Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 26-year-old woman with systemic lupus erythematosus developed massive rectal bleeding that failed to respond to medical treatment. X-rays and proctoscopy indicated that she had universal colitis. She underwent emergency subtotal colectomy because of a rapidly declining clinical course. The small intestine appeared normal. Pathological examination demonstrated a gangrenous large intestine, ischemic ulcerations, and extensive fibrinoid vasculitis that was typical of systemic lupus. The patient has had no further gastrointestinal complaints for 2 years since surgery.
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PMID:Diffuse ischemic colitis associated with systemic lupus erythematosus--response to subtotal colectomy. 71 Aug 67

A patient is described with stable primary biliary cirrhosis and recurrent gastrointestinal bleeding due to angiodysplasias in the gastrointestinal tract. This is a very rare disease association. In addition this patient showed two other disease associations, not known in the literature. She also suffered from eosinophilic colitis and had the lupus anticoagulant. These associations have not yet been described in the literature.
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PMID:Primary biliary cirrhosis associated with recurrent angiodysplastic lesions in the gastrointestinal tract, the lupus anticoagulant and eosinophilic colitis. 196 45

Sulphasalazine, devised by Dr Nana Svartz for the treatment of 'infective polyarthritis', has been used in the treatment of inflammatory bowel disease for more than 40 years. Many controlled trials have shown that sulphasalazine 4g daily will induce remissions in between one-half and three-quarters of patients with acute attacks of ulcerative colitis. When given in a dosage of 2g daily it will prevent relapses in quiescent colitis. Relapses are 5 times more likely in untreated patients. It is less effective in Crohn's disease, where it exerts only a transient benefit in patients with active colonic disease and fails to prevent relapse or recurrence. Sulphasalazine is absorbed from the small intestine, re-excreted in bile and carried to the colon, where its azo bond is split by bacteria to release sulphapyridine, which is absorbed and is responsible for most of the drug's side effects, and 5-aminosalicylic acid, which is the active therapeutic moiety of the drug and exerts a beneficial topical action on the colonic mucosa. Side effects are common but are mainly reversible and not serious. Those related to high concentrations of sulphapyridine and to poor acetylation of the drug include gastrointestinal intolerance, malaise, headache, arthralgia, drug fever, effects on red blood cells and reversible male infertility. More serious, idiosyncratic side effects are skin rashes, leucopenia and agranulocytosis. Rarely, neurotoxicity, hepatotoxicity, polyarteritis, pulmonary fibrosis, a lupus-like syndrome and haemorrhagic colitis are produced. It is possible to desensitise most patients with drug-induced skin rashes. A number of less toxic alternatives to sulphasalazine have been devised and are undergoing trial. They either convey 5-aminosalicylic acid in a coated tablet to the colon or, when conjugated to a non-toxic carrier, release 5-aminosalicylic acid by bacterial cleavage there. Sulphasalazine remains a most useful drug in the treatment of inflammatory bowel disease after 40 years of use.
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PMID:Sulphasalazine: a review of 40 years' experience. 287 47

Between January 1986 and January 1989, 524 non-typhoid salmonella strains, of which 4 (0.8%) from urine, were isolated at the Microbiology Laboratory of Department of Biomedicine (University of Pisa). These strains were isolated from a man with systematic lupus erythematosus, from two little girls with structural defects of the lower urinary tract, and from a woman with ulcerous colitis. Except the last case, the others were associated with immunological or structural abnormalities that are thought to predispose to salmonella infections.
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PMID:[Urinary infections caused by non-typhoid Salmonella]. 327 65

Antithrombin V as a pathological inhibitor of coagulation may occur in some rare cases as an accompanying symptom of various basic diseases. In the course of two years, antithrombin V could be identified in 8 patients, with plasmocytoma, lupus erythematodes visceralis, glomerulonephritis or colitis ulcerosa existing as basic diseases. Clinical findings in patients and those gained in analyzing coagulation, procedures of laboratory diagnostics for determining characteristic properties of antithrombin V as well as the therapeutic way of influencing the activity of antithrombin V are represented.
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PMID:[Antithrombin V--a rare concomitant symptom in plasmacytoma and autoimmune diseases]. 619 61

We report a 50-year-old female patient who developed ulcerative colitis 31 after years being diagnosed with systemic lupus erythematosus. The overall clinical evaluation of her SLE activity differentiated ulcerative colitis from lupus colitis. Since the association of idiopathic systemic lupus erythematosus with ulcerative colitis has rarely been reported, the combination of these two diseases may be coincidental.
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PMID:Ulcerative colitis associated with preceding systemic lupus erythematosus. 760 87

Thromboembolic disease is a well-recognized but very uncommon complication of inflammatory bowel disease. The mechanisms of the increased risk of thrombosis are not well understood: although several coagulation abnormalities have been described in inflammatory bowel disease patients, it is not clear whether they actually contribute to hypercoagulation or whether they are nonspecific markers of inflammation. Antiphospholipid antibodies (anticardiolipin antibodies and/or lupus anticoagulant) have recently been associated with an increased risk of thrombosis, particularly cerebrovascular disease in young patients. We report the case of a 33-yr-old female with severe ulcerative colitis at first attack who developed thrombosis of the superior and inferior longitudinal dural sinuses. No risk factors for thrombosis or coagulation abnormalities were observed; however, lupus anticoagulant was detected in the serum. The patient was successfully treated with osmotic agents, prophylactic anticonvulsant, and antiplatelet therapy, combined with i.v. steroids. After 6 months, the colitis is in remission, and the neurological recovery is good even if not yet complete.
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PMID:Severe ulcerative colitis, dural sinus thrombosis, and the lupus anticoagulant. 766 Nov 81

Colitis in systemic lupus erythematosus (SLE) poses a diagnostic challenge as clinical, radiological and laboratory findings are often non-specific. Fulminant amoebic colitis is a rare cause of death in SLE. Early diagnosis coupled with timely surgery can reduce the mortality. The demonstration of haematophagous trophozoites in the stool is diagnostic but insensitive. Early endoscopy with adequate specimen collection is an important part of the diagnosis. Serology is both sensitive and specific but can take up to 2-4 weeks for seroconversion making it less useful in a disease that takes a rapid downhill course if treated inappropriately. We report a fatal case of colitis in a patient with SLE due to invasive amoebiasis which was complicated by Salmonella bacteraemia, disseminated intravascular coagulation, acute oliguric renal failure and adult respiratory syndrome. We also reviewed the literature on the clinical features and diagnosis of fulminant amoebic colitis. Amoebic colitis, although rare, should be considered in the differential diagnosis of lupus patients with colitis.
Lupus 1997
PMID:Fatal amoebic colitis in a patient with SLE: a case report and review of the literature. 930 65

A registry of United States residents with chronic granulomatous disease (CGD) was established in 1993 in order to estimate the minimum incidence of this uncommon primary immunodeficiency disease and characterize its epidemiologic and clinical features. To date, 368 patients have been registered; 259 have the X-linked recessive form of CGD, 81 have 1 of the autosomal recessive forms, and in 28 the mode of inheritance is unknown. The minimum estimate of birth rate is between 1/200,000 and 1/250,000 live births for the period 1980-1989. Pneumonia was the most prevalent infection (79% of patients; Aspergillus most prevalent cause), followed by suppurative adenitis (53% of patients; Staphylococcus most prevalent cause), subcutaneous abscess (42% of patients; Staphylococcus most prevalent cause), liver abscess (27% of patients; Staphylococcus most prevalent cause), osteomyelitis (25% of patients; Serratia most prevalent cause), and sepsis (18% of patients; Salmonella most prevalent cause). Fifteen percent of patients had gastric outlet obstruction, 10% urinary tract obstruction, and 17% colitis/enteritis. Ten percent of X-linked recessive kindreds and 3% of autosomal recessive kindreds had family members with lupus. Eighteen percent of patients either were deceased when registered or died after being registered. The most common causes of death were pneumonia and/or sepsis due to Aspergillus (23 patients) or Burkholderia cepacia (12 patients). Patients with the X-linked recessive form of the disease appear to have a more serious clinical phenotype than patients with the autosomal recessive forms of the disease, based on the fact that they are diagnosed significantly earlier (mean, 3.01 years of age versus 7.81 years of age, respectively), have a significantly higher prevalence of perirectal abscess (17% versus 7%), suppurative adenitis (59% versus 32%), bacteremia/fungemia (21% versus 10%), gastric obstruction (19% versus 5%), and urinary tract obstruction (11% versus 3%), and a higher mortality (21.2% versus 8.6%).
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PMID:Chronic granulomatous disease. Report on a national registry of 368 patients. 1084 35

Vasospasm can have many different causes and can occur in a variety of diseases, including infectious, autoimmune, and ophthalmic diseases, as well as in otherwise healthy subjects. We distinguish between the primary vasospastic syndrome and secondary vasospasm. The term "vasospastic syndrome" summarizes the symptoms of patients having such a diathesis as responding with spasm to stimuli like cold or emotional stress. Secondary vasospasm can occur in a number of autoimmune diseases, such as multiple sclerosis, lupus erythematosus, antiphospholipid syndrome, rheumatoid polyarthritis, giant cell arteritis, Behcet's disease, Buerger's disease and preeclampsia, and also in infectious diseases such as AIDS. Other potential causes for vasospasm are hemorrhages, homocysteinemia, head injury, acute intermittent porphyria, sickle cell disease, anorexia nervosa, Susac syndrome, mitochondriopathies, tumors, colitis ulcerosa, Crohn's disease, arteriosclerosis and drugs. Patients with primary vasospastic syndrome tend to suffer from cold hands, low blood pressure, and even migraine and silent myocardial ischemia. Valuable diagnostic tools for vasospastic diathesis are nailfold capillary microscopy and angiography, but probably the best indicator is an increased plasma level of endothelin-1. The eye is frequently involved in the vasospastic syndrome, and ocular manifestations of vasospasm include alteration of conjunctival vessels, corneal edema, retinal arterial and venous occlusions, choroidal ischemia, amaurosis fugax, AION, and glaucoma. Since the clinical impact of vascular dysregulation has only really been appreciated in the last few years, there has been little research in the according therapeutic field. The role of calcium channel blockers, magnesium, endothelin and glutamate antagonists, and gene therapy are discussed.
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PMID:Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye. 1128 96


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