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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
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PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

Non-endemic Salmonella bacteremia tends to occur in patients with chronic disease. We reviewed all cases of Salmonella infection documented in adults at Bellevue Hospital during the years 1975-1982. Unexpectedly, the most frequent underlying disease found among bacteremic patients was systemic lupus erythematosus (SLE). Patients with SLE accounted for 6 of 30 Salmonella bacteremias as compared with 13 of 2,388 non-Salmonella gram-negative bacteremias. Salmonella was the single most frequent gram-negative isolate from the blood of SLE patients. All lupus patients with Salmonella infection were bacteremic. In contrast, isolates from blood represented only 23% of all Salmonella infections documented in the non-lupus population. Presentation was characterized by fever (greater than 103 degrees F) and abdominal pain. Four of the 6 patients were hypocomplementemic. All were receiving immunosuppressive therapy. We conclude that SLE patients in a municipal hospital setting are at increased risk for Salmonella sepsis. This should be considered when empiric antibiotic therapy is initiated.
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PMID:Salmonella bacteremia in systemic lupus erythematosus. Eight-year experience at a municipal hospital. 388 Nov 3

The study of serum from a patient with C2 deficiency is described. The patient had an episode of pneumococcal meningitis at 5 mo of age with seizures and transient hemiparesis and apparent purpuric skin lesions. He was first admitted to the University of Minnesota Hospitals at 10 yr of age following the discovery of proteinuria accidentally by his mother. Since then he has been admitted repeatedly to this hospital with numerous clinical findings including arthralgia, recurrent abdominal pain, proteinuria, membranous nephropathy, malar butterfly rash, seizures, personality aberrations, and recurrent fever. In June 1971, the patient developed positive DNA and DNP antibodies and positive LE cells. When the C profile was studied before and after recognition of lupus, C1q, C1s, and C4 dropped. C3 levels were elevated as were C5, C6, and C7, C3 proactivator had been reduced in the patient even before he developed lupus. Also because of a traumatic renal biopsy leading to a perirenal hematoma, he required surgery and a blood transfusion. 1 h after blood transfusion, a C2 titer of 23 hemolytic units was detected. Almost immediately levels of C3, C5, C6, and C7 dropped, C8 and C9 remained elevated. The addition of C2 from normal blood permitted dramatic activation of C3. These findings support the view that the rare deficiency in production of C2 predisposes to serious susceptibility to infection, vascular and mesenchymal disease as well as to renal disease and a lupus syndrome.
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PMID:C2 deficiency. Development of lupus erythematosus. 457 55

Lupus anticoagulant is an immunoglobulin that interferes with prothrombin conversion to thrombin and is manifested biochemically by prolongation of the partial thromboplastin time. Paradoxically, bleeding is rare in association with this anticoagulant, and deep leg vein thromboses, pulmonary emboli, and cerebrovascular accidents have been described in patients with this clotting inhibitor. This report describes the first case of Budd-Chiari syndrome associated with the lupus anticoagulant. The patient presented with abdominal pain and massive ascites. The Budd-Chiari syndrome was confirmed by liver biopsy and venography. No medical condition known to predispose to an increased thrombotic tendency could be identified, and the presence of the lupus anticoagulant in the patient's plasma may provide an explanation for his hypercoagulability and development of the Budd-Chiari syndrome.
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PMID:Budd-Chiari syndrome in a patient with the lupus anticoagulant. 641 18

A 58 year-old woman had atypical chronic urticaria, arthralgias and abdominal pain. Attacks of angioneurotic edema occurred. Proteinuria was discovered. She had clinical and biological signs of inflammation, leukoneutropenia , antileukocyte antibodies and low CH 50, C1q and C4 levels without functional C1 esterase deficiency. C1q precipitins were not detectable. Skin biopsy disclosed angiitis and by immunofluorescence a lupus band test was positive. Serologic investigations in search of SLE were negative. Renal biopsy showed mesangial deposits, capillary loop thickening and mesangial fixation of anti-IgG, C3 C1q and C4 antisera. In the interstitium, voluminous perivenular inflammatory infiltrates were visible. With corticosteroid treatment clinical manifestations subsided and proteinuria disappeared. This observation of McDuffie 's angiitis with renal venulitis leads to a review of the literature with discussion of the mechanisms of hypocomplementemia.
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PMID:[Hypocomplementemic urticarial vasculitis with glomerulopathy and renal venulitis]. 672 99

Lupus anticoagulant has been described in association with many autoimmune disorders. Here we describe its occurrence in a patient with ANCA-associated microscopic polyarteritis with medium vessel involvement. A 62-year-old man presented with mononeuritis multiplex and abdominal pain and was demonstrated to have multiple aneurysms on visceral angiography, consistent with the diagnosis of medium vessel vasculitis or classical polyarteritis nodosa. In addition he had active tuberculosis. He developed a deep venous thrombosis at this admission and, on one occasion, had a prolonged APTT but this was not confirmed to be due to a lupus anticoagulant. Two years later when the patient was readmitted with fevers, headaches and nasal discharge, both ANCA and a lupus anticoagulant were demonstrated in his serum, although there was no evidence of a venous thrombosis. Six months later the patient was demonstrated for the first time to have dysmorphic urinary RBC consistent with glomerular bleeding; at the same time he developed a deep venous thrombosis. ANCA was still present, but the lupus anticoagulant could not be detected. The patient was treated with cyclophosphamide and prednisolone and a Greenfield filter inserted into his inferior vena cava.
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PMID:Lupus anticoagulant in anti-neutrophil cytoplasmic antibody-associated polyarteritis. 773 54

Renal artery infarction is a very rare complication in patients with systemic lupus erythematosus (SLE), even in patients with antiphospholipid syndrome which often causes thromboembolism: Renal infarctions have only been reported in 4 SLE patients with antiphospholipid antibodies (aPL). Here we report a case of SLE without aPL who accompanied by renal and cerebral infarctions. A 42-year old Japanese woman with 8 year history of SLE manifested by arthralgia, central nervous system symptoms, positive-antinuclear and anti-DNA antibodies was admitted to our hospital for the treatment of progressive lupus nephritis. Physical examinations revealed hypertension (130-160/80-110 mmHg) without pitting pretibial edema. Laboratory evaluations showed proteinuria (3.7 g/day), normal serum creatinine level (0.9 mg/dl), low serum albumin level (2.3 g/dl) and high cholesterol level (317 mg/dl). Old cerebral infarctions were recognized by magnetic resonance imaging. However, hematological and immunological studies revealed that this case has neither a prolonged activated partial thromboplastin time, lupus anticoagulant nor anticardiolipin antibodies. Prednisolone was increased from 30 mg/every other day to 30 mg/day, and oral azathioprine, 50 mg/day, was started for the treatment of lupus nephritis. On the 11th day, she suddenly complained severe abdominal pain, which gradually localized on the right side. Computed tomography of the kidney suggested right renal infarctions, and arteriography of right renal artery confirmed both an obstruction of the ventral branch and a narrowing of the dorsal branch of right renal artery. No intra-cardiac thrombus was demonstrated by echocardiography. Following to the treatment with fibrinolytic agent and anticoagulant, her symptoms have improved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal and cerebral infarctions in a patient with systemic lupus erythematosus without antiphospholipid antibodies]. 823 16

Although an acute abdomen often occurs in lupus patients, definitive treatment is commonly delayed due to the difficulty in diagnosis. We performed an abdominal ultrasound (US) in two patients with severe abdominal pain and recognized mural thickenings of intestinal walls. In the first case high dose prednisone was given for severe abdominal pain, with subsequent perforation of sigmoid colon. Pathological specimens showed a thrombotic vasculitis in the mesenteric artery and arteriole of intestinal walls. In the second case physical examination elicited a rebound tenderness. An abdominal X-ray demonstrated a gasless ileus and US also showed marked thickening of intestinal walls, 16 mm in thickness. A CT scan revealed the same findings in the entire bowel. After high dose methylprednisolone was administered, her symptoms markedly improved. The mural thickenings disappeared within 10 days as seen by abdominal ultrasound examination. The US is very useful in order to make an early diagnosis of intestinal vasculitis, showing as edema (but non-specific) of intestinal wall and we can use it safely and repetitively without exposure to radiation, compared with other examinations, such as CT scan and gastrointestinal contrast study etc. The US is not only useful in diagnosis, but also helpful for follow up of patients after the initiation of treatment.
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PMID:[Vasculitis-related acute abdomen in systemic lupus erythematosus--ultrasound appearances in lupus patients with intra-abdominal vasculitis]. 834 66

A 34-years-old woman was admitted to our department in February, 1992, because of nausea, vomiting, abdominal pain and diarrhea. She had been diagnosed as systemic lupus erythematosus (SLE) in 1988 and treated with prednisolone at the dose of 5 mg a day. In December, 1991, gastrointestinal symptoms developed followed by anuria on March 3, 1992. The laboratory findings revealed no activities in SLE. Computed tomography (CT) showed bilateral hydroureteronephrosis, swelling of bladder and gastrointestinal wall, and ascites. Under the diagnosis of lupus cystitis, corticosteroid therapy was started with 125 mg of methylprednisolone. Her symptoms improved immediately. Abnormal findings shown in the previous CT disappeared concomitantly. Lupus cystitis was reported by Orth et al. 1983 as severe fetal syndrome. However, because early corticosteroid therapy appears to reverse acute manifestation of lupus cystitis without complications, attention should be paid on lupus cystitis in patients with SLE with gastrointestinal symptoms of unknown etiology and decreasing urinary volume.
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PMID:[A case of lupus cystitis successfully treated with corticosteroid accompanied by gastrointestinal symptoms]. 859 60

Spontaneous liver rupture is uncommon, difficult to diagnose and carries a universally high mortality. It has been well documented to occur as a complication of primary or secondary hepatic malignancy. Similarly, there are 28 cases of ruptured haemangiomata described in the world literature. It is also well described in severe pregnancy-induced hypertension and is said to carry a mortality of 18% for patients treated by packing and drainage of the haematoma and 75% for patients treated with liver resection. Two female patients aged 60 and 61 presented to our accident and emergency department. One had a history of hypertension only and the other a history of a bleeding diathesis from the lupus anticoagulant. Both presented with hypotension and abdominal pain and both were diagnosed by abdominal CT scan. One was treated with hepatic artery ligation and tamponade and the other with liver resection and correction of the coagulopathy. Neither had any evidence of a ruptured hemangioma or tumor at laparotomy or on histological examination, and both are alive and well. The conclusions to be drawn from this review and our own recent experience is that the treatment of choice for ruptured haemangiomata is liver resection and, for rupture during pregnancy, is tamponade with packs and evacuation of the haematoma. Hepatic arteriography and embolisation, if possible, is a useful adjunct. Correction of any coagulopathy is essential. We can only speculate that the aetiology in our patients was uncontrolled hypertension in one and coagulopathy in the other.
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PMID:Two cases of spontaneous liver rupture and literature review. 880 90


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