The effectiveness of oral 5-aminosalicylic acid (0.5 g t.i.d.) and of salazosulfapyridine (1.0 g t.i.d.) was compared in a randomized controlled study in two groups with 30 patients each with ulcerative colitis and with Crohn's disease. Persistent complaints within the first 5 days were treated with additional methyl-prednisolone (40 mg/d initially). After treatment for 8 weeks patients with ulcerative colitis showed morphologic remissions in 60% of the 5-aminosalicylic acid group and in 53% of the salazosulfapyridine group. Clinical improvement was achieved in 86% in both groups. Clinical improvement in Crohn's disease was seen in 87% of patients of the 5-aminosalicylic acid group and in 80% of the salazosulfapyridine group. This was evidenced by the significant fall (P = 0,0001) of the mean activity index. Additional steroid medication was nearly equal in both treatment groups. There were no side effects during treatment with 5-aminosalicylic acid. In contrast, salazosulfapyridine had to be withdrawn in four patients due to signs of intolerance. 5-Aminosalicylic acid can thus be considered a valuable alternative to conventional treatment on the basis of equal effectiveness as salazosulfapyridine and lack of undesirable side effects.
In eosinophilia of undetermined origin parasitic infection should be considered and any previous visit to countries with endemic parasitic disease taken into account.
A 29-year-old woman with chronic bronchial asthma and inflammatory bowel disease, previously classified as idiopathic, was hospitalized because of bouts of fever and increasing dyspnoea and diarrhoea. Chest radiograph showed extensive bilateral pulmonary infiltrates. Thought to be suffering from bacterial pneumonia she was treated with broad-spectrum antibiotic, but without improvement even after a change of antibiotics. Numerous diagnostic tests failed to find any causative organism. Subsequently she was found to have peripheral eosinophilia and pericardial effusion associated with echocardiographic and electrocardiographic signs of myocarditis, which raised the suspicion of allergic granulomatous vasculitis (Churg-Strauss syndrome). The patient's acute illness contraindicated a lung biopsy, but the clinical picture left no doubt of the true diagnosis. Treatment with methylprednisolone (initially 250 mg, then 80 mg daily) rapidly improved the clinical, radiological and biochemical findings. But four months later, under maintenance treatment with 15 mg methylprednisolone daily, she experienced another bout of colitis and, a few days later, pulmonary recurrence of the Churg-Strauss syndrome, both clinically and radiologically. The dose of methylprednisolone was raised to 60 mg daily. The inflammatory bowel disease, endoscopically manifesting as ulcerative colitis, was most likely part of the systemic vasculitis.-This case demonstrates that colitis can be the primary manifestation of Churg-Strauss syndrome.
Somatostatin receptor scintigraphy (SRS) was performed in 14 patients (five men, nine women; mean age 51.5 [20-71] years) with Zollinger-Ellison syndrome (ZES), a gastrinoma proven in 7 and suspected on clinical or biochemical grounds in 7. The results were compared with those obtained by other methods (ultrasound, computed tomography, angiography). All 12 known tumour manifestations were demonstrated by SRS in seven patients with histologically confirmed gastrinoma. In four patients previously non-localized tumour was revealed by SRS, while in seven other patients the procedure led to modification of the treatment (primary tumour resection: n = 3, resection of metastases: n = 2, percutaneous radiation or chemoembolization: one each). These results suggest the following indications for SRS: (1) staging or re-staging in histologically proven gastrinoma and (2) search for primary tumour in clinically and biochemically suspected ZES.
In a 39-year-old man there occurred, over a period of four years, mesenteric vein thrombosis with haemorrhagic infarction of the intestines, as well as multiple bleedings from oesophageal varices due to portal hypertension caused by portal vein thrombosis. Search for the cause of the thrombosis tendency revealed congenital protein C deficiency. Splenectomy and a disconnection operation were performed, followed by administration of anticoagulants. Since then the patient has been free of symptoms, and there have been no further variceal bleedings or thromboses.
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