The American journal of medicine
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Angiotensin-converting enzyme (ACE) inhibitors have been designed to reduce the generation of angiotensin II, i.e., to block the renin-angiotensin system. Interestingly, there exists a considerable dissociation between the time course of ACE inhibition and that of blockade of the renin-angiotensin system. Due to the greatly improved methodology used to estimate the degree of ACE inhibition in vitro and in vivo, it has become evident that the compensatory increase in renin levels in response to ACE inhibition is the key factor determining the degree and duration of blockade of the renin-angiotensin system resulting from ACE inhibition. A better understanding of these relationships would seem to be useful in determining duration of action and particularly the optimal dose of any ACE inhibitor.
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A variety of pulmonary complications related to the use of freebase cocaine have been reported in the medical literature. Pulmonary barotrauma, hypersensitivity pneumonitis, pulmonary hemorrhage, obliterative bronchiolitis, asthma, and pulmonary edema have all recently been described. The number of reports are few, reflecting either the low incidence of these complications or the lack of recognition of these phenomena as cocaine-related illnesses. ⋯ Whether cardiogenic or non-cardiogenic factors play a role in the development of pulmonary edema in freebase smokers has not yet been determined. Likewise, the roles of either cocaine, tobacco, or adulterants in producing the observed abnormalities of lung function remain controversial. Further reporting of freebase-related pulmonary complications, as well as the development of appropriate animal models, is needed.
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Patients with multiple myeloma have been shown to have defective opsonization and C3 deposition. Previous studies have suggested that defective C3 deposition may be related to a failure of C3 activation in myeloma serum, the mechanism of which is unknown. We therefore decided to investigate the underlying mechanism responsible for the failure in C3 activation and deposition. ⋯ The defect in C3 activation and deposition in multiple myeloma cannot be explained on the basis of a single complement component abnormality but rather is due to a heterogeneous group of complement abnormalities. Although no correlation between in vitro abnormalities and clinical status was identified in this small group of patients, it is likely that the described complement defects play an important role in defective host defense in multiple myeloma.
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The effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on the gastric mucosa are well documented. The complex mechanisms of gastric damage, however, are not fully understood. This review examines current knowledge about the normal function of the gastric mucosal barrier; the role of prostaglandins in cytoprotection and repair; the mechanisms by which aspirin and other weak organic acids are absorbed by the stomach; and the subsequent cascade of events--including ion trapping and back diffusion of hydrogen ions--that leads to gastric erosion and bleeding. A hypothesis describing NSAIDs' dual insult on the stomach is advanced.