Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper we searched for vertebral deformities in a group of 70 premenopausal systemic lupus erythematosus (SLE) patients (31.8 +/- 8.1 years old) and compared them to a matched control group of 22 healthy women (32.0 +/- 8.9 years old). Patients and controls performed spine X-ray (XR) morphometry and lumbar spine and femoral neck bone mineral density (BMD). Clinical data was obtained by a questionnaire and charts review. Thoracic or lumbar spine fracture was observed in 15 (21.4%) SLE patients, while no deformities were found in the control group (P = 0.018). BMD was not different amongst SLE patients and controls and between SLE patients with or without deformities. Although BMD could not predict what patient have deformity, seven patients (46.6%) with deformity had a lumbar spine or femoral neck Z-score less than - 1 SD [median = -0.59 (-3.72 to +0.88) and -0.20 (-4.05 to + 1.87)] respectively. In addition, we found a negative correlation between number of fracture per patient and lumbar spine and femoral neck BMD (R = 0.58, P = 0.04 and R = 0.84, P = <0.0001 respectively). No significant correlation was found between number of deformities and clinical data. This is the first study to search for vertebral deformities in SLE patients and to demonstrate a high prevalence of deformities in a relative young SLE population. These findings bring up the necessity to look for spine deformities in this group of women regardless the BMD.
Lupus 2005
PMID:High prevalence of vertebral deformity in premenopausal systemic lupus erythematosus patients. 1613 May 9

Acquired hemophilia is a rare coagulopathy in adults, associated with bleeding complications. Although the etiology of this disorder remains obscure, an autoimmune mechanism produces the development of autoantibodies against factor VIII. About half of cases are associated with other conditions, mainly post-partum, underlying cancer, autoimmune disease. An 81-year-old male was admitted to the hospital with extensive hematomas (neck, chest, arms and lower limbs). There was no family or personal history of congenital bleeding diathesis. He had chronic bronchitis and cerebrovascular disease; no drugs had been used during the month prior to noted symptoms. Laboratory parameters revealed: hemoglobin 10.9 g%, normal platelet count and white blood cells, prolonged activated partial thromboplastin time (98 s), with normal prothrombin time and fibrinogen concentration. An activated partial thromboplastin time mixing study did not show any correction, suggesting a coagulation inhibitor. Lupus anticoagulant and anticardiolipin antibodies were negative. Biochemical, immunological tests and tumor markers were normal. Thoracic and abdominal computed tomographic scan did not reveal pathological images or hematomas. Analysis of clotting factors revealed decreased factor VIII (< 2%) and elevated factor VIII inhibitor (55 Bethesda units). Idiopathic acquired hemophilia diagnosis was made. Red blood cell transfusion and human factor VIII (2000 U/day for 7 days) infusion were initiated, intravenously with methylprednisolone. A progressive improvement in clinical conditions and laboratory parameters was observed. After 18 days the patient was discharged and treated with prednisone. At follow-up control the clinical conditions and laboratory parameters were normal.
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PMID:[Acquired factor VIII hemophilia in a geriatric patient]. 1625 Jan 80

Patients with systemic lupus erythematosus (SLE) have an impairment in phenotype and function of endothelial progenitor cells (EPCs) which is mediated by interferon alpha (IFN-alpha). We assessed whether murine lupus models also exhibit vasculogenesis abnormalities and their potential association with endothelial dysfunction. Phenotype and function of EPCs and type I IFN gene signatures in EPC compartments were assessed in female New Zealand Black/New Zealand White F(1) (NZB/W), B6.MRL-Fas(lpr)/J (B6/lpr) and control mice. Thoracic aorta endothelial and smooth muscle function were measured in response to acetylcholine or sodium nitropruside, respectively. NZB/W mice displayed reduced numbers, increased apoptosis and impaired function of EPCs. These abnormalities correlated with significant decreases in endothelium-dependent vasomotor responses and with increased type I IFN signatures in EPC compartments. In contrast, B6/lpr mice showed improvement in endothelium-dependent and endothelial-independent responses, no abnormalities in EPC phenotype or function and downregulation of type I IFN signatures in EPC compartments. These results indicate that NZB/W mice represent a good model to study the mechanisms leading to endothelial dysfunction and abnormal vasculogenesis in lupus. These results further support the hypothesis that type I IFNs may play an important role in premature vascular damage and, potentially, atherosclerosis development in SLE.
Lupus 2010 Mar
PMID:Lupus-prone New Zealand Black/New Zealand White F1 mice display endothelial dysfunction and abnormal phenotype and function of endothelial progenitor cells. 2006 18