Bilateral combined occlusion of the central retinal artery and vein secondary to thrombotic thrombocytopenic purpura.
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Biomedical subjects
Publications and source records attributed to S L Sessoms.
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OBJECTIVES: Systemic sclerosis (SSc) and calcinosis, Raynaud's phenomenon, esophageal disease, sclerodactyly, telangiectasia (CREST) syndrome present distinctive microvasculature lesions that are thought to be responsible for tissue damage and disease progression. Involvement of the gastrointestinal tract may lead to the occurrence of profuse hemorrhage. We performed a study to assess the incidence and characteristics of gastrointestinal hemorrhage in a large group of patients with SSc and CREST syndrome. METHODS: We reviewed the medical records of 144 patients with SSc/CREST seen at our institution during the period 1985-1996. Endoscopic findings and clinical data were correlated. Data are expressed as means +/- SD. RESULTS: Twenty-two of 144 (15.2%) patients had at least one episode of gastrointestinal hemorrhage (16 women, 6 men; mean age, 59.4 +/- 17.6 yr). Eight patients (8/22; 36%) had multiple episodes and four (4/22; 18%) required chronic transfusion therapy. Mucosal telangiectasias were the most common cause of bleeding (9/22; 40.9%), followed by peptic ulcer disease (7/22; 31.8%) and erosive gastritis (3/22; 13.6%). Bleeding telangiectasias occurred in the entire gastrointestinal tract, including oral cavity (n = 1), esophagus (n = 1), stomach (n = 3), duodenum (n = 1), ileum (n = 1), cecum (n = 2), and colon (n = 2). Mortality was 22.7% in patients with gastrointestinal bleeding, compared with 7.3% in patients without bleeding. CONCLUSIONS: Patients with SSc/CREST syndrome are at risk of developing severe gastrointestinal hemorrhage. This complication is associated with frequent hospitalization, blood transfusions, and increased mortality. Mucosal telangiectasias are the most common source of bleeding. Appropriate endoscopic intervention is recommended in evaluating and preventing bleeding in patients with SSc/CREST.
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The management of pyoderma gangrenosum often requires systemic drug therapy, such as corticosteroids, sulfones, or immunosuppressants, either alone or in combination. Inconsistent response to therapy is a source of frustration to both patient and physician. Several reports in the literature document the successful treatment of pyoderma gangrenosum with hyperbaric oxygen therapy. In our patient, a woman with severe rheumatoid arthritis and diabetes mellitus, hyperbaric oxygen therapy not only promoted healing of pyoderma gangrenosum but permitted reduction of systemic corticosteroids.
This study investigates whether patients who take nonsteroidal antiinflammatory drugs are more likely to have Helicobacter pylori gastritis than age-matched individuals who do not take nonsteroidal antiinflammatory drugs, and whether patients who take nonsteroidal antiinflammatory drugs who are also infected with H. pylori are more likely to have dyspepsia, mucosal damage, or ulcers than those who are not infected. Two studies were performed, one serological and the other endoscopic, both in arthritis patients receiving nonsteroidal antiinflammatory drugs chronically. The presence of H. pylori was identified with a sensitive enzyme-linked immunosorbent assay test. One hundred eighty-three patients participated in the serological study and 75 patients in the endoscopic study. The frequency of H. pylori infection increased with age, independent of nonsteroidal antiinflammatory drug use; the age-adjusted frequency of H. pylori infection in arthritis patients paralleled that of 351 asymptomatic individuals without arthritis. The frequency of H. pylori infection increased from 30.7% in age group 21-30 years to 73.4% in age group 61-75 years. Nonsteroidal antiinflammatory drug-induced mucosal injury, either hemorrhages or erosions, was more frequent in those without H. pylori infection than with infection (61% vs. 32% for hemorrhages and 57% vs. 34% for erosions for those without and with H. pylori infection; only the difference in the frequency of hemorrhages was significant, P less than 0.05). No difference was observed in the presence of dyspeptic symptoms between those with and without H. pylori infection. These data suggest that nonsteroidal antiinflammatory drug-induced damage to the gastroduodenal mucosa does not increase the susceptibility to H. pylori infection.
Gastroduodenal intolerance is one of the major factors limiting the use of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) in patients with rheumatic diseases. We previously demonstrated that dyspepsia was not a marker for ulcer in NSAID users. We have now evaluated dyspeptic symptoms in 245 arthritic patients (receiving 13 different NSAIDs) from the practices of two rheumatologists. Fifty-seven patients (23%) gave a history of previous peptic ulcers. Heartburn, indigestion, or sour stomach at least once within the past year was present in 62.5%; 36.7% had experienced these symptoms within the previous 2 months and 28.6% within the previous week. Only 39 patients (15.9%) had experienced dyspepsia more than once daily within the previous month, and 8 (3.3%) had dyspepsia greater than 5 times/day. Thirty-four of the 39 patients with daily dyspepsia claimed to obtain relief with cimetidine or antacids (34 patients) or food (2 patients), whereas 3 had not discovered anything that provided relief. Women smokers were more likely than nonsmokers to experience dyspepsia (p less than 0.001). Neither men smokers nor those with a history of previous ulcer were more likely to have dyspepsia than nonsmokers or those without a history of ulcer (p greater than 0.5). We were not able to find a statistical association between any NSAID, or combination of NSAIDs, and the frequency of dyspepsia.
An uncontrolled series of 10 patients with severe systemic lupus erythematosus (SLE), resistant to or intolerant of other medications, were treated with a monthly intravenous bolus of cyclophosphamide. Nine of 10 patients experienced some beneficial results, several of which were quite dramatic and associated with substantial and protracted reductions in steroid requirement. Significant drug toxicity was noted in several patients. This therapy can be a useful therapeutic adjunct in carefully selected cases; however, we are not attempting to liberalize therapeutic indications for cyclophosphamide administration in SLE.