Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare SLE patient with central nervous system involvement (CNS-SLE) who relapsed presenting new symptoms associated with the development of serum anti-Sm antibody and was then successfully treated with cyclophosphamide (CY) pulse therapy is presented here. A 47-years old housewife was admitted to Kushiro City General Hospital because of fever, limb erythema and drowsy consciousness in September 1995. On the basis of convulsion, proteinuria, leukopenia, thrombopenia, serum positive tests for both anti-nuclear antibody and anti-SSA antibody and low complement levels, as well as elevations of IgG index and IL-6 in the cerebrospinal fluid (CSF), she was diagnosed as having CNS-SLE. Serum tests for anti CL-beta 2 GPI antibody and lupus anticoaglant was negative. Serum test for HBs antigen was positive. She was treated successfully with methylprednisolone (mPSL) pulse therapy and plasma exchange (PE). Prednisolone was gradually tapered to the dosage of 17.5 mg per day and she was discharged in April 1996. She was re-admitted because of fever, an exacerbation of skin eruption and arthralgia in October 1996. Serum anti-Sm antibody was found to be positive. mPSL pulse therapy was not effective. On the basis of hallucination and elevations of IgG index and IL-6 in the CSF, a diagnosis of relapsed CNS-SLE was made. However the level of IFN-alpha in the CSF was normal. Although PE was not effective, CY pulse therapy was markedly effective.
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PMID:[A recovered case of SLE with central nervous system involvement who relapsed presenting new symptoms associated with development of serum anti-Sm antibody]. 956 77

A 20-year-old woman with arthralgia, serositis, thrombocytopenia, proteinuria, muscle weakness, elevated creatinine kinase, and positive anti-Sm antibody was diagnosed as having polymyositis and systemic lupus erythematosus (SLE). She had persistent high temperature, sinus tachycardia, hyperhidrosis, mydriasis, visual disturbance, hallucination, and loss of consciousness. Levels of plasma adrenaline, noradrenaline, and dopamine and cerebrospinal fluid interleukin (IL)-6 and IL-8 were all high. A diagnosis of sympathetic hyperfunction accompanied by central nervous system (CNS) involvement in SLE was made parenteral. Pulse administration of high dose corticosteroid therapy was effective. This is the first reported case of a connective tissue disease with CNS involvement manifesting as sympathetic hyperfunction with high plasma catecholamine levels.
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PMID:Acute sympathetic hyperfunction in overlapping syndromes of systemic lupus erythematosus and polymyositis. 971 13

Anti-glomerular basement membrane (anti-GBM) antibody disease is a rare type of small-vessel vasculitis. Posterior reversible encephalopathy syndrome (PRES) is a syndrome of heterogeneous aetiologies grouped together based on similar neuroimaging findings. We report a rare case of a patient who received treatment for anti-GBM antibody disease who developed PRES. A 33-year-old woman presented with severe generalised oedema, proteinuria, haematuria, and cylindruria. She was diagnosed with anti-GBM antibody disease based on positive findings for anti-GBM antibodies and urinalysis. Haemodialysis was eventually required. She received steroid therapy, plasma exchange therapy, and intravenous cyclophosphamide, along with a red blood cell transfusion for progressive anaemia. After the transfusion, she experienced nausea, severe headache, visual hallucinations, and agitation followed by seizures and a rapid increase in blood pressure. Imaging studies led to a diagnosis of PRES. Renal failure improved with the decrease in anti-GBM antibodies, and haemodialysis was discontinued. Phenytoin was administered, and seizures disappeared. Although we cannot rule out the possibility that the treatment this patient underwent for anti-GBM antibody disease led to the development of PRES, we speculate that endothelial dysfunction leading to the development of PRES is caused not only by known risk factors such as cytotoxic agents, blood transfusions, or renal failure, but also by immunological abnormalities and subsequent inflammatory reactions due to anti-GBM antibody disease. These factors may be shared pathophysiologic mechanisms of PRES and anti-GBM antibody disease.
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PMID:Anti-glomerular basement membrane antibody disease complicated by posterior reversible encephalopathy syndrome. 3286 22