabolism. 627 May 20

Use of tobacco, moderate to heavy alcohol ingestion, infrequent consumption of raw fruits and vegetables, and low income accounted for more [figure: see text] than 98% of the SCE rates among both African American and white men and for 99% of the excess incidence among African Americans compared to whites in a case-control study in three areas of the United States [14]. Thus, it is likely that declines in the prevalence of smoking and drinking, especially among men, and increased intake of fresh fruits and vegetables may have contributed to the downward incidence and mortality rate trends reported for SCE. In addition, it seems plausible that obesity, GERD, and possibly reductions in H. pylori prevalence have contributed to the upward trends in ACE rates. Reductions in smoking, improved diet, and reductions in H. pylori prevalence probably have contributed to the consistent reductions observed for NGA. Contributing factors are less clear for the rising incidence rates of GCA during the 1970s and 1980s. These incidence rates have not continued to rise in recent years.
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PMID:Epidemiologic trends in esophageal and gastric cancer in the United States. 1242 48