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)

The results obtained from the first 20 cases of Discoid Lupus Erithematosus treated with Thalidomide showed evidence of its great efficacy, evident from the first 15 days of treatment. In the incipient cases the results were even spectacular. 2. The minimum dosage used by the authors seems to be adequate on the basis of the results obtained. 3. The precise mode of action of thalidomide but it is thought that in acts on the hypothalamus. 4. The intolerance to Thalidomide and its undesireable side effects consisted slight somnolence; only one case had fever, cephalea, arthralgia, vertigo, nausea and urticaria which is unknown made it necessary to discontinue the medication. 5. The teratogenic effect of thalidomide obliges us to redouble the vigilance in women in age of reproduction by using of parenteral contraceptives applied by or in presence of the investigator. This study included one case that started treatment during the 7th month of pregnancy, without any problem and with an excellent result. The patient gave birth to a healthy full term infant. 6. It is recognized that this preliminary study should be continued with a greater number of cases and that these should be continued for a longer follow-up evaluation. At the present time, the authors believe that thalidomide is the best treatment for Discoid Lupus Erythematosus.
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PMID:[Fixed lupus erythematosus (its treatment with thalidomide)]. 36 11

A case of systemic lupus erythematosus (SLE) with benign intracranial hypertension (BIH) is reported. A 41-year-old male with a history of SLE starting in 1982 was admitted to our hospital in December 1989 because of headache and vertigo. Laboratory examinations on admission showed proteinuria, mild anemia, and positive antinuclear and anti-Sm antibodies. No abnormal findings except high pressure of 350 mmH2O were observed in his cerebrospinal fluid (CSF). Fundoscopic examinations showed marked bilateral papilledema and retinal bleeding. Brain CT, MRI and angiography revealed diffuse brain edema without space occupying lesion and cerebrovascular diseases. Because there were no diseases such as endocrinological disorders, severe anemia, and no history of the administration of drugs which might cause intracranial hypertension, the diagnosis of BIH was made. Subsequently, he was treated with intravenous methylprednisolone therapy and osmotic diuretics and his clinical symptoms and pressure of CSF gradually improved. The decrease of CSF adsorption was observed with RI cisternography in our case. Psychosis, seizures and meningitis are common CNS manifestations in SLE patients. But BIH is very rare and its cause is unclear. Only 17 cases of SLE with BIH have been reported. The pathogenesis and treatment of BIH in SLE patients were discussed in this paper.
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PMID:[Systemic lupus erythematosus associated with benign intracranial hypertension: a case report]. 160 19

A total of 60 patients with systemic lupus erythematosus (SLE) were under observation; 36 of them had clinical symptoms of the CNS affection and 25 persons included into the control group exhibited no psychic disorders during the clinical examination. Besides, routine clinico-laboratory examinations accepted in rheumatology, the patients were subjected to cranial computer tomography (CT), electroencephalography, examination of cerebral hemodynamics with a radionuclide partechnetate 99mC as well as to psychological testing. Neuropsychic disorders developed during the first four years after the onset of the disease and are grouped in the following way: neurological, border-line, neuropsychic, affective, psychotic, intellectual-mnestic. Moderate affection of the CNS in SLE is characterized by a complex of subjective and objective symptoms: headache, deterioration of memory, insomnia, vertigo, irritability, depressed mood, assymetry of the face innervation, coordinatory disorders. Diffuse widening of the subarchnoidal space, diffuse cerebral changes, interhemispheric assymetry of the venous and arterial phases of cerebral circulation: the most peculiar symptoms of the CNS affection in SLE according to CT and EEG and radionuclide studies of cerebral hemodynamics. Focal changes in the CNS were observed in 50% of the patients with neuropsychic disorders.
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PMID:[Diagnosis of lesions of the central nervous system in patients with systemic lupus erythematosus]. 166 90

The entity of generalized livedo racemose and cerebrovascular bleeding disorders was introduced in 1965 by I. B. Sneddon describing 5 cases. it is not clear what role oral contraceptives and smoking play in the etiology of this syndrome. The case of a 44-year old multipara is described who had taken pills up to 1980 and smoked 5-10 cigarettes a day. In 1980 just before age 35 she suffered an apoplectic insult with hemisyndrome on the left side that she recovered from. An acute hypoglossal, and trigeminal paresis appeared on the left side. Computer tomogram showed a hypodense field in the area of both hemispheres of the brain. An audible mesosystolic click led to the diagnosis of suspecting cerebral embolism with mitral valve prolapse. Therapy was started with thrombocyte aggregation inhibitors. Although the prolapse could not be showed by echocardiography, the frontal mitral valve was slightly thickened. Another hospitalization in 1985 owing to a recurring attack of vertigo revealed higher blood pressure. She received betablocker treatment. In 1987 sudden weakness in the left arm and speech disorders ensued, and skin color alterations were manifest characteristic of generalized racemose livedo. Skin necrosis appeared on both toes. Sneddon syndrome was diagnosed, and full anticoagulation therapy was started with cumarin. The sensomotoric and speech symptoms receded only slightly. In 1988 a light cerebral insult occurred with the deterioration of the speech disorder. Laboratory finding showed immunoglobulin G (IgG) anticardiolipin antibodies (ACA) with 255 U/ml (normal range 0-10 U/ml), and normal IgM anticardiolipin antibodies with 8 U.ml (range of 0-10 U.ml). ACA has been detected in patients with lupus erythematosus and racemose livedo indicating the possible association of Sneddon syndrome with systemic lupus erythematosus.
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PMID:[Sneddon syndrome]. 187 23

A 28 year old woman with systemic lupus erythematosus who developed chronic lupus peritonitis and ascites is described. Lupus peritonitis appeared with abdominal fullness, postprandial abdominal discomfort, and painless ascites. Four months later the patient developed vertigo, headaches, visual disturbances, serositis, and glomerulonephritis. Lupus peritonitis and the other disease manifestations responded to treatment with intravenous pulse methylprednisolone (four 1 g/m2 injections at one week intervals), oral azathioprine (200 mg daily), and diuretics.
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PMID:Chronic lupus peritonitis with ascites. 201 11

A rare case of systemic lupus erythematosus (SLE) associated with lateral medullary syndrome and unilateral internuclear ophthalmoplegia was reported. A 15 year old girl was admitted to Kyushu University hospital on 2 September in 1987 because of vertigo, occular symptom, and sensory disturbance. She had noted vertigo since 28 August. On admission she had nystagmus, left Horner syndrome, sensory disturbance of left hemiface and right limbs and trunk and mild hemiparesis of right limbs. She also had a discoid erythema behind the left ear, butterfly rash on her cheek. She developed right internuclear ophthalmoplegia on 6 September. Investigations revealed biological false positive of serological test for syphilis, positive antinuclear antibodies, and prolonged APTT. Peripheral blood cell count and erythrocyte sedimentation rate were normal. There was no proteinuria. Computed tomography and magnetic resonance imaging failed to detect any lesions in the brain. Cerebrospinal fluid cell count was 20/3 and Ig-G index was 17.1%. Her neurological signs were thought to be related to SLE. Lupus anticoagulant might be responsible for the development of impairment of central nervous system (CNS). She was treated with prednisolone, initial dose of 40mg, and the symptoms and signs were improved quickly. Early diagnosis and treatment for SLE with CNS involvement is primarily important.
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PMID:[A case of systemic lupus erythematosus associated with lateral medullary syndrome and unilateral internuclear ophthalmoplegia]. 250 Oct 49

The three best-described genetic polymorphisms of drug metabolism--the debrisoquin/sparteine type of oxidative polymorphism (hereafter referred to as the debrisoquin polymorphism), the polymorphism of N-acetylation, and the mephenytoin type of oxidative polymorphism--are reviewed. For all three polymorphisms, the poor-metabolizer phenotype is inherited as an autosomal recessive trait. The debrisoquin and mephenytoin oxidative polymorphisms involve defects in two separate cytochrome P450 enzymes. The prevalence of the poor-metabolizer phenotype for debrisoquin ranges between 2% and 10% for groups of various ethnic origins. The poor-metabolizer phenotype for mephenytoin comprises about 5% of the Caucasian population and about 20% of the Japanese population. N-acetyltransferase is a cytosolic enzyme whose clinical polymorphism was discovered using isoniazid as the substrate probe. The prevalence of the slow-acetylator phenotype among American and European Caucasian and American black groups is about 50%; among the Japanese it is about 10%. More than 20 agents are substrates for debrisoquin hydroxylase, about 15 for N-acetyltransferase, and 3-5 for mephenytoin. In poor metabolizers, debrisoquin can cause hypotension, and sparteine can cause blurred vision, headache, and dizziness. Clinical consequences of the slow-acetylator phenotype include increased susceptibility to systemic lupus erythematosus induced by procainamide and hydralazine, peripheral neuropathy induced by isoniazid, hydralazine, and dapsone, and sulfasalazine-induced dose-related leukopenia, nausea, vomiting, headache, and vertigo. After administration of mephenytoin, poor metabolizers have increased somnolence and intellectual impairment. Awareness of genetic polymorphisms of drug metabolism should improve understanding of interindividual variability in drug disposition and response.
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PMID:Polymorphic drug metabolism. 268 60

Thirty patients with SLE were studied retrospectively and subjected to clinical neurological examination. The accumulated neurological manifestations from the beginning of the disease until the time of examination were thus collected. Twenty-five patients (83%) had experienced neuropsychiatric manifestations while 11 patients (37%) had neuromuscular manifestations. The most frequent single symptom was migraine which had occurred in 40% of the patients. This was followed by severe protracted headache in 20%, vertigo in 20%, and psychiatric problems in 17%. Carpal tunnel syndrome and muscular weakness both occurring in 23% of the patients were the most prevalent neuromuscular manifestations, followed by myositis in 10%.
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PMID:Clinical neuropsychiatric and neuromuscular manifestations in systemic lupus erythematosus. 283 97

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

To determine the utility of magnetic resonance imaging (MRI) of the brain in diagnosing active neuropsychiatric disease in systemic lupus erythematosus (NP-SLE), a prospective study of 51 hospitalized systemic lupus erythematosus (SLE) patients during 64 separate episodes of suspected NP-SLE was initiated. In addition to standard hematology, chemistry, and serological tests, the workup included MRI in all patients. A computed tomographic scan of the brain was obtained in patients enrolled in the first year of the study. Of the 64 neuropsychiatric episodes, 42 were attributable to NP-SLE and 22 were attributed to causes other than SLE. Neuropsychiatric complaints unrelated to lupus included depression (n = 6), seizures (n = 5), headache (n = 3), altered mental status (n = 2), aseptic meningitis (n = 2), cardiovascular accident (n = 2), transient ischemic attack (n = 1), and vertigo (n = 1). The MRI was abnormal in 34 of 64 (53%) episodes. MRI abnormalities were more common in patients with focal neurological deficits (19/26) than in those without focal findings (15/38; P = .008) and in patients with nephritis (19/24) than in those without renal disease (15/40; P = .002). MRI abnormalities were as frequent in NP-SLE (25/42) as in cases with non-NP-SLE-related causes (9/22). Periventricular increased signal (PIS) was a frequent MRI finding (10/64). Enlargement of the prepontine cistern, an MRI finding not previously described in NP-SLE, was seen (14/64). Both findings were associated with the presence of hypertension and lupus nephritis. PIS similar to that seen in our patients has been described in otherwise healthy elderly individuals with risk factors for stroke, suggesting that vascular abnormalities may be important in the etiology of these lesions. In conclusion, abnormalities in brain MRI occur frequently in NP-SLE, especially in patients with focal neurological deficits. However, the presence of similar MRI abnormalities in SLE patients with neuropsychiatric symptoms and findings with non-SLE-related causes limits the specificity of the MRI for diagnosing NP-SLE.
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PMID:Magnetic resonance imaging of the brain in neuropsychiatric systemic lupus erythematosus. 851 97


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