Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with connective tissue disease presenting with both protein-losing enteropathy and pancreatic involvement is reported. A 52-year-old female was admitted because of mild epigastralgia, anasarca and ascites. Serum albumin, transferrin and zinc, showed low levels. An Upper G.I. series and endoscopy showed thickened folds of the duodenum and the jejunum. Biopsy specimens revealed lymphangiectasia in edematous villi. 99mTc-labeled human serum albumin scintigram showed abnormal radioactivity in the small intestine 90 minutes after intravenous injection, indicating protein-losing enteropathy. Hypoalbuminemia was ameliorated by glucocorticoid therapy, but recurred twice when glucocorticoid treatment was tapered. Hypoalbuminemia has not occurred since intestinal lymphangiectasia was improved with glucocorticoid treatment. Levels of elastase 1 and lipase were high in serum and ascites on admission. Endoscopic retrograde pancreatogram showed no abnormalities. Serum pancreatic enzymes were also ameliorated by glucocorticoid therapy, but slightly high levels continued for about one year and a half. This case might have been diagnosed as systemic lupus erythematosus although mixed connective tissue disease was also suspected. There are few reports of protein-losing enteropathy and pancreatic involvement associated with connective tissue diseases. Protein-losing enteropathy and pancreatic involvement were ameliorated with glucocorticoid treatment, suggesting participation of immunological mechanisms.
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PMID:Protein-losing enteropathy and pancreatic involvement in a case of connective tissue disease. 157 30

Patients treated with corticosteroids often have a dyslipoproteinemia characterized by elevated plasma levels of triglyceride and low density lipoprotein cholesterol and/or decreased levels of the high density lipoprotein2 fraction of high density lipoprotein cholesterol. This study was undertaken to determine if such patients also have elevated apolipoprotein-B (apoB) levels and/or abnormalities of the activities of the triglyceride lipases in postheparin plasma. Plasma lipoprotein levels and the postheparin activities of hepatic lipase and lipoprotein lipase were measured in 28 women with systemic lupus erythematosus (SLE) who were treated with prednisone, 10 women with SLE not treated with prednisone, and 15 normal women. The prednisone-treated group had higher mean plasma levels of triglyceride [2.06 +/- 1.3 (+/- SD) vs. 1.15 +/- 0.35 and 0.95 +/- 0.46 mmol/L; P less than 0.01], low density lipoprotein cholesterol [3.41 +/- 1.4 (+/- SD) vs. 2.79 +/- 0.67 and 2.84 +/- 0.70 mmol/L; P less than 0.01], and apoB [1.16 +/- 0.35 (+/- SD) vs. 0.82 +/- 0.13 and 0.76 +/- 0.22 g/L] than the other 2 groups. Forty-three percent of the prednisone-treated group had apoB levels of 1.20 g/L or more compared to 7% of normal subjects and none of the untreated SLE group (P less than 0.05). However, of the 12 prednisone-treated patients with elevated plasma apoB levels 5 had normal plasma lipid levels. There were no differences in the postheparin lipase activities among the 3 groups. These data indicate that corticosteroid-treated patients have elevations in apoB as well as hyperlipidemia. The lipoprotein abnormalities may explain the increased risk of atherosclerosis reported in these patients.
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PMID:Elevated apolipoprotein-B levels in corticosteroid-treated patients with systemic lupus erythematosus. 341 Sep 32

Deficiency of hepatic lipase (HL) may play a role in the lipoprotein abnormalities in chronic inflammatory states which are characterized by reticuloendothelial-system activation and cytokine release. HL triacylglycerol hydrolase activity was measured in heparin perfusates of livers from autoimmune MRL/lpr mice, which spontaneously develop a condition closely resembling human lupus erythematosis and exhibit spontaneous Kupffer-cell activation after 8 weeks of age, as well as from normal mice treated with Corynebacterium parvum or polyinosinic-polycytidylic acid complex [poly(I.C)] to induce Kupffer-cell activation. HL activity in MRL/lpr mice older than 8 weeks was 29.5% (P = 0.002) of that in age-matched control MRL/++ mice. Treatment of normal mice with C. parvum or poly(I.C) resulted in HL activities 18.6% (P = 0.004) and 13.1% (P = 0.007) respectively of untreated controls. Northern-blot hybridization of liver poly(A)+ RNA showed no differences in HL mRNA abundance in MRL/++ mice compared with the MRL/lpr autoimmune strain after 8 weeks of age, or in normal control mice compared with those treated with C. parvum, indicating attenuation of HL activity at the translational or post-translational level. Deficiency of this enzyme may represent one of the mechanisms contributing to the dyslipoproteinaemia of autoimmune disease and chronic infection.
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PMID:Modulation of murine hepatic lipase activity by exogenous and endogenous Kupffer-cell activation. 850 53

We describe a patient with systemic lupus erythematosus (SLE) who presented with severe refractory pannicular lesions diffusely involving the buttocks and lower extremities. Due to the severity of these lesions, a biopsy was performed, which implicated panniculitis associated with pancreatic disease, rather than lupus panniculitis. Serum amylase was normal, but the serum lipase was markedly elevated. An abdominal computerized tomographic scan demonstrated a pancreatic mass, which upon laparotomy was found to be an acinar cell carcinoma. After resection of the mass, her symptoms improved, where they had not responded to prior immunosuppressive therapy. She has subsequently remained well without recurrence of the disease. This case illustrates that an uncharacteristic presentation of panniculitis in a patient with lupus does not necessarily imply lupus panniculitis, and a biopsy is imperative to distinguish other sometimes life threatening etiologies.
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PMID:Panniculitis of pancreatic disease masquerading as systemic lupus erythematosus panniculitis. 859 65

We report the case of a 61-year-old woman, who suffered from abdominal pain, nausea, vomiting and fever. She had a past medical history of acute rheumatism, pyelonephritis and systemic scleroderma. Since 1971 she was hospitalized many times because of recurrent abdominal pain with increased serum amylase and lipase values. On admission, she was in distress and demonstrated clinical signs of acute pancreatitis. The link between systemic lupus erythematosus and acute pancreatitis is discussed in view of the reported cases of the world literature.
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PMID:Pancreatitis in systemic scleroderma. 936 Feb 94

We report the fourth case of simultaneous macroamylasemia and macrolipasemia. A 39-year-old woman had been treated for systemic lupus erythematosus from 1982 to 1993. She was found to have an unexplained increase in serum amylase and lipase activities since 1996. Immunoprecipitation assay showed that amylase was bound to IgA2-kappa and IgA1-kappa (IgA2 > IgA1), whereas lipase was bound to IgA1-kappa. During a follow-up period up to December 1999, the patient did not develop any additional autoimmune or lymphoproliferative disorders. In the situation of atypical clinical features associated with hyperamylasemia and hyperlipasemia, the possibility of macroenzymes should be considered.
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PMID:Simultaneous macroamylasemia and macrolipasemia in a patient with systemic lupus erythematosus in remission. 1119 4

Systemic lupus erythematosus (SLE) is an uncommon etiology of pancreatic disease. Up to now, only 3 cases of chronic pancreatitis associated with SLE have been reported in adults. We report the case of a 14-year-old girl with SLE and calcifying chronic pancreatitis. At the age of 4 she was diagnosed with SLE. She presented with several acute exacerbations of SLE that were managed with prednisone and azathioprine. At the age of 9, she was admitted with abdominal pain and elevation of serum amylase and lipase levels; no gallstones were found on ultrasound, and treatment with azathioprine was withdrawn. Thereafter, she developed numerous episodes of acute pancreatitis. Later, an ERCP showed pancreatic calcifications and distortion of the main pancreatic duct, both findings consistent with established chronic pancreatitis. At the age of 14, her condition worsened progressively, and a surgical procedure (corporo-caudal spleno-pancreatectomy) was performed. The pathology specimen showed acinar atrophy and intense fibrosis. After surgery, the patient has remained pain-free and is enjoying a normal life.
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PMID:Chronic pancreatitis associated with systemic lupus erythematosus in a young girl. 1450 37

Systemic lupus erythematosus presenting as acute pancreatitis is rare. We report a case of a 12-year-old girl with a 1-year history of systemic lupus erythematosus who developed active pancreatitis. The pancreatitis was first manifested by nausea, vomiting, fever, and abdominal pain. Elevated serum amylase (578 U/L) and lipase levels (5588 U/L), and pancreatic enlargement on ultrasound and computerized tomography confirmed the diagnosis. She responded well to high-dose corticosteroid. The high titer of antinuclear antibodies (1:1280) and low level of complement components (C3, 42.9 mg/dL; C4, 2.3 mg/dL) during the pancreatitis attack suggested that the pancreatitis may have been due to systemic lupus erythematosus exacerbation and not related to drug therapy.
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PMID:Systemic lupus erythematosus-related acute pancreatitis: a case report. 1458 68

Acute pancreatitis (AP) rarely complicates the clinical course of systemic lupus erythematosus (SLE). AP as the initial manifestation of SLE is exceptional, but its outcome is often fatal. Corticosteroids have been suspected to play a role in the development of AP, but the therapeutic benefit seems to be far above the risk of exacerbation of pancreatic lesions. We report a 13-y-old girl presenting with arthralgia and malaise, followed by abdominal pain, generalized oedema and haemodynamic instability. Increased CRP (325 ng/ml), serum amylase (14,000 IU/l) and lipase (2500 IU/l) levels suggested AP. Acute anuric renal failure required haemodialysis. Multiorgan involvement suggested SLE, which was confirmed 3 d later by increased anti-ds-DNA levels. Three methylprednisolone pulses were administered promptly, followed by oral prednisone (1.5 mg/kg/d) and six pulses of cyclophosphamide (500 mg/1.73 m2/2 wk). Mycophenolate mofetil was introduced for long-term disease control. Amylase and lipase levels decreased over 4 wk. Renal function was normal after 3 wk and proteinuria negative after 6 wk. This case suggests that steroid pulse therapy should be promptly administered if clinical and biochemical investigations suggest SLE to be responsible for AP. Aggressive treatment may be life saving.
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PMID:Acute pancreatitis in paediatric systemic lupus erythematosus. 1637 10

A number of lupus patients develop episodes of acute "idiopathic" pancreatitis, unrelated to the known causes of mechanical obstruction of the pancreatic duct or toxic-metabolic etiologies. This lupus-associated pancreatitis is rare. The estimated annual incidence was 0.4-1.1/1000 lupus patients. A literature search found detailed descriptions of this condition in 77 lupus patients. Their median age was 27, and 88% were females. Abdominal pain was the most frequent pancreatitis-related symptom (88%). In 97% the diagnosis of pancreatitis was based on laboratory evidence of elevated serum amylase or lipase. Most cases were unrelated to treatment with steroids or azathioprine. Most of the patients (84%) had active lupus at the time of pancreatitis. Mortality rate was 27%, higher than in non-SLE associated pancreatitis. Active lupus and several biochemical abnormalities, but not treatment with steroids or azathioprine, were significantly associated with increased mortality. Treatment with steroids lowered the mortality by 67% compared to non-treated patients.
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PMID:Lupus-associated pancreatitis. 1678 55


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