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.
Clin Pharmacol Ther 1977 Sep
PMID:Clinical consequences of polymorphic acetylation of basic drugs. 1 87

It is reported on course and problems of the diagnosis of a lupus erythematodes visceralis with epilepsy. In the demonstrated case the initial stage was characterized by the nearly simultaneous appearance of relapsing arthritides and epilepsy. The diagnosis was made in the stage of an acute exacerbation with cardiac symptomatology which began after the medicamentous treatment with diphenylhydantoin. Up to this moment an oligosymptomatic lupus erythematodes visceralis had not yet been diagnosed. Anamnestic data and the laboratory-clinical findings of the further course of the disease proved the actual lupus erythematodes visceralis. It is referred to the necessity of an aimed anamnesis and a determination of the antinuclear factors before every application ofhydantoin derivations when an epilepsy and joint symptomatology are present.
Z Gesamte Inn Med 1978 Sep 15
PMID:[The coincidence of visceral lupus erythematosus and epilepsy]. 3 Feb 20

The cases of 20 patients, each of whom has a positive lupus erythematosus cell preparation and a negative antinuclear factor test, are presented. The concept of a false-positive lupus erythematosus preparation is suggested. Five common mechanisms causing a false-negative antinuclear factor test are discussed and evaluated. Clinical material from the 20 patients is described and pitfalls in diagnosing systemic lupus erythematosus are reviewed.
Am J Clin Pathol 1976 Sep
PMID:Lupus erythematosus cell preparation-antinuclear factor incongruity. A review of diagnostic tests for systemic lupus erythematosus. 6 Aug 80

The literature concerning the laboratory procedures presently available to aid in the diagnosis of systemic lupus erythematosus (SLE) was reviewed to determine which of these techniques could be most valuable in the detection and management of SLE patients. The LE cell test, once the laboratory basis for SLE diagnosis, was concluded to be insensitive, non-specific, and did not correspond to clinical activity of the patient. A second procedure, antinuclear-antibody detection, although very sensitive, was not specific for SLE; therefore, its value is limited for use as a screening technique to rule out SLE. The Farr anti-DNA precipitate immunoassay, used for the measurement of antibodies to DNA, was sensitive and specific, and also correlated well with the clinical condition of the patient. Therefore, the Farr binding assay is recommended as the laboratory procedure of choice since it is useful in monitoring disease activity and may contribute to earlier diagnosis and more precise management of SLE patients.
Am J Med Technol 1977 Sep
PMID:Laboratory procedures used in the diagnosis of systemic lupus erythematosus: a review. 7 51

Circulating immune complexes have been detected in 100% of 59 patients with dermatitis herpetiformis (D.H.), and in 100% of 27 patients with coeliac disease (C.D.). Three methods for detecting immune complexes were employed: radiobioassay, which gave an incidence of 77% in D.H. and 81% in C.D.; C1q binding activity, with which the incidence was 83% and 96%, respectively; and precipitation with 4% polyethylene glycol (69% positivity in D.H., 100% in C.D.). The immune complexes in D.H. and C.D. were compared with those in sera from 23 patients with systemic lupus erythematosus (S.L.E.). Multiple complexes of differing properties were found in D.H. and C.D. but not in S.L.E. The varying nature of the complexes in D.H. and C.D. may account for the damage to different tissues (skin, small intestine, reticuloendothelial system). Low third component of complement was found in 49% and low C4 in 20% of D.H. patients. C3 hypocomplementaemia was found in 26% of patients with C.D.
Lancet 1976 Sep 04
PMID:Multiple immune complexes and hypocomplementaemia in dermatitis herpetiformis and coeliac disease. 7 60

Inhibition of prostaglandin synthesis at the prostaglandin synthetase and phospholipase steps could account for acute changes in renal function which are sometimes induced in patients with systemic lupus erythematosus (S.L.E.) by nonsteroidal anti-inflammatory drugs and high-dose corticosteriids, respectively. Renal function in S.L.E. patients seems to be more susceptible to inhibition of prostaglandin synthesis than in normal subjects. This susceptibility, in conjunction with increased urinary excretion of prostaglandin compounds, indicates that renal function in S.L.E. patients may depend on enhanced renal prostaglandin production for the maintenance of renal haemodynamics.
Lancet 1978 Sep 09
PMID:Renal prostaglandins in systemic lupus erythematosus. 7 20

In healthy subjects with normal renal function beta2-microglobulin (beta2m) is constantly produced in the body. It is eliminated almost exclusively by the kidneys, predominantly by glomerular filtration but possibly also by some direct uptake from the blood. After glomerular filtration more than 99,9% of excreted protein is reabsorbed in the kidney tubules where it is catabolized. The main factor, influencing on the serum level of beta2m is the GFR. Determination of S-beta2m appears to be more effective than analysis of S-creatinine for the detection of a slightly reduced GFR. A relatively high S-beta2m, in comparison with the GFR, may be seen in e.g. malignant proliferative disorders and SLE. This indicates an increased production of the protein. An entirely free passage over the glomerular membranes is not likely for beta2m in healthy subjects but the sieving coefficient might approach 1,0 in renal disease. The increased glomerular elimination of the protein could then possibly be counterbalanced by an increased synthesis, which should explain the pronounced relationship at a log/log scale between S-beta2m and the GFR. An increased excretion of beta2m in the urine is a sensitive indicator of proximal tubular dysfunction in many clinical conditions. In marked renal insufficiency there is, however, an obligatory 100-1 000-fold increase of the normal excretion, not related to the kind of renal disorder. In studies of the protein precautions are necessary to avoid degradation of the protein, in urine with a low pH.
Pathol Biol (Paris) 1978 Sep
PMID:The serum level and urinary excretion of beta2-microglobulin in health and renal disease. 8 68

Circulating antibodies against certain nuclear acidic protein antigens have been shown to have diagnostic and prognostic importance in connective tissue disease. We describe a new precipitin system found in the sera of patients with systemic lupus erythematosus. The antigen, called MA, was prepared from calf thymus nuclei, and was shown to be distinct from other nuclear acidic protein antigens by physicochemical and immunologic techniques. MA antibodies were detected in the serum of 12 of 66 lupus patients and in none of 554 sera from normal controls or patients with other rheumatic diseases. Lupus patients having MA antibodies had more severe disease than did lupus patients with Sm or native DNA antibodies, manifested by recalcitrant skin rashes and a significantly greater incidence of hypocomplementemia, serious renal disease, hypertension, hepatosplenomegaly, lymphadenopathy, and neurological disease (P values range from 0.025 to 0.005). The presence of circulating MA antigen was demonstrated in three lupus patients immediately before a flare of nephritis. These data suggest that MA is a nuclear acidic protein antigen that may identify a subset of lupus patients with very severe disease. The presence of the antigen in the circulation before clinical flares suggests a possible biologic role for the MA system in an immune complex nephritis.
J Clin Invest 1979 Sep
PMID:Characterization of a distinct nuclear acidic protein antigen (MA) and clinical findings in systemic lupus erythematosus patients with MA antibodies. 8 19

Monoclonal rheumatoid factors (MCRF) have previously been used in a variety of assays for the detection of IgG-containing circulating immune complexes. We have isolated a MCRF from a patient with a lymphoproliferative disorder and have used a nephelometric technique to characterize its reaction with heat-aggreagated gammaglobulin (HAGG) used as a source of artificial immune complexes. The method is simple, economical and rapid and will detect as little as 6 microgram/ml of HAGG over a wide range of physicochemical conditions. A clinical study demonstrated that the sera from thirty-five out of fifty-eight patients (59%) with rheumatoid arthritis and twenty-one out of seventy-four patients (28%) with systemic lupus erythematosus (SLE) gave increased precipitation with MCRF compared with 232 blood donors. However, in marked contrast to previous studies, sucrose gradient ultracentrifugal analysis of nine strongly precipitating sera revealed that in eight the MCRF precipitated with material sedimenting in the monomeric IgG position. In only one specimen did the MCRF react with material sedimenting in heavier regions. It is suggested that different MCRFs vary in the specificity for binding IgG complexes and these reagents should be carefully characterized before becoming established in nephelometric assays for circulating immune complexes.
Clin Exp Immunol 1979 Sep
PMID:A nephelometric study of the reaction of monoclonal rheumatoid factor with heat aggregated gamma globulin and sera from patients with immune complex diseases. 9 79

Acute lupus pneumonitis was the presenting manifestation of systemic lupus erythematosus in six of 12 cases in this series. The clinical picture was characterized by severe dyspnea, tachypnea, fever and arterial hypoxemia. Radiographic findings included an acinar filling pattern which was invariably found in the lower lobes and was bilateral in 10 of the cases. Studies failed to reveal evidence of infection as a cause of the acute pulmonary infiltrates. All patients were treated with oxygen and corticosteroids; seven received azathioprine. Six patients survived and are clinically well 14 months to four years following their acute illness. Three of these patients have residual interstitial infiltrates with persistent pulmonary function test abnormalities indicating progression to chronic interstitial pneumonitis. Histologic sections of the lungs available from four patients revealed hyaline membranes and interstitial edema (four cases), acute alveolitis (two cases), arteriolar thrombosis (one case) and a prominent lymphocytic interstitial pneumonitis with organizing bronchiolitis (one case).
Medicine (Baltimore) 1975 Sep
PMID:Pulmonary manifestations of systemic lupus erythematosus: review of twelve cases of acute lupus pneumonitis. 12 38


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