The American journal of medicine
-
During the last 15 years, there has been a dramatic decline in the incidence of bleeding from stress-related mucosal damage. This decrease probably relates to an increased understanding of those mechanisms responsible for the pathogenesis of stress-related mucosal damage and the application of this knowledge to prophylaxis and treatment. ⋯ The nearly routine use of prophylactic antacid and/or histamine (H2)-receptor antagonist therapy to adequately buffer intragastric acidity is another factor that has minimized the development of stress-related damage. As continued understanding of the mechanisms responsible for stress damage is obtained and therapy applied appropriately, this disease should become a disorder of only historical interest in years to come.
-
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) is an autosomal dominant, systemic fibrovascular dysplasia in which telangiectases, arteriovenous malformations, and aneurysms may be widely distributed throughout the body vasculature. Major clinical manifestations include: recurrent bleeding from mucosal telangiectases and arteriovenous malformations; hypoxemia, cerebral embolism, and brain abscess due to pulmonary arteriovenous fistulas; high-output congestive heart failure and portosystemic encephalopathy from hepatic arteriovenous malformations; and a variety of neurologic symptoms due to central nervous system angiodysplasia. ⋯ Ligation, resection, or embolization may be indicated for pulmonary arteriovenous fistulas. The prognosis and survival of patients with hereditary hemorrhagic telangiectasia are favorable, providing treatable complications are accurately diagnosed.
-
Randomized clinical trials have become the accepted scientific standard for evaluating therapeutic efficacy. Contradictory results from multiple randomized clinical trials on the same topic have been attributed either to methodologic deficiencies in the design of one of the trials or to small sample sizes that did not provide assurance that a meaningful therapeutic difference would be detected. When 36 topics with conflicting results that included over 200 randomized clinical trials in cardiology and gastroenterology were reviewed, it was discovered that results of randomized clinical trials often disagree because the complexity of the randomized clinical trial design and the clinical setting creates inconsistencies and variation in the therapeutic evaluation. ⋯ The design issues include eligibility criteria and the selection of study groups, baseline differences in the available population, variability in indications for the principal and concomitant therapies, protocol requirements of the randomized clinical trial, and management of intermediate outcomes. The issues in interpreting the trials include the regulatory effects of treatments, the frailty of double-blinding, and the occurrence of unexpected trial outcomes. The results of this review suggest that pooled analyses of conflicting results of randomized clinical trials (meta-analyses) may be misleading by obscuring important distinctions among trials, and that enhanced flexibility in strategies for data analysis will be needed to ensure the clinical applicability of randomized clinical trial results.
-
Changes occur in lipid and lipoprotein concentrations with age that increase the risk of developing atherosclerotic disease. In children and young adults (less than 20 years of age), the plasma total cholesterol concentration decreases between the ages of 10 and 20 years. After age 20, the plasma total cholesterol concentration increases progressively, and in men reaches a plateau between the ages of 50 and 60 years, whereas in women, it reaches a peak between 60 and 70 years of age. ⋯ The triglyceride concentration increases progressively in men, reaching peak values between 40 and 50 years of age, and then declining slightly thereafter. In women, the triglyceride concentration increases throughout their lifetime, but is always higher in those using estrogens. Whether these changes in lipoprotein concentrations merely accompany the increasing prevalence of atherosclerotic vascular disease that occurs with age, or contribute to it, is unknown at this time.
-
Because a prospective controlled investigation showed a highly significant association of the onset of acute myocardial infarction with signs of preceding respiratory infection, the clinical, laboratory, experimental, and epidemiologic evidence more directly supporting this association was analyzed. Inflammation--specifically of infectious, usually viral, origin--has been shown by several lines of evidence to be capable of precipitating or mimicking clinical myocardial infarction. Myocardial biopsy is producing rapidly increasing confirmation that myocarditis can perfectly mimic clinical acute myocardial infarction. ⋯ Effects of blood-borne infectious agents, particularly viremia, on platelets in vivo and in vitro--aggregation and lysis with release of vasoactive substances--have even more serious potential for coronary thrombosis and vasospasm. It is not clear whether such mechanisms operate entirely independently or are more potent in high-risk patients, particularly in view of the demonstrable hypercoagulable state in many patients with coronary disease. Because of the great importance of confirming precipitating mechanisms for acute myocardial infarction (as well as its frequent mimic, myocarditis), intensive investigation of the relation between infection and infarction has important preventive and therapeutic implications.