Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with systemic lupus erythematosus (SLE) are reported to have an increased risk of malignancy, especially lymphoproliferative disorders. We decribe the occurrence of ileocaecal intussusception secondary to Burkitt's lymphoma in a patient with SLE. A 23-year-old woman, who had been diagnosed with SLE 2 years ago, developed intermittent abdominal pain with a palpable mass. Computed tomography and a double-contrast barium enema showed a lobulated mass with intussusception at the ileocaecal junction. Right hemicolectomy and splenectomy was performed after histopathological examinations on colonoscopic biopsy revealed Burkitt's lymphoma. Fourteen months after chemotherapy, there is no evidence of recurrence of the Burkitt's lymphoma. When a patient with SLE has abdominal complaints, besides serositis, lupus enteritis such as peptic ulcer disease, mesenteric vasculitis with or without complications and pancreatitis, we have to consider intussusception secondary to gastrointestinal lymphoma as one of the differential diagnoses. Therefore, we should thoroughly investigate patients with SLE presenting with abdominal pain and not simply consider it afeature of lupus enteritis until other causes have been ruled out.
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PMID:Burkitt's lymphoma presenting as ileocaecal intussusception in systemic lupus erythematosus. 1120 54

We report two cases of systemic lupus erythematosus (SLE) diagnosed when acute peritonitis was appeared. Case 1 was a 20 year-old woman suffering from stomachache and right lower abdominal pain. Case 2 was a 40 year-old woman with diarrhea, epigastralgia, pollakisuria. In both cases, their peritoneal fluids were exudative with positive autoantibodies. After high dose steroid therapy, abdominal symptoms and ascites improved promptly. However, due to the complication of lupus nephritis, additional therapy was necessary. To characterize the feature of lupus peritonitis (LP), we examined the clinical and laboratory findings of LP from the literature. In patients with acute LP, abdominal pain, vomiting, diarrhea were significantly more common compared with chronic LP patients (P < 0.05), and fever, arthritis, central nervous system involvement and cystitis were more common. In patients with chronic LP, pleural effusion and pericardial effusion were more common compared with acute LP patients. Gastrointestinal manifestations such as abdominal pain, vomiting and diarrhea were more common in patients with acute LP compared with patients with chronic LP. Most patients with chronic LP were asymptomatic, ascites and serositis being the only clinical findings. The response to steroid therapy was better in acute LP.
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PMID:[Two cases of acute lupus peritonitis]. 1121 Jul 76

There are many causes of acute abdominal pain, or abdominal "crises," in patients with systemic lupus erythematosus (SLE), most frequently the causes are serositis or vasculitis. Vasculitis generally causes small vessel abnormalities and may present with symptoms owing to mucosal damage, such as pain, diarrhea, or bleeding. We present a patient with SLE who had the acute onset of severe abdominal pain while hospitalized for a lupus flare and who was found to have a ruptured ileocolic aneurysm with intraperitoneal bleeding. She was successfully managed with angiographic embolization, without further complications. Although angiography is well established as a therapeutic intervention for mesenteric aneurysms of various etiologies, this is the first case of an SLE-related ileocolic aneurysm so managed. This entity should be considered in the differential diagnosis of abdominal pain in patients with lupus, and angiographic embolization should be considered in its management.
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PMID:Lupus abdominal crisis owing to rupture of an ileocolic aneurysm with successful angiographic treatment. 1127 82

The case of a 21-year-old African-American woman who presented with abdominal pain, diarrhea and hydronephrosis and who proved to have protein-losing enteropathy secondary to systemic lupus erythematosus is discussed. This is an unusual complication of lupus.
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PMID:Protein-losing enteropathy in a young African-American woman with abdominal pain, diarrhea and hydronephrosis. 1178 72

A 50-year-old woman with a 4-year history of Evans syndrome was admitted to our hospital because of progressive nausea, appetite loss, body weight loss, diarrhea and abdominal pain. Abdominal ultrasonography revealed pleural effusion, ascites, bilateral hydronephrosis, dilatation of the bilateral ureter, and irregular wall thickness of the urinary bladder. Immunological studies revealed decreased complement components (C3; 72 mg/dl, C4; 7 mg/dl, CH50; 28.8 mg/dl), a x 80 antinuclear antibody titer (homogeneous pattern), antibody against single-stranded DNA 19 U/ml, anti-SS-A antibody over 500 U/ml and negativity for antibody against double-stranded DNA (anti-dsDNA Ab). Although the patient did not fulfill the criteria for systemic lupus erythematosus (SLE), we diagnosed her as having lupus cystitis. Bolus methylprednisolone (mPSL) therapy (1,000 mg mPSL over 3 days, div) was administered, followed by 60 mg PSL, and this led to immediate improvement of the patient's symptoms and laboratory data. Later, anti-dsDNA Ab became positive, and the patient thereby fulfilled the criteria for SLE. Lupus cystitis following Evans syndrome has rarely been reported. The present such case was treated successfully with bolus mPSL therapy.
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PMID:[Lupus cystitis in the course of Evans syndrome]. 1186 59

A 24-year-old Japanese man was admitted because of massive haematemesis and melaena with persistent abdominal pain. Markedly bloody ascites and severely oedematous small intestine were recognized, and angiography then revealed superior mesenteric vein thrombosis. After resection of the necrotic small intestine, continuous intravenous infusion of heparin and urokinase was performed. This patient had no familial or personal history of thrombosis. On the 15th day after operation, an initial search for lupus anticoagulant revealed that the prothrombin time (PT) ratio and dilute activated partial thromboplastin time (aPTT) were positive under heparin treatment, without evidence of rheumatic or connective tissue disease. Thrombocytopenia was observed with a nearly normocellular bone marrow. A follow-up examination 1 year later still revealed an increased aPTT. However, all tests for antiphospholipid antibodies had been negative including dilute aPTT for about 2 years since the 15th day after operation. These findings suggest that, in this patient, superior mesenteric vein thrombosis has not been associated with primary antiphospholipid syndrome but is probably idiopathic. Positive tests for lupus anticoagulant in the initial period may be unreliable due to heparin treatment.
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PMID:Superior mesenteric vein thrombosis presented transient false positivity for lupus anticoagulant under heparin treatment. 1198 2

A 40 year-old female patient was admitted to the hospital with ascites and abdominal pain developed in the last five days. The ascitic fluid was an exudate with negative results for common diseases. Antinuclear antibodies and anti-DNA were positive and a low activity of serum complement was found. The renal biopsy disclosed a lupus glomerulonephritis grade IV. She received oral prednisone and a pulse of cyclophosphamide with gradual resolution of the ascites.
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PMID:[ASCITES AS MAIN PRESENTATION IN SYSTEMIC LUPUS ERYTHEMATOSUS] 1214 May 80

To describe the clinical and immunologic characteristics of patients with adrenal involvement and antiphospholipid syndrome (APS), we conducted a computer-assisted (PubMed) search of the literature to identify all cases of primary adrenal insufficiency associated with antiphospholipid antibodies published in English, French, and Spanish from 1983 (when APS was first defined) through March 2002. We reviewed 86 patients (80 from the literature plus 6 from our cohort); 55% were male, and the mean age at presentation was 43 +/- 16 years. Sixty-one (71%) patients had primary APS, and 14 (16%) had systemic lupus erythematosus. In 31 (36%) patients, adrenal insufficiency was the first clinical manifestation of APS. Abdominal pain was present in 55% of patients, followed by hypotension (54%), fever (40%), nausea or vomiting (31%), weakness or fatigue (31%), and lethargy or altered mental status (19%). The main finding in imaging techniques was compatible with adrenal hemorrhage (59%) and in histopathologic study was a hemorrhagic infarction with vessel thrombosis (55%). Lupus anticoagulant was detected in 97% of patients and the anticardiolipin antibodies titer was positive in 93% of patients. Most patients (95%) were positive for the IgG isotype of anticardiolipin antibodies, whereas 40% were positive for the IgM isotype. Baseline cortisol levels were decreased in 98% of patients, ACTH hormone levels were increased in 96% of patients, and the cosyntropin stimulation test was positive in 100% of patients tested. Steroid replacement therapy was the most frequent treatment (84%), followed by anticoagulation (52%) and aspirin (6%). Thirty-two of 35 (91%) patients with prolonged anticoagulant therapy were in good health with a mean follow-up of 25 months, whereas 25 of the 69 (36%) patients with outcome data available had died. The results of the present review stress the clinical importance of systematic screening for lupus anticoagulant and anticardiolipin antibodies in all cases of adrenal hemorrhage or infarction. An initial screening for hypoadrenalism is mandatory in any antiphospholipid antibody-positive patient who complains of abdominal pain and undue weakness or asthenia.
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PMID:Adrenal involvement in the antiphospholipid syndrome: clinical and immunologic characteristics of 86 patients. 1264 Jan 87

The case of a 42-year-old female with Budd-Chiari syndrome (BCS) and lupus anticoagulant is reported. This patient, who had been on chronic anticoagulants for her lupus anticoagulant, presented with abdominal pain, dyspnea on exertion, engorged abdominal wall venous collaterals, and hepatomegaly. A dynamic computerized tomography of the abdomen showed complete suprahepatic inferior vena caval occlusion at the junction with the right atrium. IVC venogram confirmed the diagnosis and also demonstrated patency of the hepatic veins. Free hepatic venous pressure was 25-26 mm Hg. Histopathologic examination of the liver showed marked central venous congestion with significant bridging fibrosis. The total caval occlusion and overt calcification of the clot precluded radiologic angioplasty, and the patient underwent a successful surgical thrombectomy with cavoplasty utilizing an autologous venous patch. Several weeks following surgery, she was free of symptoms and resumed her usual daily activities. Follow-up venography showed a widely opened cava with normal free hepatic vein pressures. Repeat liver biopsy at 6 months showed complete resolution of the hepatic venous congestion and a decrease in the degree of fibrosis.
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PMID:Suprahepatic Budd-Chiari syndrome treated with thrombectomy and cavoplasty. 1292 61

Portal vein thrombosis (PVT) has rarely been documented in patients after splenectomy for gastric malignancy. We report a case of PVT that occurred after splenectomy as part of an en-bloc node dissection performed to treat gastric malignant lymphoma. A 38-year-old man underwent total gastrectomy and splenectomy with en-bloc D2 lymph node dissection. The spleen weighed 480 g. On postoperative day (POD) 31, the patient complained of abdominal pain in the right upper quadrant accompanied by fever. Moderate elevations of C-reactive protein (CRP), aspartate transaminase (AST), and alanine transaminase (ALT) were noted. Contrast-enhanced computed tomography (CT) and ultrasonography disclosed thrombus in the portal vein and the splenic vein. There were no abnormalities in the levels of lupus anticoagulant, protein C antigen, protein S antigen, or antithrombin III (AT III). A diagnosis of PVT was made, and prompt treatment, including intravenous heparin combined with tissue plasminogen activator (tPA) was initiated, followed by longterm warfarin. This treatment resulted in clinical improvement, but failed to achieve thrombolysis in the portal vein. At follow-up after 6 months, the patient complained of postprandial abdominal pain with persistent peripheral edema and ascites. This case indicates that splenectomy for en-bloc node dissection in gastric malignancy is a possible cause of PVT. Because both the symptoms and the laboratory data in PVT are nonspecific, a high level of clinical suspicion and a low threshold for obtaining imaging examinations are important in the early diagnosis of PVT. Surgeons should remember PVT among several other complications whenever patients treated with radical gastrectomies are symptomatic and imaging studies are considered necessary.
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PMID:Portal vein thrombosis after splenectomy for gastric malignant lymphoma. 1471 20


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