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 clinical consequences (therapeutic and toxic) of drug acetylation polymorphism are reviewed for procainamide, hydralazine, phenelzine, isoniazid, and salicylazosulfapyridine. Genetic slow acetylators are more likely than rapid acetylators to experience the following adverse drug reactions: (1) earlier development of procainamide-induced antinuclear antibody; (2) earlier and more frequent development of procainamide-induced systemic lupus erythematosus (SLE); (3) hydralazine-induced SLE; (4) spontaneous SLE; (5) drowsiness and nausea from phenelzine; (6) cyanosis, hemolysis, and transient reticulocytosis from salicylazosulfapyridine; and (7) polyneuropathy after isoniazid therapy. The incidence of isoniazid hepatitis may, however, be more common in rapid than than in slow acetylators. Genetic slow acetylators are also more likely than rapid acetylators to experience greater therapeutic responses from similar doses of the following: phenelzine, hydralazine provided beta blockers are concurrently used, and isoniazid if once weekly therapy is used. Thus, knowledge of the acetylator phenotype of a patient can help determine the relative risk for some drug-related toxic and therapeutic responses.
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PMID:Clinical consequences of polymorphic acetylation of basic drugs. 1 87

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

In a warm desertic and irrigated region, with population 250 000 Northwest of Mexico, in Hermosillo, Sonora, along 8 weeks, 51 patients showed the following clinical data: fever, vomiting, neck rigidity, drowsiness and increase of cells and proteins in the CSF. In 12 patients good correlations were found between positive serologic results using SLE antigen by means of HI, CF and NT. Four paired sera showed fourfold increases in titers to SLE by means of HI or CF. With VEE antigen no such increases were found. The cases were scattered geographically, most of them occurred within an urban area, and affected people in 13 localities. The outbreak developed from August to September, 1974, the attack rate was 22/100 000, 69% of the patients being children under 15 years of age. The case fatality rate was 20%. A prosperous chicken industry existed in the region and epizootics were not reported in either domestic or wild animals at that time.
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PMID:[Saint Louis encephalomyelitis in Hermosillo, Sonora, Mexico. Its epidemiology]. 61 46

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

A 17-year-old female with a 5-year history of disseminated lupus erythematosus has remained without immunosuppressive therapy for the last 3 years. She was admitted to the hospital for acute abdominal pain, generalized edema, and rapidly developing dyspnea and somnolence. Although all symptoms were consistent with active SLE, septicemia was suspected because of leukocytosis (20,000/microliters), greatly elevated C-reactive protein (45 mg/dl), and normal complement values (C3 0.74 g/l, C4 0.21 g/l). Directly after bacterial blood cultures were prepared, a combined treatment was instituted consisting of plasmapheresis (3 x 2.1 l against fresh frozen plasma), antibiotics, prednisolone, and cyclophosphamide following the last plasmapheresis. Within three days cerebral function returned to normal, edema improved, and CRP fell to 0.5 mg/dl. The blood cultures and pericardial effusion displayed meningococcal colonies.
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PMID:Successful therapy of meningococcal sepsis in acute disseminated lupus erythematosus with plasmapheresis, immunosuppression, and antibiotics. 223 29

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

Twenty three patients with SLE and cutaneous lesions not responsive to chloroquine, photoprotectors and corticosteroid in doses < 0.5 mg/kg/day were treated with thalidomide 300 mg/day. Three patients presented side effects and had to discontinue treatment. Eighteen of the remaining 20 patients (90%) had complete remission of the cutaneous lesions and 2 had partial improvement. Another important parameter of improvement was a reduction in the average prednisone dose required from 40.5 mg/day to 17.4 mg/day. The most frequent side effects were drowsiness in 52% of cases and abdominal distention in 22%. These symptoms were reversed by dose reductions in all but one patient. Thalidomide was shown to be efficient in the treatment of cutaneous lesions unresponsive to more usual treatments.
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PMID:Treatment of the cutaneous lesions of systemic lupus erythematosus with thalidomide. 827 83

A 30-year-old woman, diagnosed as having systemic lupus erythematosus at the age of 18, presented with excessive sleepiness and cataplectic attacks. Sleep laboratory findings were consistent with narcolepsy. To the best of our knowledge an association between these 2 diseases has never been reported. The unrelated course of narcolepsy and lupus symptoms in our patient suggests a lack of common pathogenetic mechanisms and this association is more likely explained by genetic factors.
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PMID:Narcolepsy in systemic lupus erythematosus. 847 79

Various diseases often occur after delivery but the systemic examinations have not been studied before. Thyroid dysfunction frequently (4.4%) occurs after delivery through an immune rebound mechanism. If postpartum women complain of the symptoms caused by thyrotoxicosis (palpitation, weight loss, increased sweating, finger tremor, fatigue) or hypothyroidism (edema, cold intolerance, hoarseness, sleepiness, fatigue), it is essential to examine thyroid hormones, thyroid stimulating hormone, anti-thyroid microsomal antibody (MCHA) and anti-TSH receptor antibody. To predict who will develop postpartum thyroid dysfunction, the measurement of MCHA during pregnancy is useful because 62% of the subjects with positive MCHA show thyroid dysfunction after delivery. The individuals at high risk of postpartum onset of Graves' thyrotoxicosis can be found early in their pregnancy by the detection of thyroid stimulating antibody (TSAb). Other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, autoimmune hypophysitis and so on, also could develop after delivery. These findings indicate that laboratory tests in the postpartum period are essential to diagnose postpartum onset of autoimmune diseases and the measurement of autoantibodies in early pregnancy is useful for prediction of their onset in the postpartum period.
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PMID:[Postgravid health care and laboratory tests]. 855 72

Phenobarbital (phenobarbitone) and phenytoin are the most useful anticonvulsants in neonates because adverse effects are most readily reversed when these drugs are used. Most anticonvulsants are very rarely associated with haematological adverse effects. Platelet function is particularly vulnerable to valproic acid (sodium valproate) therapy. Barbiturates and phenytoin can precipitate metabolic bone disease. Although very infrequent, lymphadenopathy is most common with phenytoin, and lupus-like illnesses with ethosuximide. Valproic acid may precipitate underlying metabolic disorders. Nephrolithiasis can occur with topiramate. Liver disease is most likely with felbamate or valproic acid, but can occur with other anticonvulsants. Valproic acid and ethosuximide are the main precipitants of gastrointestinal symptomatology; while valproic acid and vigabatrin are frequently associated with excessive bodyweight gain. Rash is most likely to occur with barbiturates, but there is a high risk of this adverse effect if large doses of lamotrigine are given with valproic acid. Adverse cosmetic effects are most likely with phenytoin, but valproic acid may cause alopecia. All anticonvulsants may cause unwanted neurological effects: when they occur, diplopia is usually precipitated by carbamazepine; tremor by valproic acid; and other motor disturbances are probably most common with phenytoin. Most anticonvulsants can cause drowsiness. Phenobarbital leads anticonvulsants as a cause of behavioural difficulties. Effects of anticonvulsants on cognitive function are difficult to assess, but subtle changes have been reported for all anticonvulsants in use up to the 1980s. Compared with other anticonvulsant drugs, phenytoin and felbamate are more often discontinued as a result of unwanted effects.
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PMID:A comparative review of the adverse effects of anticonvulsants in children with epilepsy. 896 93


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