Journal of the Association for Academic Minority Physicians : the official publication of the Association for Academic Minority Physicians最新文献

A 47-year-old man with a prior gunshot wound presented with arthritis, constipation, abdominal pain, and weight loss. Arthrocentesis did not reveal the cause of the arthritic complaints, but lead poisoning was suspected and confirmed. We present this case along with a short review of the literature pertaining to this often overlooked and reversible cause of lead poisoning.

Colorectal cancer can develop by two distinct pathogenic mechanisms: one involving chromosomal breakage and aneuploidy (called chromosomal instability) and one involving mutations at DNA micro-satellite sequences (termed micro-satellite instability). Relatively few reports consider these mechanisms of colorectal cancer development across racial or ethnic groups. Available data indicate a moderate increase in colorectal cancer risk among Ashkenazi Jews who have a mutational polymorphism at codon 1307 in the APC gene. In American blacks, there is evidence for a higher prevalence of right-sided colonic tumors and an earlier age of onset of colorectal cancer. In addition, blacks have the highest colon cancer incidence in the United States among ethnic groups and have poorer 5-year survival rates compared with whites. While some differences may be attributed to health care access and socioeconomic differences, these do not completely explain all the variances. In the chromosomal instability pathway, there are polymorphisms within the P53 gene that are more prevalent in blacks, but the significance of these polymorphisms is not fully known. Blacks are more likely to demonstrate micro-satellite instability in their tumors; however, the mechanism for this phenomenon in blacks is unexplored. Differences in diet among racial and ethnic groups and polymorphic variations in drug metabolizing or acetylation genes have not been adequately cataloged. Identification of genetic and environmental factors among racial and ethnic groups should offer some insights into the observed epidemiologic data and advance opportunities to better understand the control and development of colorectal cancer.

Colorectal cancer is a major public health problem. It is also one of the most preventable cancers. Although the colorectal cancer incidence and mortality in whites have been declining over the past 2 decades, these statistics are rising in nearly all ethnic minority groups. The development of colorectal cancer is influenced by exogenous factors, such as dietary constituents and drugs. While reputable data on the chemopreventive effects of diet and drugs, such as nonsteroidal anti-inflammatory drugs (NSAIDs), in specific minority groups are limited, evidence suggests that dietary factors may affect colorectal carcinogenesis in various ethnic minority groups. Clearly, more studies are necessary to resolve these questions. Because the risk of colorectal cancer is increasing in minority patients, they cannot wait for the results of such studies. Therefore, until definitive data are available, it is prudent for physicians to recommend that all individuals be screened for colorectal cancer according to accepted guidelines and to educate them regarding healthful eating habits that will prevent the development of colorectal cancer. Physicians should be particularly vigilant in recommending these approaches to minority patients. Patients should be advised to consume a well-balanced, low-fat, high-fiber diet that is rich in fruits and vegetables.

Essential hypertension affects more than 40 million Americans, or one in four adults. The prevalence of hypertension is greater among the African-American population, with a distressingly high rate of end-organ complications. Although diabetes mellitus has surpassed hyper tension as the dominant etiology of end-stage renal disease in the United States, kidney failure secondary to hypertensive nephrosclerosis remains a significant problem, particularly among African Americans. During the past decade, a shift in the paradigm for the renin-angiotensin system (RAS) has evolved from a circulating vasoactive cascade toward angiotensin II (ANG II) formation at the cellular level. The molecular components of the RAS have been identified in cells, documenting the existence of an autocrine tissue RAS, as well as the presence of enzymes, which catalyze the formation of ANG II by angiotensin-converting-enzyme-independent pathways, providing new targets for therapeutic intervention. The latter challenge has important clinical implications, in view of recent evidence implicating ANG II in pathologic cell growth and cell death and fundamental events in the remodeling of the vascular wall and myocardium in the setting of hypertension. This review focuses on ANG II as a major determinant of end-organ damage in essential hypertension; the benefits of ANG II blockade at the end-organ level, which appear to be independent of the blood pressure-lowering effect; and the emerging role for ANG II receptor antagonists as first-line agents in the treatment of essential hypertension.

Previous clinical and experimental investigations have suggested that pentoxifylline, a methylxanthine, can improve cerebrovascular circulation and reduce cerebral edema in cerebrovascular disorders. Pentoxifylline's mechanism of action includes such rheologic effects as enhanced red cell deformability, alterations in leukocyte activation, and modification of coagulation parameters. The purpose of our investigation was to determine the effects of pentoxifylline in an experimental spinal cord injury model. A compression device was used to cause a reproducible spinal cord injury in adult female albino rats. Spinal cord blood flow was monitored using a laser Doppler flow meter pre- and postinjury for 4 hours. The experimental group (N = 7) was injected with pentoxifylline 10 minutes prior to injury. The control group (N = 5) received an identical protocol, except that this group was injected with an equal amount of saline. Results of this investigation revealed that pentoxifylline treatment significantly increased spinal cord blood flow. In the pentoxifylline-treated group, spinal cord blood flow was significantly higher from 120 to 240 minutes postinjury compared with that of the control group. We conclude that via its multiple physiologic effects, pentoxifylline significantly improves spinal cord blood flow in experimental spinal cord injury.

Meningitis is often associated with hyponatremia due to inappropriate secretion of antidiuretic hormone, and diabetes insipidus is associated with bacterial meningitis. This article describes a patient with acquired immunodeficiency syndrome who experienced recurrent episodes of central diabetes insipidus in association with recurrent fungal meningitis. Desmopressin was effective in controlling the polyuria until the episodes of meningitis resolved.

Colorectal cancer is the third leading cause of cancer-related mortality and a significant public health problem in the United States. Aspirin and other nonsteroidal anti-inflammatory drugs reduced the incidence of colorectal cancers and related mortality by 30% to 60% as well as the incidence of colonic adenomas. This effect is presumably due to an inhibition of cyclooxygenase 2, an inducible enzyme involved in the synthesis of prostaglandins. Prostaglandins are increased in colorectal neoplasms. Aspirin's effect appears to be dose related and enhanced by long-term exposure. Two prospective studies, however, failed to show a protective benefit of aspirin in colorectal cancer. When used long term, aspirin has significant adverse effects and is poorly tolerated. The gastrointestinal toxicity of aspirin is dose related, but even low doses of aspirin (75 mg per day) when used regularly result in significantly higher gastrointestinal toxicity, manifested by melena, hematemesis, and peptic ulcer disease, in aspirin users compared with nonusers. Furthermore, some studies indicate an increased risk of hemorrhagic strokes in aspirin users. Presently, aspirin should not be recommended for the primary chemoprevention of colorectal cancer in the general population due to significant risks of serious cerebrovascular and gastrointestinal adverse effects associated with long-term aspirin use.

Noncirrhotic portal hypertension results from thrombosis of the extrahepatic portal vein that subsequently is recanalized. Liver function is preserved. In the adult, esophageal variceal hemorrhage is the most common presentation and may occur years after the portal vein thrombosis. We report the case of a 34-year-old man who presented with recurrent esophageal variceal hemorrhage. After ultrasonographic and angiographic evaluation, a diagnosis of idiopathic noncirrhotic portal hypertension was made. Due to recurrent esophageal variceal bleeding, the patient required surgical intervention to control bleeding. The incidence of noncirrhotic portal hypertension is unknown. Multiple etiologies may cause the disorder, although nearly half are idiopathic. The pathogenesis, clinical manifestations, diagnostic evaluation, natural history, prognosis, and management of noncirrhotic portal hypertension are discussed. Endoscopic management of esophageal variceal bleeding is the preferred therapy. However, when endoscopic treatment fails to control variceal hemorrhage, a distal splenorenal shunt is likely to be the most successful operation.