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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatitis is a rare complication of paediatric systemic lupus erythematosus (SLE). We describe a child with severe form of SLE who initially developed acute pancreatitis, subsequently complicated by extensive pancreatic pseudocyst. The treatment and outcome are discussed.
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PMID:Pancreatic pseudocyst in paediatric systemic lupus erythematosus. 1211 36

Urticarial vasculitis, a form of leukocytoclastic vasculitis involving the postcapillary venules, is classified as a type III hypersensitivity reaction and has been associated with connective tissue disease. The lesions resemble urticaria and typically persist for more than 24 hours. Urticarial vasculitis usually affects young women, and the diagnosis is confirmed at histologic examination. Patients with urticarial vasculitis can be divided into 2 types--those with normal complement levels and those with hypocomplementemic urticarial vasculitis (HUV). Patients with normocomplementemic urticarial vasculitis have a milder course than do patients with HUV, a condition that has a strong association with systemic lupus erythematosus. Angioedema, ocular inflammation, obstructive lung disease, and glomerulonephritis are commonly associated with HUV. We describe the case of a girl with systemic lupus erythematosus and HUV who also had pancreatitis, hypothyroidism, and elevated levels of antiphospholipid antibodies.
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PMID:Hypocomplementemic urticarial vasculitis: report of a 12-year-old girl with systemic lupus erythematosus. 1239 49

Pancreatitis is a well-established but unusual complication of thrombotic thrombocytopenic purpura (TTP). It is also an unusual complication of systemic lupus erythematosus (SLE). However, TTP occurring as a consequence of acute pancreatitis in a patient with SLE has never been reported. We report a 24-year-old African American woman with active systemic lupus (SLE) who developed thrombotic thrombocytopenic purpura (TTP) following an episode of acute pancreatitis. The TTP was manifested by low-grade fever, microangiopathic hemolytic anemia, renal insufficiency, altered mental status, seizures and thrombocytopenia. The patient was initially treated with pulse corticosteroids with inadequate response and subsequently with daily plasmaphresis, leading to full remission. This case represents first report of pancreatitis leading to TTP in a patient with systemic lupus erythematosus.
Lupus 2003
PMID:Pancreatitis leading to thrombotic thrombocytopenic purpura in systemic lupus erythematosus: a case report and review of literature. 1263 Jul 59

We describe the case of a 23-year-old woman with a mild form of systemic lupus erythematosus who presented a febrile illness rapidly followed by general worsening, neurologic involvement, renal failure and coma. While hospitalized in the intensive care unit she also suffered from acute pancreatitis, microangiopathic hemolitic anemia, thrombocytopenia and prolongation of clotting times. Despite aggressive treatment the patient died at day 17 of hospitalization in the intensive care unit. At autopsy necrotico-hemorragic pancreatitis, diffuse pneumonia, peritonitis and cerebral edema were present. Most striking was the presence of invasive aspergillosis, which was detected in all organs examined. In this case thrombotic thrombocytopenic purpura, invasive aspergillosis and multiorgan failure including acute pancreatitis were present. The relationship between the three entities is complex, and it is difficult to establish which of the different events took place first and triggered the others.
Lupus 2003
PMID:A fatal case of systemic lupus erythematosus complicated by acute pancreatitis, invasive aspergillosis and features of thrombotic thrombocytopenic purpura. 1276 8

Osteonecrosis is a clinical entity characterized by death of bone marrow and trabecular bone as a result of disruption of blood supply to the bone (1,2). Other aspects of this condition include avascular necrosis, aseptic necrosis, and osseous ischemic necrosis of bones. Osteonecrosis is classified into two main forms; post-traumatic and nontraumatic. The post-traumatic form of osteonecrosis usually develops as a result of traumatic displacement of bone fragments, which leads to impaired blood supply and ischemia to the affected bone. Osteonecrosis of the femoral head is common following fracture of the femoral neck. A variety of systemic diseases and clinical conditions are associated with nontraumatic osteonecrosis. These include autoimmune rheumatic diseases, alcoholism, pregnancy, Gaucher's disease, thrombophilia, corticosteroid therapy, Sickle-cell anemia, pancreatitis, inflammatory bowel diseases, and use of cytotoxic drugs and others. Idiopathic forms of osteonecrosis have also been reported (2-4). Among the rheumatic diseases, osteonecrosis is strongly associated with systemic lupus erythematosus (SLE) (5). However, osteonecrosis has been diagnosed in patients with primary antiphospholipid syndrome (APS) (6), rheumatoid arthritis (7), and systemic vasculitis (8). This article reviews the causes, clinical and epidemiological features, diagnosis, and treatment options for osteonecrosis among patients with SLE.
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PMID:Osteonecrosis in patients with SLE. 1279 57

Antibodies (Abs) to carbonic anhydrase (isoforms CA-I and CA-II) have been considered pathogenic factors in the development of autoimmune pancreatitis. Besides, such autoAbs might accelerate the pancreatic damage in alcoholic chronic pancreatitis (CP). The aim of the present study was to evaluate the presence of serum Abs to CA-I and CA-II in CP and the relative affinity of these Abs. Serum anti-CA-I and -CA-II Abs were measured in 89 patients with CP (48 alcoholic and 41 nonalcoholic) by an ELISA technique. The prevalence of those autoAbs in CP was compared with other autoimmune diseases where they have also been found. The presence of other serological manifestations of autoimmunity, such as hypergammaglobulinemia or antinuclear Abs, was determined in CP patients as well. Elevated serum levels of both anti-CA-I (24%) and -CA-II (18%) Abs were observed in CP, although their prevalence was lower than in autoimmune diseases like rheumatoid arthritis (44 and 25%, respectively) or systemic lupus erythematosus (39% for anti-CA-I Abs). Furthermore, these Abs were of low average avidity. On the other hand, a significantly higher proportion of nonalcoholic CP had anti-CA-II Abs with respect to alcoholic CP (15.2 vs. 2.4%, p < 0.05). Anti-CA-I and -CA-II Abs might be helpful in the diagnosis of autoimmune CP, and the detection of the latter Abs seems to discard alcoholic etiology. Although it does not discard any pathogenic role in autoimmune CP, the low-avidity of anti-CA Abs argues against such idea.
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PMID:Low-avidity antibodies to carbonic anhydrase-I and -II in autoimmune chronic pancreatitis. 1280 41

Symptoms of leukoencephalopathy led to hospital admission of a 59-year-old woman. In addition, a tumor of unknown nature in the pancreas was identified by abdominal ultrasound and CT scan. Following explorative laparotomy and pancreas tail resection, histopathologic analysis revealed a pancreatic pseudotumor with chronic fibrotic pancreatitis. Systemic lupus erythematosus (SLE) was diagnosed due to the presence of antinuclear antibodies (ANA) in serum, antiphospholipid antibodies, and involvement of the central nervous system. Leukoencephalopathy related to anticardiolipin antibodies in serum is a known but rare manifestation of SLE. The concomitant occurrence of chronic pancreatitis can be caused by the development of SLE-induced vasculitis in the pancreas. Subsequent complications of pancreatitis are responsible for the critical, life-threatening state of these patients and may be prevented by early identification of anticardiolipin antibodies and therapy for SLE.
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PMID:Leukoencephalopathy and chronic pancreatitis as concomitant manifestations of systemic lupus erythematosus related to anticardiolipin antibodies. 1293 45

The chief dangers reported with some common drugs are reviewed. Hazards of antibiotic therapy include: the increasing incidence of sensitization to penicillin with occasional anaphylactic reactions; aplastic anemia with chloramphenicol, and the poor tolerance of infants for chloramphenicol; staphylococcal enterocolitis; unnecessary "prophylactic" use of antibiotics. Thiazide diuretics may precipitate potassium depletion, skin reactions, pancreatitis, blood dyscrasias, gout, diabetes mellitus and hepatic coma. Reserpine can increase gastric acidity, induce mental depression, and when used with digitalis lead to ventricular premature beats. Hydralazine may aggravate angina pectoris, cause tachycardia, and bring about a syndrome resembling disseminated lupus erythematosus. Guanethidine may result in loose stools, impotence, and postural hypotension. Hazards of phenothiazines include jaundice, parkinsonian states and tremors, convulsions, hypotension, and blood dyscrasias. The butanediols have numerous side effects including gastrointestinal, cutaneous and hypotensive reactions. Prolonged corticosteroid therapy introduces a new danger in surgical treatment. The progesterone-like drugs may induce masculinization of the female fetus.
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PMID:Dangers in the use of some potent drugs. 1398 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

The aim of this study was to evaluate whether corticosteroid use is the etiological agent in acute pancreatitis in patients with systemic lupus erythematosus, or whether it is related to the underlying connective tissue disorder. Hospital admissions at Thomas Jefferson University Hospital between 1982 and 2002 that carried the dual diagnosis of systemic lupus erythematosus and pancreatitis were identified, and demographic data, clinical interventions and parameters of clinical progression of their disease were identified. From 2947 admissions with systemic lupus erythematosus 25 (0.85%) were diagnosed as having acute pancreatitis; 76% of cases had active systemic lupus erythematosus on presentation, with an average of 4.4 organ involvement, and a clustering of renal disease (56%), pleural effusion (48%) and arthritis (44%) in these patients. Fifteen patients with active disease and three whose disease was inactive received increased doses of corticosteroids, and four active cases and one inactive one stayed on the same doses. Two inactive patients received no corticosteroids before or after the diagnosis of pancreatitis. Eighty-two percent of patients had clinical and laboratory improvement on the higher or maintenance dose of corticosteroids. We therefore concluded that acute pancreatitis is a rare manifestation of systemic lupus erythematosus, and corticosteroids do not appear to be the etiological agent.
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PMID:Systemic lupus erythematosus and acute pancreatitis: a case series. 1504 30


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