Biomedical subjects
Publications and source records attributed to C M Wilcox.
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OBJECTIVES: The role of vascular ectasia (VE) as a cause of bleeding in the upper GI tract (UGIB) in patients with chronic renal failure (CRF) is controversial. We evaluated the prevalence VE as a cause of UGIB in patients with CRF and examined factors associated with its presence. METHODS: Over a 50-month period (from August 1, 1990, to September 30, 1994) all patients with UGIB evaluated by our gastroenterology consultative service at a large inner city hospital were prospectively identified. CRF was defined as a serum creatinine concentration > or = 2 mg/dl for the 6 months before and after the bleeding episode. Endoscopy was performed in all patients, usually within 48 h of admission. VE was considered causative if the typical endoscopic features were observed in the absence of other potential bleeding sources. RESULTS: Of the 727 patients with UGIB undergoing endoscopy, 60 (8%) had CRF. The mean age of these patients was 61 +/- 15 yr, and the mean serum creatinine concentration was 5.6 mg/dl (range, 2-29.4 mg/dl). Hypertension and diabetes mellitus were the most common causes of renal failure. Gastric ulcer (37%) and duodenal (23%) ulcer were the most frequently identified causes of UGIB, followed by VE in eight patients (13%). VE was significantly more common in patients with CRF (13 vs 1.3%, p < 0.01). The prevalence of VE as a cause of UGIB was related to duration of renal failure (p = 0.004) and need for hemodialysis (p < 0.0001). VE was also the most frequent cause of recurrent bleeding in these patients. CONCLUSIONS: The most common cause of UGIB in patients with CRF is peptic ulcer disease. VE is more frequent in patients with CRF than in those with normal renal function, and its prevalence seems to be related to the duration and severity of renal disease.
OBJECTIVE: To determine the causes of esophageal ulceration, the response rate to currently available therapies, and the long-term outcome in patients with human immunodeficiency virus (HIV) infection. DESIGN: Prospective cohort study. SETTING: An urban county hospital. PATIENTS: Consecutive patients with HIV infection and endoscopically detected esophageal ulceration during a 4-year period. INTERVENTION: Causes of ulcers were determined from clinical, endoscopic, and pathologic findings. Standard medical therapies for the identified causes were instituted, and ulcer healing was endoscopically confirmed when possible. MEASUREMENTS: Symptomatic and endoscopic response to therapy and long-term outcome, including survival. RESULTS: 100 patients with esophageal ulcer were identified. Ulcers caused by cytomegalovirus alone were the most common (n = 45); idiopathic ulcers were almost as frequent (n = 40). Herpes simplex virus esophagitis alone was identified as a cause in only 5 patients. Several potential causes of ulcer were found in 5 patients, including Candida esophagitis in 27 patients. Ten patients developed more than one cause of ulceration during long-term follow-up. Eighty-five patients had specific medical therapy for their identified disorders and had an overall response rate of 98%. Median survival from time of diagnosis was 8.9 months (range, 2 days to > 42 months). A difference in median survival was found between patients with cytomegalovirus esophagitis and those with idiopathic esophageal ulcer (7.6 months compared with 13.1 months; P = 0.03). CONCLUSIONS: Given 1) the broad spectrum of causes of esophageal ulceration, 2) that each of these causes requires specific therapy, and 3) the apparent high response rate, it is important to do endoscopic evaluation with mucosal biopsy in patients with HIV infection so that a diagnosis can be established and appropriate therapy instituted. Despite effective therapy, long-term survival is poor; however, long-term remission and survival may occur in some patients.
There are many options as to the accuracy of a patient's subjective localization of an obstructing esophageal lesion. However, there are few studies specifically examining this issue. Over a 35-month period, all patients evaluated by our gastroenterology service undergoing endoscopy for dysphagia were prospectively identified. The patient's subjective localization for the level of obstruction was evaluated by an investigator blinded to the results of prior barium esophagography and recorded on a schematic of the bony skeleton. At the time of endoscopy, the most proximal level of the obstructing lesion was documented. In all, 139 patients with dysphagia and an esophageal stricture were evaluated. Barium esophagograms were performed prior to endoscopy in all but nine patients (6.5%). The most common lesions causing dysphagia were carcinoma (34.5%), gastroesophageal reflux disease (22.3%), and a Schatzki's ring (15.8%). The level of obstruction was localized exactly in 30 patients (21.6%), within +/- 2 cm in 72 (52%), and within +/- 4 cm in 31 additional patients (74%). Eight patients (15%) with a distal esophageal lesion localized the obstruction to the proximal esophagus, whereas only two patients (5%) with a lesion in the proximal esophagus localized the level of obstruction to the distal esophagus. Overall, patients with distal obstructing lesions were more likely to have referral > 6 cm proximally than proximal lesions with referral to the distal esophagus (P = 0.003). There were no significant differences in accuracy based on the cause of dysphagia. In conclusion, a patient's subjective localization of the level of an esophageal stricture is highly accurate. Patients appear to be most accurate in localizing proximal rather than distal lesions.
PURPOSE: Although cytomegalovirus (CMV) esophagitis is an important complication of acquired immunodeficiency syndrome, there has been little study specifically addressing the response to currently available antiviral therapy, relapse rate without maintenance therapy, and long-term outcome. PATIENTS AND METHODS: Over a 45-month period, 44 patients with CMV esophagitis established endoscopically and histopathologically were prospectively identified from among all human immunodeficiency virus (HIV)-infected patients undergoing endoscopy. Induction therapy consisted of intravenous ganciclovir at 10 mg/kg per day for approximately 14 days. Foscarnet was given at 60 mg/kg every 8 hours for nonresponders to ganciclovir. RESULTS: Of these patients, 35 completed induction ganciclovir therapy, resulting in a complete response in 17 (49%) and a partial response in 10 (29%), yielding a 77% overall response rate. Seven of 8 nonresponders were subsequently treated with foscarnet, with a clinical response seen in 5 patients. In the 18 eventual complete responders to ganciclovir or foscarnet followed up without maintenance therapy, 7 (39%) relapsed at a median of 4 months (range 2 to 18 months). In all cases, relapse was manifested by recurrent odynophagia. Reinduction ganciclovir therapy yielded a complete response in 1 patient and a partial response in 2, and induction foscarnet treatment resulted in a complete response in the other treated patients. During long-term follow-up, 1 complete responder developed CMV colitis with concurrent retinitis, and 4 other patients developed retinitis. The median survival after diagnosis was 8.2 months, although survival for greater than 1 year was seen in 4 patients. No patient died as a direct result of esophageal disease, although ulcer-related bleeding may have contributed to death in 2 patients with end-stage liver diseases and hepatic encephalopathy. CONCLUSIONS: CMV esophagitis has a favorable response to induction ganciclovir therapy, and a long-term remission may occur after induction therapy alone. Despite the favorable response to ganciclovir therapy, the long-term survival is poor, reflecting the severe immunodeficiency of these patients.
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Computed tomography (CT) is increasingly used to evaluate abdominal diseases, including those of the colon. Recent CT studies have documented colonic abnormalities in patients with pseudomembranous colitis; however, these findings are not widely appreciated by primary care physicians. Over a 25-month period, we prospectively identified 13 patients who had proven pseudomembranous colitis evaluated by abdominal CT. The primary indications for CT were abdominal pain with or without fever in 9 patients, fever of unknown origin in 1, evaluation of other abdominal processes in 1, and as part of this study after documentation of pseudomembranous colitis in 2. Importantly, the diagnosis of pseudomembranous colitis was first considered on the basis of the CT findings in 9 patients with abdominal pain or fever. Diffuse thickening of the colonic wall, ranging from 4 to 40 mm, was the most common radiologic finding, seen in 8 patients (62%). In 3 cases, wall thickening was seen in the descending colon and rectosigmoid, with one of these also having a thickened transverse colon. Colonic wall thickening, which may be dramatic, appears to be an almost uniform accompaniment of pseudomembranous colitis and may be present without clinically severe disease. These CT findings in the appropriate clinical setting should suggest colitis due to Clostridium difficile and prompt the appropriate evaluation for this disease.
We report the case of a 55-year-old woman who was thought to have systemic lupus erythematosus (SLE) for more than 13 years before Crohn's colitis was correctly diagnosed. The differentiation of Crohn's disease from SLE may be difficult, as illustrated by our case. Gastrointestinal symptoms, laboratory studies, and radiographic findings may appear similar between the two diseases. The correct diagnosis has important treatment and prognostic implications.
OBJECTIVE: Although the presence of oropharyngeal (OP) candidiasis plays an important role in the evaluation of human immunodeficiency virus (HIV)-infected patients with esophageal symptoms, there is little information on the utility of OP findings in patients with esophageal ulceration. METHODS: Over a 54-month period, all HIV-infected patients with esophageal ulceration had careful inspection of the oropharynx at the time of presentation with esophageal complaints and at endoscopy. HIV-infected patients without esophageal ulceration undergoing endoscopy during the last 30 months had OP findings similarly documented. OP ulceration ulceration was determined based on clinical, endoscopic, and histopathological findings. RESULTS: Of the 124 patients identified with esophageal ulcer, 14 (11%) had coexistent OP ulceration: herpes simplex virus, four; idiopathic esophageal ulcer, four; cytomegalovirus, three; herpes simplex virus and cytomegalovirus, two; idiopathic and cytomegalovirus, one. Four patients had OP ulcer without esophageal ulcer; only one of these patients had esophageal symptoms. All OP lesions healed with therapy for the esophageal ulcer. Twenty-eight patients with esophageal ulcer had OP candidiasis (23%); 21 of these patients (75%) also had Candida esophagitis. The sensitivity and specificity of OP ulcer for esophageal ulcer were 11% and 97%, respectively. The positive and negative predictive values of OP candidiasis for esophageal candidiasis were 90% and 82%, respectively. CONCLUSIONS: OP ulceration is uncommon in patients with esophageal ulceration, with the exception of herpes simplex virus esophagitis. OP candidiasis is common in patients with underlying esophageal ulcer, potentially resulting in diagnostic confusion. OP candidiasis appears to be a moderately useful diagnostic marker for Candida esophagitis.
Recent studies suggest human immunodeficiency virus (HIV) may be the cause of HIV-associated idiopathic esophageal ulcer (IEU). However, other causes of esophageal disease in HIV-infected patients have not been evaluated for appropriate comparison. Over a 14-month period 13 patients with IEU as determined by clinical, endoscopic, and pathologic criteria were identified. During the same period nine HIV-infected patients with cytomegalovirus (CMV) esophagitis and one HIV-infected patient each with herpes simplex virus esophagitis and gastroesophageal reflux disease (GERD) were also identified. Polymerase chain reaction (PCR) and in situ DNA hybridization (ISH) were performed on paraffin-embedded tissue formed on paraffin-embedded tissue of endoscopic biopsies of ulcer tissue using standard techniques. Eleven of 13 IEU patients (85%) as compared to seven of nine patients (78%) with CMV had HIV detected by PCR (P = 0.38). HIV was also detected in ulcer tissue from biopsy material from the patient with GERD but not herpes simplex virus esophagitis. In PCR-positive patients, ISH confirmed the presence of HIV in four patients (57%) with CMV and eight (73%) with IEU (p = 0.31). HIV was found only in inflammatory cells and not squamous epithelial cells. Given the similar prevalence of detection of HIV by PCR and ISH in ulcer tissue from both groups of HIV-infected patients as well as the location in rare inflammatory cells, we conclude that HIV infection of squamous mucosa does not appear to be the primary cause of IEU.
Enterocytozoon bieneusi is the most frequently reported microsporidial infection of humans. In patients with the acquired immunodeficiency syndrome, Enterocytozoon infects the lining epithelial cells of the small intestine, hepatobiliary tract, and gallbladder. Because Enterocytozoon has been thought to be limited to infecting lining epithelial cells, the mechanism of spread of E bieneusi within the intestine, to the biliary tract, and, in two case reports, to distant organs remains unknown. This report describes a patient with acquired immunodeficiency syndrome and intestinal microsporidiosis due to E bieneusi. Histopathologic examination of well-oriented biopsies from the duodenum and jejunum revealed both intra- and extracellular spores of Enterocytozoon extending deeply into the lamina propria, where they were located adjacent to capillaries. The patient has not developed disseminated disease 20 months after the initial diagnosis. In this patient, the demonstration of E bieneusi spores in extraepithelial tissues does not appear to be associated with development of subsequent systemic infection.
OBJECTIVE: To test the hypothesis that the regular use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is negatively associated with the risk of subsequent colorectal cancer. DESIGN: Case-control study with four age- and sex-matched control subjects for each incident colorectal cancer case. POPULATION AND SETTING: Patient population of a large municipal teaching hospital in Atlanta, Ga. MAIN OUTCOME MEASURE: Odds of colorectal cancer as a function of aspirin, nonaspirin NSAIDs, and acetaminophen dispensed to the study population in the 4 years prior to incident colorectal cancer diagnosis. MAIN RESULTS: The risk of colorectal cancer estimated by odds ratios decreased with increasing days of exposure to aspirin linearly in a dose-dependent fashion (likelihood ratio statistic: for cumulative days, P < .001; for cumulative dose, P < .001). The coefficient for days of exposure to aspirin was highly significant even when modeled as a continuous variable (P = .001). There appeared to be a threshold above which nonaspirin NSAIDs afforded protection (likelihood ratio statistic: for cumulative days, P = .021; for cumulative dose, P = .019). Acetaminophen conferred no risk reduction. CONCLUSION: The results of previous experimental animal models, interventional case studies, and some but not all epidemiological investigations and the present data point toward a causal relationship between NSAID use and the prevention of cancer of the large bowel and rectum. Because of the potential gastrointestinal and renal side effects of NSAID use, particularly in the elderly, chemoprevention trials are now needed to allow risk-benefit analysis in populations at high risk for colorectal cancer.
BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) are a well-established cause of gastrointestinal disease. There appears to be an association with peptic ulcer disease complications, specifically ulcer-related bleeding. Studies addressing this relationship have primarily evaluated prescription use of these agents. There has been little study of over-the-counter NSAID use in patients with either ulcer or nonulcer-related upper gastrointestinal hemorrhage. METHODS: Consecutive patients with upper gastrointestinal hemorrhage evaluated by a gastroenterology consultative service at a large inner-city hospital from August 1, 1990 to July 31, 1992 were identified. The use of any prescription or over-the-counter NSAID during the week before admission was prospectively assessed. Computerized pharmacy records were available for confirmation of prescription drug use. RESULTS: During the 2-year period of study, 421 patients were evaluated for upper gastrointestinal hemorrhage. The mean age of the patients was 50 years and the majority were male and black. The most common cause of bleeding was peptic ulcer disease, identified in over 50% of patients. Use of an over-the-counter aspirin or nonaspirin NSAID was reported in 145 patients (35%) and 36 patients (9%), respectively, during the week before admission. Prescription use of a nonaspirin NSAID or aspirin was reported in 56 patients (14%) and 27 patients (6%), respectively. The overall prevalence of NSAID use during the week before admission was 56% (95% confidence interval, 51.2% to 60.8%). The use of any NSAID was significantly associated with gastric compared with duodenal ulcer hemorrhage, and ulcer-related bleeding compared with variceal hemorrhage. CONCLUSIONS: Over-the-counter NSAID use is frequent in our patient population and exceeds prescription use. Although ulcer-related bleeding was significantly associated with use of these drugs, NSAIDs were commonly used in patients with nonulcer-related upper gastrointestinal hemorrhage as well. Over-the-counter NSAID use may represent a more important cause of peptic ulcer disease and ulcer-related hemorrhage than previously appreciated.
The variable appearance of gut-associated lymphoid tissue at videocolonoscopy has not been well documented. Over a 3-year period all patients undergoing high resolution videcolonoscopy underwent biopsy of any identified abnormalities for correlating histopathologic findings with endoscopic appearance. We identified several distinct patterns for lymphoid tissue: small well-circumscribed nodules, red rings, large coalescing vesicles with or without central pits, or white plaques. A mass-like appearance of the ileocecal valve was present in one patient. Although individually each of these patterns appeared characteristic, overall, variability appeared dependent on the colonic location and underlying disease. Prominent lymphoid tissue was most frequently seen in patients with underlying disorders resulting in stimulation of the immune system. We take this to mean that there is a broader spectrum of colonic lymphoid tissue as assessed by videocolonoscopy than previously appreciated. The variability of these normal structures has potential diagnostic implications.
This report of disseminated pneumocystosis in an HIV-infected patient describes an unusual presentation consisting of splenic disease mimicking lymphoma, absence of typical roentgenographic signs of pulmonary or disseminated pneumocystis, and absence of use of aerosolized pentamidine. Because of these factors, a diagnosis of disseminated pneumocystosis was not considered. Our case in combination with other recent reports emphasizes the need to consider disseminated pneumocystosis in HIV-infected patients, even if they have no obvious pulmonary disease and have not received aerosolized pentamidine therapy. Timely recognition of this lethal infection is important for initiation of potentially curative therapy.
There are a number of potential causes for false-positive results on a barium enema study. We report three cases in which patients had to have colonoscopy because a nifedipine slow-release tablet (Procardia XL) was misinterpreted as a colonic polyp on a barium enema study. The pill did not move with abdominal compression, further suggesting that it was a polyp. Patients in whom similar lesions are identified during barium enema examination should be questioned as to whether they are taking these medications.
BACKGROUND: Although fluconazole is increasingly utilized for the therapy of Candida oesophagitis in patients with AIDS, the time course of response has not been adequately defined. METHODS: Over a 48-month period, all HIV-infected patients undergoing upper endoscopy at a large city-county hospital were identified prospectively. Symptomatic patients with endoscopic and histopathologically confirmed Candida oesophagitis in whom oral antifungal therapy had not been received within the past three months were treated in an open-label fashion with fluconazole 200 mg on the first day followed by 100 mg daily for two weeks. All patients were followed clinically to determine the rapidity of response. RESULTS: Eighteen patients were identified; all but two were male. Candida oesophagitis was graded as severe in 13 patients (72%). A complete symptomatic response was seen by five days in seven patients (39%) and by seven days in nine additional patients (cumulative response, 89%). The two other patients had improved by at least 50% at one week, with a complete symptomatic response seen at two weeks. CONCLUSIONS: Our study confirms anecdotal experience suggesting that fluconazole results in a rapid clinical response for Candida oesophagitis in patients with AIDS. Given this rapidity, a one-week course of empiric treatment with fluconazole for HIV-infected patients with newly developed esophageal symptoms could be used as an appropriate time period to assess a response prior to further diagnostic evaluation with endoscopy.
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