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)

One hundred and fifty-four patients with erythema nodosum who attended the skin clinic at Ramathibodi Hospital from January 1990 to December 2000 were evaluated retrospectively with regard to the etiology of erythema nodosum. Of 49 patients who attended the skin clinic during that time 26 returned for reevaluation. Of the 154 patients, their ages ranged from 10-72 years old; 138 were females, 16 were males. The most common cause of erythema nodosum was tuberculosis (12.3%). Upper respiratory tract infection was found in 3.9 per cent. Other causes included Behcet's disease, sytemic lupus erythematous, drugs, pregnancy, chronic myeloid leukemia, leprosy, Reiter's syndrome and inflammatory bowel disease. Of the 26 patients who returned for reevaluation, pulmonary tuberculosis was identified in only one patient who had developed erythema nodosum 16 months earlier. In conclusion, it was found that tuberculosis is still a predominant cause of erythema nodosum among Thai patients.
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PMID:Long-term follow-up of erythema nodosum. 1497 15

Bloom syndrome (BS) is a rare autosomal genetic disorder characterized by lupus-like erythematous telangi-ectasias of the face, sun sensitivity, infertility, stunted growth, upper respiratory infection, and gastrointestinal infections commonly associated with decreased immuno-globulin levels. The syndrome is associated with immuno-deficiency of a generalized type, ranging from mild and essentially asympto-matic to severe. Chromosomal abnormalities are hallmarks of the disorder, and high frequencies of sister chromatid exchanges and quadriradial configurations in lymphocytes and fibroblasts are diagnostic features. BS is caused by mutations in BLM, a member of the RecQ helicase family. We determined whether BLM deficiency has any effects on cell growth and death in BLM-deficient cells and mice. BLM-deficient EB-virus-transformed cell lines from BS patients and embryonic fibroblasts from BLM-/- mice showed slower growth than wild-type cells. BLM-deficient cells showed abnormal p53 protein expression after irradiation. In BLM-/- mice, small body size, reduced number of fetal liver cells and increased cell death were observed. BLM deficiency causes the up-regulation of p53, double-strand break and apoptosis, which are likely observed in irradiated control cells. Slow cell growth and increased cell death may be one of the causes of the small body size associated with BS patients.
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PMID:Augmented cell death with Bloom syndrome helicase deficiency. 2156 87

A 40-year-old woman with antiphospholipid syndrome presented with a 5-day history of right upper quadrant (RUQ) pain, radiating posteriorly, associated with fever and vomiting. She was admitted 1-week prior with an upper respiratory infection and erythema multiforme. Clinical assessment revealed sepsis with RUQ tenderness and positive Murphy's sign. Laboratory results showed raised inflammatory markers, along with renal and liver impairment. CT showed bilateral adrenal infarction and inferior vena cava thrombus. The patient was managed for sepsis and started on heparin. Further immunological investigations revealed a diagnosis of systemic lupus erythematous, an exacerbation of which culminated in lupus myocarditis. This case illustrates the importance of promptly recognising adrenal insufficiency in patients with antiphospholipid syndrome and the possible causative agents, which require careful consideration and exclusion to prevent further thrombotic events. It also highlights the importance of undertaking imaging, namely CT, in patients with antiphospholipid syndrome presenting with abdominal pain as well as considering concomitant autoimmune conditions.
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PMID:Non-haemorrhagic, bilateral adrenal infarction in a patient with antiphospholipid syndrome along with lupus myocarditis. 2744 Aug 55