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)

Kikuchi-Fujimoto disease (KFD) is a benign and self-limited disorder, characterized by regional cervical lymphadenopathy with tenderness, usually accompanied with mild fever and night sweats. Less frequent symptoms include weight loss, nausea, vomiting, sore throat. Kikuchi-Fujimoto disease is an extremely rare disease known to have a worldwide distribution with higher prevalence among Japanese and other Asiatic individuals. The clinical, histopathological and immunohistochemical features appear to point to a viral etiology, a hypothesis that still has not been proven. KFD is generally diagnosed on the basis of an excisional biopsy of affected lymph nodes. Its recognition is crucial especially because this disease can be mistaken for systemic lupus erythematosus, malignant lymphoma or even, though rarely, for adenocarcinoma. Clinicians' and pathologists' awareness of this disorder may help prevent misdiagnosis and inappropriate treatment. The diagnosis of KFD merits active consideration in any nodal biopsy showing fragmentation, necrosis and karyorrhexis, especially in young individuals presenting with posterior cervical lymphadenopathy. Treatment is symptomatic (analgesics-antipyretics, non-steroidal anti-inflammatory drugs and, rarely, corticosteroids). Spontaneous recovery occurs in 1 to 4 months. Patients with Kikuchi-Fujimoto disease should be followed-up for several years to survey the possibility of the development of systemic lupus erythematosus.
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PMID:Kikuchi-Fujimoto disease. 1672 18

The spectrum of diseases found in series of fever of unknown origin shows variation in relation to selection bias; particularly, selection of the most difficult cases in tertiary reference university centres. We present a series of 144 patients presenting to a non-university hospital between 1999 and 2005 (secondary level of the health care system) with a community-acquired fever of unknown origin. In 37 cases (25.7%), the reason for fever could not be explained. Among the 107 patients with a final diagnosis (74.3%), non-infectious inflammatory disorders represented the most prevalent category (35.5%), surpassing infections (30.8%), miscellaneous causes (20.6%) and malignancies (13.5%). 13 entities accounted for over 68% of diagnoses (sinusitis and occult dental infections, Q fever, Epstein-Barr virus and cytomegalovirus infections, lymphoma, colo-rectal adenocarcinoma, adult-onset Still disease, systemic lupus erythematosus, giant cell arteritis and/or polymyalgia rheumatica, rheumatoid arthritis, polyarteritis nodosa, factitious fever and habitual hyperthermia). As demonstrated in other studies, non-infectious inflammatory diseases emerge as the most prevalent diagnostic category. Giant cell arteritis and polymyalgia rheumatica were particularly frequent in the elderly. Epstein-Barr virus and cytomegalovirus infections and habitual hyperthermia were particularly frequent in the youngest patients. There were no major differences in repartition of diagnostic categories between this series and historical university series.
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PMID:Fever of unknown origin in adults: evaluation of 144 cases in a non-university hospital. 1757 41

A 49-year-old man was urgently admitted due to edema in both leg and left toe pain. A chest radiograph revealed a solitary nodule in the right lung field. Detailed investigations including bronchoscopy and renal biopsy led to a simultaneous diagnosis of clinical stage IIIB pulmonary adenocarcinoma, minimal change nephrotic syndrome, antiphospholipid syndrome, and warm-type autoimmune hemolytic anemia. Prednisolone was administered for nephrotic syndrome, antiphospholipid syndrome and warm-type autoimmune hemolytic anemia, and 6 courses of chemotherapy with 70Gy radio-therapy were performed. The pulmonary nodule significantly decreased in size and the other three autoimmune diseases appeared to be well-controlled. Thirteen months after admission, multiple brain metastases developed along with worsening antiphospholipid syndrome symptoms including lupus anticoagulant. Following whole-brain irradiation, the brain metastases decreased in size and antiphospholipid syndrome symptoms improved. Thirty-nine months after the initial visit, the primary lung cancer, its brain metastasis and the 3 other autoimmune diseases appeared to be well-controlled. The temporal correlation of the lung cancer and the three autoimmune diseases suggests the latter may be paraneoplastic syndrome.
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PMID:[A case of pulmonary adenocarcinoma accompanied by minimal change nephrotic syndrome, antiphospholipid syndrome and warm-type autoimmune hemolytic anemia]. 1703 7

Defective CD3zeta chain expression has been reported in T lymphocytes of patients with inflammatory diseases, such as systemic lupus erythematosus or osteoarthritis, and with cancer. In lupus, the absent CD3zeta chain is replaced by the FcRgamma chain, rendering the T cells hyper responsive. However, there are no data on T lymphocytes from patients with cancer. In this study, the presence of the FcRgamma chain and its associated kinase, Syk, was analysed in patients with gastric adenocarcinoma and healthy subjects. Western blot and immunoprecipitation experiments were carried out with total cell or lipid raft extracts from fresh peripheral blood mononuclear cells or T lymphocytes, and Herpesvirus saimiri-derived T-cell lines (of blood or tissue origin). Our results revealed that the absent CD3zeta chain in cancer T lymphocytes was not replaced by FcRgamma either in fresh T cells or T-cell lines, in contrast to lupus T cells. This altered expression of signalling molecules in T lymphocytes of cancer patients, would explain their low proliferative capacity. Our T-cell lines represent tools to unveil the signalling abnormalities of cancer T lymphocytes.
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PMID:FcRgamma chain does not replace CD3zeta chain in CD3zeta-deficient T lymphocytes of patients with gastric adenocarcinoma. 1713 55

Hereditary activated protein C resistance (aPCR) has been identified as an important risk factor for the occurrence of thromboembolic events. It is most frequently hereditary, and caused by a point mutation in factor V, named Factor V Leiden (FVL), which renders it resistant to the anticoagulant action of circulating protein C. However, aPCR can also be found in absence of FVL (acquired aPCR), associated to lupus anticoagulant, pregnancy or neoplasms. We report a case of deep venous thrombosis (DVT) in a 54 year-old woman, with no digestive symptoms and negative screening for biochemical tumor markers, who presented with DVT from FVL-negative aPCR, one year before being diagnosed of colonic adenocarcinoma. Once complete remission of the carcinoma was reached, aPCR returned to normal values. In thrombophilia screening studies, the finding of aPCR may be caused by acute-phase reactants or neoplastic processes, and therefore require evolutive evaluation and genetic search for FVL.
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PMID:[Hypercoagulable state due to acquired protein C resistance, harbinger of colonic neoplasm?]. 1737 Nov 49

There is a high incidence of thrombosis in cancer patients. Retrospective studies indicate that lupus anticoagulant (LA) antibodies can be a thrombosis risk factor in cancer. In 77 patients with different forms of cancer LA and thrombosis incidence were retrospectively evaluated. In a prospective study, with 42 lung adenocarcinoma patients, we measured plasma LA, fibrinogen, factor VIII (FVIII), and thrombosis incidence. A high frequency of LA and thrombosis were observed in both studies. In isolation LA, increased levels of FVIII and fibrinogen could not be considered good markers for the development of thrombosis.
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PMID:Lupus anticoagulant activity as a thrombosis risk factor in lung adenocarcinoma patients. 1780 32

In the present study, we determined from a single-center data the treatment continuation, discontinuation and reasons for discontinuation in the patients with active rheumatoid arthritis (RA) or spondyloarthropathies (SpA) who were treated with etanercept or adalimumab. All RA and SpA patients, who were treated with etanercept (n = 53) or adalimumab (n = 43) as their first biological treatment according to national guidelines in the Center for Rheumatic Diseases, Tampere University Hospital during the years 1999-2005, were analyzed at baseline and after 1-year treatment. The treatment was regarded ineffective if the clinical response was lower than ACR50 in RA or the reduction of BASDAI was lower than 50% or 2 cm in SpA. After 1 year, the continuation rate was 74% with etanercept and 60% with adalimumab. Mean prednisolone dose among continuers was diminished by 52% in etanercept-treated patients and by 44% in adalimumab-treated patients. During 1-year follow-up, 14 (26%) of the etanercept-treated patients and 17 (40%) of the adalimumab-treated patients discontinued the medication. Eleven patients were regarded as poor responders, seven in etanercept group and four in adalimumab group. Adverse events (mainly infections and injection reactions) caused six discontinuations in etanercept-treated group and 11 discontinuations in adalimumab-treated group. Etanercept was discontinued due to other adverse event in two patients: in one patient due to adenocarcinoma of ovary and in one patient due to drug-related leukopenia. One patient treated with adalimumab developed clinical and immunological features of systemic lupus erythematosus (SLE). In the present study, etanercept and adalimumab treatments were started in patients who had active RA or SpA despite ongoing treatment with combinations of traditional disease modifying antirheumatic drugs (DMARDs). Thirty-nine (74%) patients and twenty-six (60%) patients achieved at least 50% response when etanercept or adalimumab was added to their earlier DMARD treatment. Adverse events (mainly infections and injection reactions) were in line with previous reports. Three rare adverse events were reported: one patient with ovarial carcinoma, one with leukopenia and one with features of drug-induced SLE.
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PMID:Etanercept and adalimumab treatment in patients with rheumatoid arthritis and spondyloarthropathies in clinical practice: adverse events and other reasons leading to discontinuation of the treatment. 1784 78

Kikuchi-Fujimoto disease is characterized by fever and lymphadenopathy, usually localized in the cervical region. This disease principally affects young females. It can be confused with lymphoma, adenocarcinoma metastasis and tuberculosis. We report two cases of Kikuchi-Fujimoto disease. In the first case, a 28-year-old female had been treated for tuberculosis one year prior and presented with a clinical and histological profile compatible with Kikuchi-Fujimoto disease. The second patient, a 58-year-old female, initially received treatment for Wegener's granulomatosis and, subsequently, for tuberculosis. Histopathological examination followed by immunohistochemical analysis confirmed the diagnosis of Kikuchi-Fujimoto disease in both cases. After the definitive diagnosis had been made, both patients were treated symptomatically, and both presented clinical improvement within one month. Subsequently, the latter patient developed systemic lupus erythematosus.
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PMID:Kikuchi-Fujimoto disease. 1918 Mar 44

A 14 year-old Bangladeshi girl presented with high fever, painful swellings in the neck, anorexia, weight loss and night sweating. On examination she had multiple enlarged and tender cervical lymph nodes. Other systems were normal. Laboratory investigations for sepsis and autoimmune diseases were negative. Initial fine needle aspiration and cytology of affected lymph node was suggestive of tubercular lymphdenitis. But she did not respond to anti-tubercular treatment. Kikuchi-Fujimoto disease was diagnosed from the histopathological appearance of excised lymph node. She completely recovered with symptomatic treatment. Kikuchi-Fujimoto disease, also called Kikuchi's disease or histiocytic necrotizing lymphadenitis is a rare, benign but enigmatic disease of unknown aetiology. The disease is self-limited and has an excellent prognosis. Its recognition is crucial because it can be mistaken for systemic lupus erythematosus, malignant lymphoma, tubercular lymphadenitis or even, for metastatic adenocarcinoma. Clinicians' and pathologists' awareness of this disease may help prevent misdiagnosis and inappropriate treatment.
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PMID:Kikuchi-Fujimoto disease. 1918 59

Thrombosis is a frequent finding in cancer patients, being referred to as a poor prognostic factor. The mechanisms underlying the thrombophilic state in malignancy are not well elucidated but involve a complex interaction between tumor and host cells as well as the hemostatic system. A number of studies have demonstrated the presence of antiphospholipid antibodies (aPL) in cancer patients, suggesting a potential role in tumor-associated thrombosis. A prospective analysis has been performed in a group of lung adenocarcinoma patients in respect to the presence of aPL and thrombotic manifestations. Lupus anticoagulant (LAC) was identified in 61 out of 105 patients and it correlated highly with thrombosis (22/61, LAC positive vs 2/44, LAC negative RR=7.93; p<0.001). On the other hand, patients that displayed IgM anti-beta2-glycoprotein I (abeta2GPI) (22/80) showed an unexpected decrease in thrombosis risk (2/22, with IgM abeta2GPI vs 18/58, without IgM abeta2GPI RR=0.29; p=0.04). Considerations on the mechanisms that link cancer, thrombosis and aPL are discussed in this article.
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PMID:Lung adenocarcinoma and antiphospholipid antibodies. 1918 19


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