RESUMO
NSAIDs have been a mainstay of therapy for rheumatologic diseases for a number of years. Unfortunately, their use was accompanied by sometimes unacceptable gastrointestinal and/or renal side effects. Therefore, safer treatment options were sought. In the process of such a search, selective cyclo-oxygenase-2 inhibitors were identified. Drugs in this class have anti-inflammatory properties similar to NSAIDs and did not produce anywhere near the same pattern of NSAID-related gastrotoxicity. The enthusiasm for this class of drugs would appear, at least on the surface, to be well grounded. However, establishing the renal side effect profile of the selective cyclo-oxygenase-2 inhibitors would appear to be a work in progress. Formal studies with selective cyclo-oxygenase-2 inhibitors have not been conducted in the congestive heart failure population. Information does though exist for other patient cohorts--similarly "prostaglandin-dependent" for their integrity of renal function, such as the elderly and sodium-deplete individual. These data would strongly suggest that the selective cyclo-oxygenase-2 inhibitors could decrease glomerular filtration rate and stimulate salt and water retention, comparable to what occurs with nonselective NSAIDs. To date, no compelling information exists, which supports the notion that differences exist among the currently available selective cyclo-oxygenase-2 inhibitors--celecoxib and--in the potential to negatively impact renal function in this and similarly compromised patient populations. (c)2000 by CHF, Inc.
RESUMO
The use of angiotensin-converting enzyme inhibitors can be accompanied by a number of adverse events, including cough, angioedema, and hyperkalemia, as well as a peculiar form of functional renal insufficiency. Other, less obvious side effects accompany ACE inhibitor use, such as a reduction in red blood cell production. This feature of ACE inhibitor use may be employed to good effect, as in the management of post-transplant erythrocytosis. Alternatively, the suppressive effect of ACE inhibitors on red blood cell production may intensify the anemia of chronic renal failure and/or congestive heart failure. The untreated congestive heart failure patient typically has an increased red blood cell mass as a consequence of increased erythropoietin levels, with the latter governed by congestive heart failure-related renal hypoxia. This is not expressed as an increase in hemoglobin concentration because of the increase in plasma volume that marks advanced congestive heart failure. ACE inhibitor therapy can be expected to both reduce plasma volume and decrease red blood cell production. As a result, the hemoglobin concentration changes very little in the ACE inhibitor-treated congestive heart failure patient and usually falls in the low normal range. Recently, erythropoietin has been employed to good effect in congestive heart failure patients with borderline anemia. (c)2000 by CHF, Inc.
