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

Preterm birth rates are higher for African Americans than for whites, but the risk for recurrence is not well defined. We tested the hypothesis that the base and recurrence rates for premature births are higher for African Americans than for whites. We recruited a cohort of African-American and white women giving birth to singleton infants between 1988 and 1993 at Perinatal Network, a Midwest urban teaching hospital. These women had known reproductive history, delivered two or more singletons, and had no planned abortions, miscarriages, or induced preterm labor. Premature infants were born at less than 37 completed weeks of gestation. The total preterm birth rate among African Americans was 24.5%, significantly higher than the 11.1% for whites (relative risk, 2.22; confidence interval, 1.79 to 2.75). The preterm birth rate among African Americans for the second pregnancy was 30.6%, significantly higher than the rate of 18.2% for the first pregnancy and 24.5% for the third and fourth pregnancies. The preterm birth rates for whites were 11.7% for the first pregnancy, 9.8% for the second, and 12.9% for the third and fourth pregnancies, which were not significantly different from each other. Considering only the first two pregnancies, recurrence accounted for 32.6% of all premature births for both African Americans and whites. After the second pregnancy, 68% of African-American and 41.7% of white premature babies were born to women who had previous preterm infants. We conclude that preterm births are relatively common for African Americans and whites in the first two pregnancies. Women, particularly African-American women with a previous preterm birth at either the first or second pregnancy, require more specific management to prevent recurrence of preterm birth.

We report three children with autistic spectrum disorders who underwent upper gastrointestinal endoscopy and intravenous administration of secretin to stimulate pancreaticobiliary secretion. All three had an increased pancreaticobiliary secretory response when compared with nonautistic patients (7.5 to 10 mL/min versus 1 to 2 mL/min). Within 5 weeks of the secretin infusion, a significant amelioration of the children's gastrointestinal symptoms was observed, as was a dramatic improvement in their behavior, manifested by improved eye contact, alertness, and expansion of expressive language. These clinical observations suggest an association between gastrointestinal and brain function in patients with autistic behavior.

A 37-year-old man presented with symptoms consistent with adult-onset Still's disease. Fever and leukocytosis were prominent, and the patient was started on high-dose aspirin for possible acute rheumatic fever. He developed severe anemia as a result of glucose-6-phosphate dehydrogenase deficiency. His treatment was changed to naproxen, and he recovered with restoration of his hematologic parameters. Although Still's disease is frequently accompanied by mild-to-moderate anemia, the development of severe anemia should raise the possibilities of hemolysis secondary to glucose-6-phosphate dehydrogenase deficiency.

Identification of a cDNA clone and the genome of hepatitis C virus in 1988-1989 allowed the development of clinical tests that are now used to detect and quantify hepatitis C virus. This has largely eliminated post-transfusion hepatitis C virus infection; however, the overall incidence of chronic hepatitis C and its complications has greatly increased because of its transmission by other means, lack of a protective vaccine, and inadequate virucidal therapy. Drug abuse is the most common cause of hepatitis C; an etiologic mechanism, however, remains unknown in one third of patients referred to the New Jersey Medical School Liver Center. Response to treatment depends on the viral subtype, immune reactivity of the host, and hepatic pathologic alterations. Many patients with hepatitis C improve or are cured by administering an interferon with or without ribavirin; patients refractory to these measures exhibit persistent elevation of serum cytokines and progressive liver disease. New measures, including protease inhibitors and adjunct immunotherapy, should increase effectiveness of therapy, diminishing hepatitis C virus-induced cirrhosis and hepatocellular cancer. Populations, including the underserved, who harbor and transmit hepatitis C virus require special assistance. This is best achieved by community support groups organized through medical schools, physician associations, and churches to help prevent, detect, and treat chronic hepatitis C.

Hypertension and diabetes are overrepresented in the African-American population and can be particularly devastating in this population. These diseases share genetic predisposition, medical risk factors, and environmental influences as etiologic factors, and they may be interrelated, at least in part, by obesity and accompanying hyperinsulinemia. Noncompliance with treatment plans is a significant barrier to health improvement in both diseases, but increased attention to patient involvement in care is a potential solution to this long-standing problem. The Baltimore Alliance for the Prevention and Control of Hypertension and Diabetes was established in January 1998 to promote care to the underserved community of West Baltimore, Maryland, and to improve outcomes of hypertension and diabetes. Based at the University of Maryland School of Medicine, the Baltimore Alliance comprises a community health worker program, a church-based education and screening effort, managed care and pharmaceutical company (Hoechst Marion Roussel) partners, a health policy and services research group, and inpatient/outpatient clinical care sites in the health system. Mobilization, cultural relevance, and partnership are employed to ensure that the Alliance's goals of increased patient enrollment and retention in treatment programs will be achieved. Thereby, improved outcomes--clinical, humanistic, and economic--will result. Novel as well as classic approaches to patient education, compliance, and goal achievement are being pursued. Complete expert systems for hypertension and diabetes disease management are being created and will be implemented in the near future. Baseline practices and current outcomes are being identified to act as historical controls. The organization and administration of the Alliance will serve as a prototype that others may follow.

Post-extubation stridor is a potential complication of endotracheal intubation. The incidence, risk factors, and outcome in adult patient populations are poorly defined. It was our clinical impression that the occurrence of post-extubation stridor in our medical intensive care unit was more frequent than generally reported. We therefore monitored all intubated patients to determine the incidence of post-extubation stridor and to identify any predisposing factors. All adult patients requiring endotracheal intubation and medical intensive care admission were prospectively observed over a 5-month period in a university-affiliated medical intensive care unit. Sixty-seven patients requiring intubation and medical intensive care admission were evaluated. Twenty-two patients were excluded from analysis because no extubation was attempted. The remaining 45 patients were divided into two groups: 8 with and 37 without post-extubation stridor. Of the parameters analyzed, cuff pressure, treatment with corticosteroids at the time of extubation, and the presence of a primary neurologic process necessitating intubation differed significantly between groups. Six of the 8 patients who developed post-extubation stridor required reintubation. Four of these patients were subsequently successfully extubated, one required tracheostomy, and one patient died after a 2-week deteriorating clinical course. The incidence of significant stridor in our population was 17.8%. Medical management was successful in the majority of patients with post-extubation stridor. Routine tracheostomy following a single episode of post-extubation stridor is not indicated. Further investigation regarding risk factors and a placebo-controlled trial evaluating the efficacy of systemic corticosteroids before extubation in individuals at risk for developing post-extubation stridor are needed.

Diversion of pancreaticobiliary juice from the small intestine results in resetting of the normal negative-feedback regulation of exocrine pancreatic secretion. The mechanism by which this process occurs is not well understood. To examine this regulatory process, we investigated the effects of pancreaticobiliary juice diversion and reperfusion on exocrine pancreas using isolated rat pancreatic acini. Two groups of rats were surgically prepared for pancreaticobiliary juice diversion and reperfusion. Both groups received a liquid diet via a duodenal cannula and saline by intravenous infusion for 24 hours following surgery. Forty-eight hours after the surgery and infusions, the rats were sacrificed, and acinar cells were quickly isolated from each pancreas. Amylase release from isolated acini was measured in response to doses of cholecystokinin octapeptide (CCK-8) and carbachol. Acinar cell receptor binding was measured by using CCK-8 labeled with iodine 125 and N-tritium-methscopolamine bromide as radioligands. Amylase release in response to both CCK-8 and carbachol was significantly decreased in the diversion group when compared with that of the reperfusion group. Receptor binding sites of CCK-8 and methscopolamine bromide were similar in the diversion and reperfusion groups. The results suggest that cholecystokinin- and carbachol-mediated amylase response is affected by pancreaticobiliary juice diversion through a process that most likely involves alteration of post-receptor-mediated intracellular signaling pathways.

Oral thrush and esophagitis caused by Candida are common in patients infected with the human immunodeficiency virus. We present the case of a 33-year-old man with acquired immunodeficiency syndrome who developed dysphagia during a hospitalization for pneumonia. Signs and symptoms were consistent with Candida esophagitis. Despite therapy with fluconazole, the patient's symptoms persisted. At upper endoscopy, a 1-cm, polypoid esophageal mass at 30 cm from the incisors and several other nodular lesions were observed; white plaques were noted throughout the esophagus. Biopsy specimens of the mass contained hyphal forms consistent with Candida species. Therapy with amphotericin B improved the patient's symptoms, and resolution of the mass was confirmed by repeat upper endoscopy. We believe this is the first case in the medical literature of a Candida mass (candidoma) causing dysphagia in a patient with acquired immunodeficiency syndrome. Candidoma should be considered in the differential diagnosis of dysphagia in patients with human immunodeficiency virus infection or immunosuppression due to other causes.

A previously healthy 9-year-old white boy presented with a 13-lb weight loss over a period of 4 weeks and a 4.5-cm mass in the right lung. Histology was compatible with a plasma cell granuloma, which is the most common benign childhood lung tumor. Surgical management with segmental or wedge resection is the usual standard of care in this situation. However, it has been suggested that with a confirmed histologic diagnosis surgical resection is not warranted. This patient was managed conservatively. Repeat computed tomography scan 6 weeks later revealed significant resolution of the lesion, and at 7 months the lesion had totally resolved. Spontaneous resolution of this lesion has been rarely described in pediatric populations.