Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On routine hospital admission, 23,714 patients received a 28-test serum metabolic profile. The 33 most common diseases (4,132 patients) of liver, pancreas, and gallbladder (LPG) had unique chemical templates averaging 15 significant serum deviations. Each LPG disease differed from all others by elevations of both leucine-aminopeptidase (LAP) and alkaline phosphatase (AP) levels. LAP level was low or normal and serum glutamic oxaloacetic transaminase (SGOT) and AP levels were elevated in 43 non-LPG diseases. Patients with acute and chronic pancreatitis had elevated amylase levels. The four nonmalignant diseases of the gallbladder were associated with normal levels of amylase and lactic dehydrogenase (LDH); except for silent cholelithiasis, each showed elevated total bilirubin (BIL) levels. Patients with solitary or scattered lesions of the liver had normal bilirubin levels (2,115 patients), and those with diffuse interstitial or parencymal disease had elevated BIL levels. Cancer patients had elevated LDH and alpha1 globulin (A1G) levels, but low albumin levels. The importance of comprehensive liver profiles in the treatment of psychoses is emphasized by significant liver damage in a number of these patients. A1G was normal and LDH was elevated in patients having mononucleosis, hepatitis, lupus erythematosus, alcoholism, and alcoholic cirrhosis.
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PMID:Serum chemistry templates of disease in liver, pancreas, and gallbladder. 116 26

A case of Coombs' positive anemia in a man who had procainamide-induced lupus erythematosus syndrome is reported. The patient had a hemoglobin of 4.3 gm/dl and reticulocytopenia (3.1% corrected). Serum lactate dehydrogenase and haptoglobin levels were normal, and total bilirubin was only slightly elevated. Two other reported cases of procainamide-induced hemolytic anemia have demonstrated similar findings. Apparently, procainamide occasionally may induce a reversible, reticulocytopenic, Coombs' positive anemia that is not associated with laboratory evidence of acute hemolysis.
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PMID:Reticulocytopenic, coombs' positive anemia induced by procainamide. 685 67

A 38 year-old man with a 12-year history of noninsulin-dependent diabetes mellitus with rapidly progressive diabetic complications presented with microangiopathic hemolytic anemia and thrombocytopenia. He had no disorders that could induce microangiopathic hemolytic anemia other than diabetic microangiopathy. In addition, there was a significant negative correlation between serum lactate dehydrogenase levels and peripheral platelet counts, which suggested that the hemolysis and thrombocytopenia occurred through the same mechanism. Activated partial thromboplastin time was slightly prolonged, and lupus anticoagulant and antiphospholipid immunoglobulin G antibodies were positive. Both the hemolysis and the thrombocytopenia spontaneously improved after the initiation of hemodialysis. This is a unique case of diabetic microangiopathic hemolytic anemia and thrombocytopenia in which antiphospholipid syndrome also may be involved.
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PMID:Case report: diabetic microangiopathic hemolytic anemia and thrombocytopenia with antiphospholipid syndrome. 861 92

The case of a 75-year-old Japanese woman with adult-onset Still's disease who presented with cerebral haemorrhage is described. She had been in clinical remission for 2 years, after induction therapy including non-steroidal anti-inflammatory drugs, prednisolone, cyclophosphamide and mizoribine followed by auranofin, until her cerebral haemorrhage occurred, although her serum level of ferritin had gradually increased. After the onset of cerebral haemorrhage, the patient's serum level of thrombomodulin was elevated although c-reactive protein and lactate dehydrogenase were not increased. Anti-cardiolipin antibody and lupus anti-coagulant were not detected. Patients with adult-onset Still's disease are rarely reported to develop cerebral vascular disease, possibly because the disease is most frequent in young adults. The cerebral haemorrhage may have been caused by the vasculitis due to Still's disease.
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PMID:Cerebral haemorrhage complicating adult-onset Still's disease: a case report. 895 35

The objective of this study was to determine the incidence of pulmonary involvement in patients with systemic lupus erythematosus (SLE) and to clarify the clinical and laboratory characteristics in SLE patients with various pulmonary involvements. A retrospective study (n = 137) revealed that the types of pulmonary involvement found in SLE patients were: pleuritis (9%), interstitial pneumonia (8%), pulmonary infarction (7%), pulmonary infection (4%), pulmonary hypertension (2%), restrictive dysfunction (28%) and decreased diffusion capacity (43%). The incidences of pericarditis (P < 0.01), arthralgia (P < 0.05) and hypoalbuminemia (P < 0.05) were significantly greater in patients with pleuritis than in those without, while in patients with interstitial pneumonia, the incidence of anti-SS-A antibody (P < 0.05) and sicca syndrome (P < 0.05) were significantly greater than in those without. A longitudinal follow-up study of patient groups with various pulmonary involvements revealed: 1. significant changes of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), lactate dehydrogenase (LDH) and thrombomodulin (TM) in patients with pleuritis, and 2. significant changes of WBC and LDH in patients with interstitial pneumonia. The increased ESR, CRP and TM levels during disease episodes suggest that the involvement of inflammatory processes is related to vasculitic events in the pathogenesis of lupus pleuritis. A higher incidence of anti-SS-A antibody in lupus patients with interstitial pneumonia suggests a potential role for this autoantibody in the pathogenesis of this complication.
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PMID:Clinical and laboratory features of lupus patients with complicating pulmonary disease. 1046 59

Mycophenolic acid (MPA) reversibly inhibits inosine 5'-monophosphate dehydrogenase (IMPDH), an enzyme involved in the de novo synthesis of guanine nucleotides. Previously, mycophenolate mofetil (MMF), the pro-drug of MPA, was shown to exert beneficial effects on the systemic lupus erythematosus (SLE)-like disease in MRLlpr/lpr mice. In this study, MPA's immunomodulating effects in vitro on the B cell hybridoma MAR 18.5 were investigated. The cells were exposed for MPA at either 1 or 10 microM for 24 h, and the levels of immunoglobulins, cytokines and lactate dehydrogensase in supernatants were measured. The frequency of immunoglobulin producing cells and the proliferation and viability of the cells was also investigated. MPA exposure reduced the frequency of immunoglobulin producing cells, decreased the levels of immunoglobulins and cytokines in the supernatants, and decreased the cell proliferation. MPA was slightly cytotoxic as indicated by increased lactate dehydrogenase (LDH) levels and reduced viability. All MPA-induced effects were totally reversed by the addition of guanosine to the cultures. Thus, since activated B lymphocytes play a central role in lupus and our results show that B cells are targets for MPA, we propose that direct effects on B cells may be an important mechanism for the ameliorating effects of MMF in SLE.
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PMID:Mycophenolic acid inhibits inosine 5'-monophosphate dehydrogenase and suppresses immunoglobulin and cytokine production of B cells. 1253 32

This study aimed to investigate the effects of human anti-DNA antibodies (Ab) from patients with lupus on renal proximal tubular epithelial cells (PTEC), focusing on alterations in cell morphology and proinflammatory cytokine synthesis. Immunohistochemistry showed increased tubulointerstitial IL-6 expression and IgG deposition in renal biopsies from patients with diffuse proliferative lupus nephritis, not observed in controls or membranous lupus nephritis, which correlated with the severity of inflammatory cell infiltration. Sera from patients with lupus nephritis contained IgG that bound to cultured PTEC. Such binding increased with disease activity and correlated with the level of anti-DNA Ab. Incubation of PTEC with anti-DNA Ab that were isolated during active (active Ab) or inactive (inactive Ab) disease induced IL-6 synthesis, both apically and from the basolateral aspect. This was accompanied by altered cell morphology, increased cell proliferation (P < 0.05), and lactate dehydrogenase release (P < 0.05). The binding of inactive Ab and active Ab to PTEC resulted in differential and sequential upregulation of TNF-alpha, IL-1beta, and IL-6 secretion (P < 0.05). Early induction of TNF-alpha was observed with active Ab; the two then acted synergistically to induce IL-6 secretion. Exposure of PTEC to inactive Ab was associated with modest induction of TNF-alpha, which was not involved in downstream induction of other proinflammatory peptides. These data suggest distinct immunopathogenetic mechanisms during disease flare or remission. Conditioned media from human mesangial cells acted synergistically with anti-DNA Ab to induce cytokine secretion in PTEC. Results from these studies underscore the pivotal role of PTEC in the pathogenesis of tubulointerstitial inflammation and fibrosis in lupus nephritis.
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PMID:Effect of human anti-DNA antibodies on proximal renal tubular epithelial cell cytokine expression: implications on tubulointerstitial inflammation in lupus nephritis. 1619 22

The purpose of this study was to design chimeric human papillomavirus type-16 L1 virus-like particles (VLPs) and to explore the potential capacity of elimination to anti-dsDNA antibody-producing B cells. To test it, VLPs were achieved by combination of human papillomavirus type-16 L1 proteins inserted into a targeting peptide (DWEYSVWLSN) and plasmids encoding diphtheria toxin A ligand. Additionally, VLPs were cocultured with target cells to assess the killing efficiency by lactate dehydrogenase assay in vitro. Lastly, lupus-prone (BWF1) mice vaccinated with VLPs were used as a model to assess the killing efficiency in vivo. The results showed that the VLPs were constructed successfully, and possessed the potential of killing anti-dsDNA antibody-producing B cells with high efficiency. The findings indicate the possibility that the VLPs ablate autoreactive B cells represents a novel strategy in the immunotherapy of autoantibody-mediated diseases.
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PMID:Insertion of a targeting peptide on capsid surface loops of human papillomavirus type-16 virus-like particles mediate elimination of anti-dsDNA Abs-producing B cells with high efficiency. 1930 92

We present a case of a 28-year-old black female patient with a previous diagnosis of overlapping syndrome of lupus and rheumatoid arthritis, treated with corticosteroids and methotrexate, who was admitted to our department due to abdominal pain with vomits and diarrhea for 15 days. On complementary evaluation elevated C-reactive protein and erythrocyte sedimentation rate, lactate dehydrogenase and amylase levels were detected, C3 was reduced, blood, faeces, peritoneal fluid and urine cultures were negative; abdominal computerized tomography disclosed jejunal thickening with parietal edema, bilateral ureterohydronephrosis and bladder parietal thickening; on endoscopy with biopsy there was chronic pangastritis and duodenitis; cystoscopy with biopsy showed chronic cystitis. Those aspects suggested lupus enteritis and cystitis which appear rarely associated and have poor prognosis. This patient was treated with high dose corticosteroids followed by azathioprine and prednisolone, with clinical and imaging improvement.
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PMID:[Enteritis and cystitis - a cause of abdominal pain in lupus]. 1956 79

Macrophage activation syndrome (MAS) belongs to secondary hemophagocytic lymphohistiocytosis (HLH) syndrome. It is usually associated with rheumatic diseases. We retrospectively reviewed our hospital's medical records of 102 HLH/MAS patients from the past 20 years. Demographics, clinical data, treatment, and outcomes were analyzed. Among 102 patients, eight patients with underlying juvenile systemic lupus erythematous (two patients), mixed connective tissue disease (one patient), primary anti-phospholipid syndrome (one patient), and systemic type juvenile rheumatoid arthritis (sJRA; four patients) with 13 episodes of MAS were studied. Clinical manifestations of MAS included fever (100 %), hepatosplenomegaly (77 %), lymphadenopathy (38 %), skin rash (62 %), and neurological involvement (31 %). Laboratory features included leukopenia (54 %), anemia (46 %), thrombocytopenia (77 %), jaundice (27 %), hypofibrinogenemia (40 %), decreased erythrocyte sedimentation rate (67 %), and elevated liver enzymes (77 %), lactate dehydrogenase (100 %), ferritin (88 %), triglycerides (91 %), C-reactive protein (85 %), plasma D-dimer (50 %), and hemophagocytosis in bone marrow (83 %). The Epstein-Barr virus and adenovirus infection triggered MAS in two patients with sJRA. Methylprednisolone pulse therapy was effective in two out of three patients, and high-dose intravenous immunoglobulin (IVIG) was effective in two out of six patients. Patients with sJRA responded well to corticosteroids and cyclosporine. Complications included opportunistic infection with Pneumocystis jiroveci, multiple organ failure, and intensive care unit myopathy. The mortality rate was one out of eight (12.5 %). Our results showed that MAS could be fatal and complicate various pediatric autoimmune diseases. It generally has a good response to corticosteroids and IVIG. Prompt recognition and timely treatment can result in good outcomes.
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PMID:Clinical analysis of macrophage activation syndrome in pediatric patients with autoimmune diseases. 2261 46


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