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

Prajmalium bitartrate (Neo-Gilurytmal) was given to 19 patients, who had either runs of ventricular extrasystoles or frequent extrasystoles. The E. C. G. was continuously monitored on magnetic tape. At a dosage of 80 mg/d (20 mg every six hours) a significant reduction in ventricular extrasystoles was demonstrated on 20 separate occasions. After two hours extrasystoles decreased to 63% of the initial level. After six hours practically the full effect of the drug had been reached; the reduction in extrasystoles stabilized after 12 hours at an average of 30% of initial level. Ten hours after the last tablet had been taken the frequency of extrasystoles had risen to 57% of initial level. Comparison with procaine amide (3 g/d) in 14 patients revealed no significant difference between the two drugs. Prajmalium bitartrate was well tolerated, while three patients receiving procaine amide complained of nausea and gastrointestinal symptoms, so that treatment had to be discontinued in two. In one patient, receiving procaine amide by continuous drip, there were reversible joint pains, resembling lupus erythematodes.
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PMID:[Effect of prajmalium bitartrate and procaine amide on ventricular extrasystoles (author's transl)]. 5 39

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

Migraine is a common condition with, usually, stereotyped symptomatology, suggesting that it is a specific disease entity (a morbus sui generis). However, occasionally a migraine sufferer will exhibit atypical manifestations of the condition; also, some specific diseases such as systemic lupus erythematosus and arteriovenous malformations, may exactly mimic the symptoms of migraine. These latter considerations raise the possibility that migraine is a syndrome rather than a disease. The recent delineation of the trigeminovascular system allows a conception of migraine as being neither disease nor syndrome, but rather a constitutional predisposition of the neurovascular system to react excessively to internal or external stimuli by a pattern of hyperactivity of the brain and of the trigeminovascular apparatus. Activation of the trigeminovascular system, whether by neural impulses from the brain or humoral factors in the circulation, results in vascular headaches, while associated activity in the brain may produce such typically migrainous symptomatology as prodrome and aura, and nonspecific symptoms such as nausea, vomiting and dizziness. In this model specific diseases may gain access to the trigeminovascular apparatus, detonating it to produce vascular headaches and neurological symptomatology which may more or less exactly mimic migraine.
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PMID:Migraine--disease or syndrome? 149 11

A case of systemic lupus erythematosus (SLE) with subarachnoid hemorrhage due to a ruptured intracranial aneurysm is reported. A 31-year-old woman who had been treated with steroid for SLE was admitted to our department with severe headache, and nausea. CT scan showed subarachnoid hemorrhage and the left carotid angiogram revealed a small aneurysm at the supraclinoid portion of the left internal carotid artery. She had no neurological deficit. Hematological examination on admission showed disseminated intravascular coagulation (DIC), therefore, we decided to perform an intentionally delayed operation. In the meantime we treated the patient for DIC with FOY and methylprednisolone. The operation was performed after two weeks, when DIC had been eliminated completely. Postoperative hematological examination showed severe thrombocytopenia. We considered that SLE had come to the fore again, so we used Danazol in company with FOY and steroid. It seemed that Danazol was very effective for her. She was discharged about two months after admission with no problem. Cerebral apoplexy, such as cerebral infarction and cerebral hemorrhage, has often been seen in SLE, but subarachnoid hemorrhage due to a ruptured aneurysm is very rare. We could find only five reports of this phenomenon. Their prognoses were all, unfortunately, poor. It should be born in mind for therapy that a patient in SLE has a tendency to bleed. It seems that repeated hematological examinations and quick and proper management are important. We think that the aneurysmal formation in SLE is due to lupus vasculitis or the fragility of blood vessels due to a long use of Steroid.
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PMID:[A case of systemic lupus erythematosus with subarachnoid hemorrhage due to ruptured aneurysm]. 220 86

A 25-year-old man, who was admitted for evaluation of arthralgia and fever of 2-weeks duration, complained of a 10 kg weight loss during the previous weeks. Systemic lupus erythematosus (SLE) was diagnosed on the basis of leukopenia, LE cells, antinuclear antibodies, antibodies to double-stranded DNA, and arthritis, Malabsorption was diagnosed because of the finding of hypoalbuminemia, fat droplets in the feces, a pathological D-xylose test, and an appropriate X-ray image. Approximately half the patients with SLE develop minor expressions of gastrointestinal tract involvement, such as nausea, vomiting, and diarrhea. Major manifestations, such as intestinal obstruction or perforation, ascites, peritonitis and pancreatitis have been reported with varying frequency. Despite the frequent association of SLE with gastrointestinal manifestations, malabsorption, as in this case, has rarely been reported.
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PMID:[Malabsorption in systemic lupus erythematosus]. 235 16

A patient with systemic lupus erythematosus presenting abdominal pain, nausea, vomiting and severe mucocutaneous vasculitis had significant elevation of serum amylase and hepatic enzymes levels during a flare-up of the disease. Clinical and laboratory alterations disappeared after therapeutic increase of corticosteroids given to the patient a fact that suggested etiologic correlation between systemic lupus erythematosus, hepatitis and pancreatitis.
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PMID:[Pancreatitis and hepatitis associated with systemic lupus erythematosus]. 248 88

Thirty patients suffering from systemic lupus erythematosus (SLE) were treated with daily 20 mgs of piroxicam (Hotemin). The patients were in a mildly active stage of the disease, taking maintenance doses of corticosteroids. The duration of piroxicam therapy was 3 months. Allergy was observed in one case, intolerance (gastrointestinal symptoms, nausea, vomiting) in two; these resulted in the cessation of therapy. Twenty seven patients were on piroxicam therapy for 3 months. Signs of clinical activity diminished, corticosteroid requirement decreased, subjective complaints were reduced. The drug was tolerated. In 3 cases, due to mild water retention, diuretics were given. Gastrointestinal symptoms, transaminase elevation, changes in blood cell counts were not observed during the 3 months period.
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PMID:Treatment of systemic lupus erythematosus (SLE) with piroxicam (Hotemin-Egis). 268 85

We describe a patient with systemic lupus erythematosus (SLE) and overlapping syndrome who had repeated gastrointestinal (GI) symptoms such as nausea, vomiting and malabsorption. With a subacute process, she developed paralytic ileus and contracted bladder, and died of perforation of the ileum. When 13 reported cases with lupus cystitis were reviewed, an extremely strong correlation between GI and urinary tract symptoms was observed, indicating the presence of a unique subgroup of SLE.
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PMID:Lupus cystitis and performation of the small bowel in a patient with systemic lupus erythematosus and overlapping syndrome. 268 79

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


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