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Fifty outpatients suffering from rheumatoid disorders were treated with proglumetacin. Efficacy was classified as "good" or "very good" in 80% of cases. Besides this considerable efficacy, a tolerance classified as "good" or "very good" was observed in 86% of patients.
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Perianal complications of Crohn's disease are fairly common in the adult and pediatric populations. Transrectal ultrasonography is effective for the diagnosis and follow-up of patients with anorectal abscesses and fistulas in Crohn's disease. Metronidazole and 6-mercaptopurine therapy have been used effectively to treat perianal complications of Crohn's disease in the pediatric population. Asymptomatic perianal fistulas in a patient with Crohn's disease do not require treatment. If a fistula is symptomatic and involves only a small portion of the sphincter mechanism, conventional fistulotomy may be performed with good results. Complex fistulas that involve larger areas of the sphincter are best treated by optimizing medical management and seton placement. The management of rectovaginal fistulas in the presence of Crohn's disease is controversial. Conventional fistulotomy and transvaginal mucosal advancement flap with diverting ileostomy have been advocated as primary treatment modalities. Rectovaginal fistulas secondary to ulcerative colitis may be treated by ileoanal pouch anastomosis and primary repair.
Muscle biopsies from 21 dermatomyositis (DM) and 7 polymyositis (PM) patients were studied by conventional histoenzymatic reactions and immunoreacted with antibodies against T cells and subsets, B cells, macrophages, activated T cells, proliferating cells, transferrin and IL-2 receptors, and natural killer cells. The expression of both class I and II molecules from the major histocompatibility complex (MHC) was also tested. As control groups we used muscle biopsies from normal healthy people, from chronic alcoholics and from a cohort of HIV-1 infected patients. In DM cases, severe muscle fiber necrosis, predominant perivascular infiltrates, fibrosis and perifascicular atrophy were the rule whereas in PM cases, endomysial infiltrates and the existence of partially invaded non-necrotic cells were more frequent. Perivascular B cells were found only in some DM cases. Transferrin and IL-2 receptors, proliferating cells and NK cells were detected in some cases from both diseases. MHC class I molecules were detected mainly in perifascicular fibres in DM while in PM the stronger expression was demonstrated in non-necrotic partially invaded cells, suggesting for the latter a MHC-restricted T-cell cytotoxicity. MHC Class II molecules expression in endothelial cells was detected in a variable fashion in both diseases, probably reflecting different stages of activation of such cells.
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OBJECTIVE: To compare the prevalences of demographic, historic, and behavioral risks for pelvic inflammatory disease among women with sexually transmitted disease (STD) pelvic inflammatory disease versus those with non-STD pelvic inflammatory disease. METHODS: Subjects included patients diagnosed with acute pelvic inflammatory disease at San Francisco General Hospital between January 1, 1981 and August 20, 1989, who had been entered into clinical treatment trials. At a minimum, endocervical cultures for Neisseria gonorrhoeae and Chlamydia trachomatis were required for study eligibility. All but nine women also had upper reproductive tract cultures for N gonorrhoeae, C trachomatis, and anaerobic and facultative bacteria. Five hundred eighty-nine patients were included in this analysis. The medical records of study subjects enrolled between January 1981 and October 1986 were abstracted (n = 321). Subjects recruited after October 1986 were interviewed during hospitalization using a standardized data base instrument (n = 268). Independent variables examined included age, race, insurance status, education, pregnancy history, menstrual history, contraceptive history, sexual history, douching history, STD history, and pelvic inflammatory disease history. Both univariate associations and multivariate (multiple logistic regression) analysis were performed. RESULTS: An STD organism was present in 65% of pelvic inflammatory disease cases. Neisseria gonorrhoeae and C trachomatis were recovered from 324 (55%) and 129 (22%) of the patients, respectively. In 30% of cases only anaerobic and/or facultative bacteria were isolated. In univariate analysis of STD versus non-STD pelvic inflammatory disease, statistically significant increases in STD risks were found for the following: black race (relative risk [RR] 1.76; 95% confidence interval [CI] 1.39-2.24), two or more sexual partners in the past 30 days (RR 1.25; 95% CI 1.08-1.45), no contraception (RR 1.36; 95% CI 1.18-2.57), N gonorrhoeae with previous episode of pelvic inflammatory disease (RR 1.97, 95% CI 1.39-2.80), and reported duration of pain 3 days or less (RR 1.17; 95% CI 1.02-1.35). Risks associated with non-STD pelvic inflammatory disease included: current intrauterine device (IUD) use (RR 0.25; 95% CI 0.11-0.61), history of IUD use (RR 0.82; 95% CI 0.68-0.98), and pelvic surgery in the past 30 days (RR 0.48; 95% CI 0.30-0.76). Multivariate analysis of the risks found that black race was associated with STD pelvic inflammatory disease (odds ratio 2.56; 95% CI 1.68-3.90), and current IUD use was associated with non-STD pelvic inflammatory disease (odds ratio 3.87; 95% CI 1.30-11.53). Neither univariate nor multivariate analysis identified douching as a risk differentiating STD from non-STD pelvic inflammatory disease. CONCLUSIONS: Pelvic inflammatory disease is a complex polymicrobial disease. This study demonstrates that risk factors associated with pelvic inflammatory disease cases can be differentiated by microbial etiology. We found that black race was associated with STD pelvic inflammatory disease and recent IUD use was associated with non-STD pelvic inflammatory disease.
OBJECTIVE: To relate factor XIII levels and other prothrombotic markers to inflammatory bowel disease and investigate the frequency of valine34leucine and its effect on factor XIII cross-linking activity in patients with inflammatory bowel disease. DESIGN: Fifty patients with active inflammatory bowel disease but no venous thromboembolism (32 with ulcerative colitis, 18 with Crohn's disease), 50 patients with inactive inflammatory bowel disease but no venous thromboembolism (32 with ulcerative colitis, 18 with Crohn's disease), two age- and gender-matched healthy control groups of 100 subjects each were recruited. To further explore the relationship between valine34leucine and inflammatory bowel disease, 21 patients with the disease (13 with ulcerative colitis and eight with Crohn's disease) and venous thromoembolism (male to female ratio = 7 : 14, median age 59.5 years (range, 19-80 years)) were recruited. Two hundred and fifteen control subjects (M : F = 121 : 94, median age 62 years (28-74 years)), with venous thromboembolism (119 with deep venous thrombosis, and 96 with pulmonary embolism) were drawn from the same geographical area as the patients. METHODS: Factor XIII A, B-subunit antigen and A2B2 tetramer levels were measured using an in-house sandwich enzyme-linked immunoassay method. RESULTS: Factor XIII A2B2 tetramer and the A-subunit were significantly decreased in patients with active inflammatory bowel disease compared with controls (59% vs 95%, P < 0.0001 and 75% vs 102%, P < 0.0001, respectively), but not between the inactive inflammatory bowel disease group and controls. The D-dimer and prothrombin 1+2 fragment levels in patients with active inflammatory bowel disease were raised compared with controls (178 (152) vs 109 (84), P = 0.0007 and 82 (43) vs 55 (28), P = 0.0001, respectively). The factor XIII B-subunit and factor XIII cross-linking activity were not significantly different between patients with active or inactive inflammatory bowel disease and controls. There was no significant difference in genotype distribution in inflammatory bowel disease patients with or without venous thromboembolism and respective control subjects. Levels of tissue plasminogen activator antigen were significantly increased in patients with active inflammatory bowel disease when compared to inactive inflammatory bowel disease and controls (8.9 (3.7) vs 6.7 (3.4) vs 6.9 (3.4), P < 0.001). CONCLUSIONS: Active inflammatory bowel disease is associated with activation of coagulation. Factor XIII A and A2B2 tetramer levels were markedly decreased in active inflammatory bowel disease. Variations in the level of factor XIII in patients with inflammatory bowel disease could be multifactorial and in part may result from the increased formation of microthrombi and accelerated turnover of the factor XIII. We found no evidence of association of factor XIII valine34leucine polymorphism and inflammatory bowel disease.
BACKGROUND: Non-steroidal anti-inflammatory drugs use may protect against development of oesophageal adenocarcinoma. AIM: To define the consequences of non-steroidal anti-inflammatory drugs use in patients with Barrett's oesophagus. METHODS: Records of all Barrett's oesophagus/oesophageal adenocarcinoma patients examined in Blackpool-Wyre-Fylde area were reviewed. All surviving patients completed validated questionnaires. RESULTS: Use of non-steroidal anti-inflammatory drugs of any type and at any frequency was more prevalent in Barrett's oesophagus patients [147 (38%) Barrett's oesophagus vs. 30 (26%) oesophageal adenocarcinoma, P = 0.02]. Daily use of non-steroidal anti-inflammatory drugs was more prevalent in Barrett's oesophagus patients [88 (23%) Barrett's oesophagus vs. 14 (12%) oesophageal adenocarcinoma, P = 0.02], due to more prevalent consumption of non-aspirin non-steroidal anti-inflammatory drugs [48 (13%) Barrett's oesophagus vs. four (4%) oesophageal adenocarcinoma, P = 0.009]. There was no difference between the two groups in usage of either daily low-dose aspirin or of occasional non-steroidal anti-inflammatory drugs. In logistic regression analysis any use of non-steroidal anti-inflammatory drugs [odds ratio (OR) = 0571 (95% CI: 0.359-0.909), P = 0.018] and daily use of non-aspirin non-steroidal anti-inflammatory drugs [OR = 0.297 (95% CI: 0.097-0.911), P = 0.034] were significant protective factors. Non-steroidal anti-inflammatory drugs use did not affect the survival of oesophageal adenocarcinoma patients. Oesophageal adenocarcinoma and Barrett's oesophagus consuming non-steroidal anti-inflammatory drugs did not differ in upper gastrointestinal bleeding [26 (15%) non-steroidal anti-inflammatory drugs consumers vs. 29 (9%) non-consumers, P = 0.08], oesophageal ulcers [31 (18%) non-steroidal anti-inflammatory drug consumers vs. 49 (15%) non-consumers, P = 0.43] or stricturing [19 (11%) non-steroidal anti-inflammatory drug consumers vs. 41 (13%) non-consumers, P = 0.58]. CONCLUSIONS: (i) Daily use of non-steroidal anti-inflammatory drugs is more prevalent in Barrett's oesophagus than oesophageal adenocarcinoma patients, because of a more prevalent use of non-aspirin non-steroidal anti-inflammatory drugs. (ii) Use of non-steroidal anti-inflammatory drugs in Barrett's oesophagus patients is safe if acid suppression is adequate.