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I A Halaby

Publications and source records attributed to I A Halaby.

4 recordsLinked to original sources
PubMed1996

Collagenous colitis: pathogenesis and management.

INTRODUCTION: Collagenous colitis is a rare disease of unknown etiology that primarily affects middle-aged women. It presents with chronic watery diarrhea and thickening of the subepithelial collagen layer of the colonic mucosa in the absence of endoscopic abnormalities. PURPOSE: This study was undertaken to review the current literature on clinical course, pathology, diagnosis, and current management of collagenous colitis. RESULTS: Collagenous colitis is an inflammatory disease of the colon, clinically characterized by a waxing and waning course of watery diarrhea, an inflammatory infiltration of the colonic mucosa, and a thickening of the subepithelial collagen layer. Its pathogenesis remains unclear, but there is evidence for an inflammatory process triggered possibly by an uncommon luminal agent. Diagnosis is established by colonic biopsies; in the setting of normal colonic mucosa, the disorder is primarily managed medically with virtually no role for surgery. CONCLUSIONS: Pathogenesis of collagenous colitis remains unclear. Current data favor an inflammatory etiology, possibly involving an initiating luminal insult. Guidelines for diagnosis are being established, and medical treatment options are variably effective in the majority of cases. Very unusual refractory cases may benefit from surgical management.

Biopsy↗
PubMed1996

Population-based analysis of treatment of pancreatic cancer and Whipple resection: Department of Defense hospitals, 1989-1994.

BACKGROUND: The influence of hospital experience and referral patterns on the operative mortality rate of pancreaticoduodenectomy was studied in a worldwide hospital system. METHODS: We analyzed computerized data on pancreatic cancer patients from U.S. Department of Defense (DOD) hospitals from 1989 to 1994. RESULTS: Six hundred ninety-eight patients had pancreatic cancer, and 130 Whipple operations (105 for pancreatic and 25 for other cancers) were performed with an 8.5% 30-day operative mortality rate. Although most resections were done in teaching hospitals performing more than 1 Whipple procedure per year, their results were not superior to smaller, lower volume nonteaching hospitals. Patients transported for resection were younger than patients undergoing resection at their local DOD hospital but had similar outcomes. The operative mortality rate was higher after unusual resections and with increasing age; the tumor stage had no effect. Unresected patients undergoing combined radiation and chemotherapy had the longest survival times. Radiation therapy was associated with significantly longer survival times in patients without distant metastases, but chemotherapy was associated with a longer survival time when metastases were present. CONCLUSIONS: This mortality rate 8.5% for Whipple resections matches that from other large populations. Equivalent results were obtained in DOD teaching hospitals and smaller, community-type institutions. Because the DOD medical system minimizes financial and logistic barriers to transfer, the even distribution of DOD pancreatectomy mortality suggests that these barriers may favorably influence single institutional outcomes.

Adenocarcinoma↗
PubMed1993

Relationship between ischemia and ischemic neuronal necrosis to astrocyte expression of glial fibrillary acidic protein.

It is not entirely clear whether the proliferative changes in astrocytes following cerebral ischemia are in response to neuronal injury or are secondary to the direct effects of ischemia on the astrocytes. Therefore, the following study examined the relationship between post-ischemic astrocytosis with the extent of neuronal necrosis and the severity of the ischemia. Astrocyte reactivity was assessed by alterations in glial fibrillary acidic protein (GFAP), using immunohistochemistry and evaluation by optical density analysis. Cerebral ischemia was produced in rats by temporary occlusion of the carotid and vertebral arteris for 2, 10 and 30 min. This results in damage to the CA1 neurons after a characteristic delay of several days, the duration of which is inversely proportional to the severity of the ischemia. CA3 neurons are resistant to the ischemia and do not suffer permanent injury. The results showed that GFAP immunoreactivity significantly increased in the CA1 region after all three ischemic intervals but the rise of GFAP in the CA3 area reached significance only after 30 min of ischemia. The peak and duration of the GFAP increases thus correlated with the extent and the maturation of the neuronal necrosis. This suggests that with mild injury (2 and 10 min ischemia), post-ischemic astrocytosis is closely related to its neuronal environment rather than to the ischemic insult itself. Furthermore, the results showed an initial decrease in and delay of the subsequent GFAP rise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗