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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections are a common cause of morbidity and mortality in systemic lupus erythematosus (SLE) patients. The primary disease process and complications of drug management may contribute to this increased susceptibility. A high incidence of salmonella infections have been reported in SLE patients. We report an unusual case of a SLE patient who developed recurrent salmonella sepsis. The first episode with salmonella typhimurium was followed a few months later by an episode of salmonella enteritides sepsis.
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PMID:Recurrent salmonella sepsis with different species in a systemic lupus erythematosus patient. 892 81

The relative risk of age, sex, underlying diagnosis, corticosteroid usage, diabetes mellitus, and major nonprosthetic infection for the development of multiple prosthetic infections was assessed retrospectively. Deep infection occurred in 174 replacement arthroplasties in 145 patients between 1981 and 1993. Patients with rheumatoid arthritis had a significantly larger number of implants per patient (P < .001). Twenty-seven of 145 patients developed a second prosthetic infection, for an overall incidence of 19%. Of these 27, the underlying diagnoses were rheumatoid arthritis in 19, osteoarthritis in 6, neuropathic arthritis in 1, and systemic lupus erythematosus in 1. Rheumatoid arthritis and the occurrence of a major nonprosthetic infection (sepsis) were found to be highly associated with the development of a second prosthetic infection (P < .001 and P = .0001, respectively). In those rheumatoid patients with multiple infections, there was a significantly larger proportion with American Rheumatism Association class III and IV function than those with a single prosthetic infection (P = .0002). In 14 of the 27 cases of more than one prosthetic infection, the infected implants presented clinically within the same month. Ten of these 14 had an associated nonprosthetic infection. It is therefore not possible to accurately calculate the risk that one infected arthroplasty poses to other implants.
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PMID:Multiple prosthetic infections after total joint arthroplasty. Risk factor analysis. 893 29

Sixty-five abdominal computed tomography (CT) scans of 54 systemic lupus erythrematosus (SLE) patients were retrospectively evaluated together with their clinical records. This was to assess the spectrum of CT findings and to determine the value of abdominal CT in this group of patients. Over a 3.5-year period, abdominal CT scans had been requested for suspected renal vein or inferior vena cava thrombosis (n = 52, 80%), sepsis, mesenteric ischaemia, Conn's syndrome, evaluation of hepatosplenomegaly, portal hypertension and hydronephrosis. The most frequent indication for CT was suspected renal vein thrombosis (RVT). An SLE patient with previously stable renal function who rapidly develops nephrotic syndrome with deteriorating renal function has an increased risk of thromboembolic phenomenon. Also, renal vein thrombosis is difficult to diagnose clinically and prompt anticoagulation can help preserve remaining renal function. Of these with suspected RVT, two had RVT only and five had thrombosis in both renal veins and inferior vena cava. Two patients had CT features strongly suggestive of mesenteric ischaemia, one had bilateral hydronephrosis thought to be secondary to lupus cystitis and CT confirmed two abdominal abscesses. Other incidental CT findings were: subscapular renal haematoma, overall enlargement or diminution of renal size, serositis, bowel wall thickening, splenic, hepatic and pancreatic enlargement and mild para-aortic lymphadenopathy. Abdominal CT revealed many diverse findings and aided the management of these SLE patients.
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PMID:Abdominal computed tomography in systemic lupus erythematosus. 911 46

Despite their age, patients younger than 50 years who have collapse of their femoral condyles caused by steroid associated avascular necrosis have few options except total knee arthroplasty. There have been no specific reports of the results of total knee replacements for this disease. Between 1980 and 1993, 31 porous coated anatomic total knee replacements were performed in 21 patients younger than 50 years of age with avascular necrosis of the femoral condyles and tibial plateaus. There were 17 women and 4 men, with an average age of 36 years (range, 22-48 years). Seventeen of 21 patients had systemic lupus erythematosus, and all patients had a history of corticosteroid use. Patients underwent a complete clinical and radiographic evaluation at final followup that averaged 8.2 years (range, 2-16 years). Overall, there were 17 good and excellent results (55%). Eleven knees were revised for aseptic loosening (37%), and 3 additional knees (10%) ultimately were revised for deep sepsis. All 6 knees in patients with no diagnosis of systemic lupus erythematosus had excellent clinical results. There were only 11 of 25 successful outcomes (44%) in the patients with systemic lupus erythematosus. There were no differences in results when patients were stratified by degree of steroid use, cemented versus cementless fixation, or activity level.
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PMID:Total knee arthroplasty for corticosteroid associated avascular necrosis of the knee. 917 Mar 73

Lymphohistiocyte activation syndromes associated with the Epstein-Barr virus and characterized by activation and proliferation of T-cells and macrophages reflecting an inappropriate response of the host to the viral infection. The clinical manifestations are often alarming symptoms suggestive of severe sepsis. Most patients have a known underlying disease (hemopathy, lupus, Still's disease, HIV infection, bone marrow or organ transplantation). In the few cases that occur in the apparent absence of any risk factors, investigations should be done to look for a predisposing inherited disease, such as familial lymphohistiocytosis of Purtilo syndrome in boys. The treatment rests on immunosuppressive agents followed by bone marrow transplantation, which can provide a definitive cure in genetic forms.
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PMID:[Lymphohistiocyte activation syndromes associated with Epstein-Barr virus]. 924 35

Neonatal seizures in the neonatal period are symptoms of numerous underlying disorders of the neonate. We present a case in which neonatal seizures due to cerebral infarction led to a diagnosis in the mother. Neonatal convulsions caused by cerebral artery thrombosis is relatively rare in the neonatal period and is often secondary to indwelling intravascular catheters that cause thromboembolism, but may be associated with many conditions.1 Cerebral artery thrombosis in newborns, in which antiphospholipid antibodies (APA) were found in the mother, has been described in three case reports. Two of these premature infants were born with other risk factors for thrombosis. APA could not be identified in any of these three infants. In the two cases reported by Silver et al the diagnosis was made several months after birth. This case is unique in the fact that no other risk factors for thrombosis could be identified to explain the infarction, and that APA were found in the offspring of an apparently healthy mother. Whether the prior fetal death was caused by APA remains unclear. The finding of lupus anticoagulant in her child led to the diagnosis of antiphospholipid antibody syndrome in her. We believe that in case of cerebral artery thrombosis in a neonate, with no trivial cause such as an indwelling catheter or sepsis, both mother and infant should be tested for presence of APA, even when the mother seems healthy.
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PMID:An unusual cause of neonatal seizures in a newborn infant. 931 May 41

Mixed connective tissue disease (MCTD) was first reported 25 years ago. This report provides an assessment of the course of juvenile (J) MCTD in 224 patients available in the literature until 1996, including our own 33 patients. Most patients improved and remissions were observed in 3-5% (up to 27%). Among the long-term problems, a loss in joint function was seen in up to 29% of the cases, renal involvement in up to 47%, restrictive lung disease in up to 54% and gastrointestinal manifestations consisting of oesophageal dysmotility in up to 29%. Cerebral involvement was rare but severe. Cardiovascular problems observed include cardiomyopathy, myopericarditis and pulmonary hypertension. Among other long-term problems were Raynaud's phenomenon and scleroderma-like skin changes in up to 86% of the patients. Seventeen of the 224 patients had died (7.6%) because of sepsis or infection (7), cerebral complications (3), heart failure (2), pulmonary hypertension (2), renal failure (2) or gastrointestinal bleeding (1). The mortality rate of JMCTD seems to be in the same range as that of juvenile systemic lupus erythematosus, dermatomyositis and scleroderma. When compared with the other connective tissue diseases, however, mainly minor long-term problems are seen in the surviving patients.
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PMID:Course of mixed connective tissue disease in children. 945 80

Leukemia inhibitory factor (LIF) exhibits multiple biological activities in various tissues, and we have shown that LIF activates POMC gene transcription in response to immune signals. As higher serum levels of LIF have been reported in septicemia, we measured LIF values in biological fluids by RIA. Immunoreactive LIF was detected in 303 of 428 human serum samples. Circulating LIF detection rates were 69% in acute inflammatory diseases, 83% in chronic inflammatory diseases, 61% in noninflammatory diseases, and 90% in cancer patients. Serum concentrations of human LIF was higher in patients with inflammatory disease than in noninflammatory disease (0.80 +/- 0.10 vs. 0.53 +/- 0.02 ng/mL; P < 0.05) or in cancer patients (0.44 +/- 0.06; P < 0.05). Higher serum human LIF levels were found in septicemia (0.78 +/- 0.14 ng/mL), pneumonia (0.80 +/- 0.10 ng/mL), acute bronchitis (0.88 +/- 0.09 ng/mL), other infections (1.01 +/- 0.17 ng/mL), and systemic lupus erythematosus (SLE; 0.79 +/- 0.06 ng/mL). In 7 septicemia patients, Gram-negative infection was associated with higher LIF levels (1.06 +/- 0.16 ng/mL) than was Gram-positive infection (0.58 +/- 0.14 ng/mL). In patients with acute inflammatory disease, serum LIF levels decreased within several days after hospitalization. To test circulating mouse (m) LIF changes in response to inflammatory stress, lipopolysaccharide (LPS) was injected ip to mice. LPS increased serum mLIF values concordantly with ACTH levels. After i.p. injection of 80 microg LPS, serum mLIF increased by 144% (P < 0.05), 173% (P < 0.05), and 134% at 30, 90, and 120 min respectively. In vitro, however, LPS did not increase ACTH and mLIF secretion from dispersed mouse primary pituitary cells. These results suggest that LIF is an important participant in the pathogenesis of the acute inflammatory response. The elevated serum LIF levels observed in inflammation do not appear to originate from the pituitary.
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PMID:Measurement of leukemia inhibitory factor in biological fluids by radioimmunoassay. 954 56

We describe here the broad spectrum of acute renal insufficiency occurring in the course of human immunoinsufficiency virus infection. In our renal unit in Tenon hospital, 90 human immunoinsufficiency virus-infected adult patients were admitted for acute renal insufficiency between June 1988 and December 1996. Sixty out of them had a pathological diagnosis. The remaining patients did not have renal biopsy because of obstructive renal failure (n = 2), bleeding risk (n = 11), or clinically evident hypovolemic and/or sepsis-related acute tubular necrosis (n = 17). Nine different causes of acute renal insufficiency were listed. Human immunoinsufficiency virus-associated nephropathy, the most specific human immunoinsufficiency virus-related renal disease, which was diagnosed in 14 patients, is characterized by focal and segmental glomerulosclerosis with an important hyperplasia and/or proliferation of podocytes and huge tubular distension. The rapid progression to end-stage renal failure was not a constant feature since 10/14 patients had a partial renal recovery. Hemolytic-uremic syndrome was the other major cause of acute renal failure in these patients (32 cases) and was found to be associated with active cytomegalovirus infection. Cytomegalovirus-infected cells were present in half of the renal biopsies performed in this group of patients. Furthermore, these patients had an increased plasma tissue-type plasminogen activator activity whereas its type 1 inhibitor was not significantly increased, as opposed to non human immunoinsufficiency virus-associated hemolytic-uremic syndrome. Half of the patients had a complete renal recovery. The other causes of acute renal insufficiency were 1) intratubular deposition of either drugs (Adiazine, Foscavir, Indinavir) in 13 patients, or monoclonal light chain in one patient with B cell-lymphoma; 2) lupus-like glomerulonephritis characterized in one case by a complete clinical remission after 6 month-treatment by antiproteases; 3) acute tubular necrosis. In this setting, rhabdomyolysis could reveal HIV infection. The heterogeneity of renal diseases could be explained by the variation of human immunoinsufficiency virus-associated infections along time and by the different drugs which permit a better survival. We can hypothesize that new HIV-associated diseases will occur with the long term use of antiproteases.
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PMID:[Human immunodeficiency virus and acute renal insufficiency]. 961 98

A 64-year-old woman with an 11-year history of systemic lupus erythematosus and amputation of her left lower leg as a consequence of arterial embolism, presented with two large, non-healing ulcers on her right shank. Pyoderma gangrenosum associated with secondary antiphospholipid syndrome was diagnosed based upon the typical clinical features and increased antibodies to cardiolipin. Although an aggressive therapy with corticosteroids and cyclosporine was started, her condition continued to worsen. She finally died as a result of sepsis. We discuss the difficulties in diagnosis and therapy of SLE combined with the antiphospholipid syndrome and pyoderma gangrenosum.
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PMID:Pyoderma gangrenosum associated with the secondary antiphospholipid syndrome. 964 13


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