Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper reports a case of hemolytic anemia induced by procainamide hydrochloride treatment. Decreases in hemoglobin concentration are correlated with 11 months of procainamide treatment along with a marked increase in hemoglobin following cessation of the drug. The patient exhibited no symptoms suggestive of drug-induced Lupus Erythematosus that has been frequently reported as a sequela of procainamide therapy. Direct antiglobulin tests were consistently positive throughout the clinical course, and an ether-eluate prepared from the patient's red blood cells showed panagglutinability. The antibody in the eluate reacted with Rhnull, D--, LW negative, and U negative red blood cells without addition of procainamide or pretreatment of red blood cells with the drug. It is noted that this antibody reacts similarly to the antibody produced as a consequence of alpha-methyl-dopa therapy.
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PMID:Procainamide-induced hemolytic anemia. 41 35

A prospective study of systemic lupus erythematosus (SLE) patients under high doses of corticosteroid therapy (greater than 30 mg/day prednisolone) for a five-year period elucidated some risk factors of avascular necrosis of the femoral head (ANFH). A complete survey was performed on 62 patients, of whom nine patients developed ANFH during the period of study. The risk factors in the causation of ANFH were ascertained on the basis of characteristic clinical features of SLE, a typical pattern of laboratory data at the onset of ANFH, and the mode of glucocorticosteroid administration observed from a statistical point of view. The risk factors include stomatitis, drug-induced lupus, lupus erythematosus cell positive rheumatoid arthritis, interstitial pneumonitis, and thrombocytopenic purpura (characteristic clinical features); increased total cholesterol, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, alkaline phosphatase, red blood cell, hemoglobin, and albumin/globulin; advanced renal failure (pattern abnormality of laboratory data); and a rash introduction of high-dose corticosteroid therapy (greater than or equal to 30 mg/day prednisolone) without corticosteroid preloading (mode of administration).
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PMID:Risk factors of avascular necrosis of the femoral head in patients with systemic lupus erythematosus under high-dose corticosteroid therapy. 155 61

We examined weights and hematologic profiles of gray wolf (Canis lupus) pups and the associated wolf density in the east-central Superior National Forest of northeastern Minnesota (USA) during 1970 to 1988. We collected weight and hematologic data from 117 pups (57 females, 60 males) during 1 September to 22 November each year. The wolf density (wolves/800 km2) trend was divided into three phases: high (72 +/- 7), 1970 to 1975; medium (44 +/- 2), 1976 to 1983; and low (27 +/- 2), 1984 to 1988. Wolf numbers declined (P = 0.0001) 39 and 63% from 1970 to 1975 to 1976 to 1983 and from 1970 to 1975 to 1984 to 1988, respectively. Weight was similar between male and female pups and did not vary as wolf density changed. Mean hemoglobin (P = 0.04), red (P = 0.0001) and white blood cells (P = 0.002), mean corpuscular volume, mean corpuscular hemoglobin concentration and mean corpuscular hemoglobin (P = 0.0001) did differ among the multi-annual phases of changing wolf density. Weight and hematologic data also were compared to values from captive wolf pups. The high, but declining wolf density was associated with macrocytic, normochromic anemia in wolf pups, whereas the lowest density coincided with a hypochromic anemia. Although hematologic values show promise for assessing wolf pup condition and wolf population status, they must be used cautiously until data are available from other populations.
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PMID:Gray wolf density and its association with weights and hematology of pups from 1970 to 1988. 175 28

Hematologic reference values were determined for a captive population of 11 Mexican wolves (Canis lupus baileyi). Wolf pups from 4 to 24 weeks old had progressive age-related increases in PCV, hemoglobin concentration, mean cell volume, and RBC counts similar to those seen in domestic dog pups (C familiaris). Hematologic indices in wolves older than 24 weeks were comparable to those of the adult domestic dog; however, PCV, hemoglobin concentration, and RBC counts were higher.
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PMID:Hematologic values of captive Mexican wolves. 178 34

A prospective study was performed to investigate the outcome and complications of pregnancy in patients with systemic lupus erythematosus. Twenty-nine pregnancies occurred in 22 patients. There were 12 abortions, two spontaneous and 10 induced. Fifteen women had 17 live-born neonates. Neonatal complications included nine premature deliveries, two cases of intrauterine growth retardation, and one of Treacher Collins syndrome. Obstetric complications included threatened abortion (two), placenta previa (two), and preeclampsia (three). Cesarean sections were necessary in five patients. There was no maternal or neonatal mortality. Thirteen episodes of systemic lupus erythematosus relapses were detected by incidents of increasing proteinuria (six), arthritis (four), and vasculitic rash (two). There were no statistical differences in changes in hemoglobin level, erythrocyte sedimentation rate, albumin level, antinuclear antibody titer, or C3 or C4 level between the patients who relapsed and those who did not. Pregnancy could induce a flare of systemic lupus erythematosus in previously normal patients or patients with previously inactive disease. The overall neonatal and maternal survival was good, even in patients who presented during pregnancy. Spontaneous fetal loss was low (2/29 [6.9%]); both cases occurred in mothers with inactive lupus.
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PMID:Outcome of pregnancy in patients with systemic lupus erythematosus. A prospective study. 199 54

A number of lines of evidence suggest that the lupus-like symptoms associated with procainamide therapy may be caused by products of metabolic N-oxidation. In the present study, the perfusion of the isolated rat liver with a hemoglobin-free solution containing procainamide (100 microM) resulted in the rapid appearance of the N-oxidation metabolite procainamide hydroxylamine in the perfusate. Addition of procainamide hydroxylamine in vitro to whole rat blood (1-40 microM) resulted in a concentration-dependent loss of proliferative response among mononuclear cells isolated from the treated blood and cultured with mitogens (phytohemagglutinin, PHA-P: concanavalin A, Con A; and pokeweed mitogen, PWM), as well as a loss of viability. Similar effects on lymphocyte mitogen responsiveness were observed when procainamide hydroxylamine (1-40 microM) was added to rat whole splenic cell populations. Carbon monoxide or ascorbic acid pretreatment inhibited the toxicity of procainamide hydroxylamine to lymphocytes in whole blood, but only carbon monoxide pretreatment inhibited procainamide hydroxylamine-induced methemoglobin formation. These observations are consistent with the participation of hemoglobin in a redox cycle with procainamide hydroxylamine, generating products which are primarily responsible for its cytotoxicity in blood.
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PMID:Procainamide hydroxylamine lymphocyte toxicity--I. Evidence for participation by hemoglobin. 247 7

Evidence suggests that N-oxidized metabolites of procainamide may be responsible for the development of lupus-like symptoms associated with procainamide therapy. The human hepatic microsomal metabolism of procainamide has been previously reported to result in formation of the N-hydroxylamine derivative of procainamide (procainamide hydroxylamine [PAHA]). The objective of this study was to examine the effects of PAHA on human lymphocytes and adherent cells (monocytes and macrophages). When incubated with lymphocytes in whole blood, PAHA enhanced the response to mitogen and immunoglobulin secretion at lower concentrations (less than or equal to 4 mumol/L) but suppressed these functions at higher concentrations. The cytotoxic effects were nonselective for T lymphocytes and B lymphocytes and appeared to involve an interaction between PAHA and hemoglobin. When erythrocytes were removed or when hemoglobin was converted to carboxyhemoglobin, the suppressive effects of PAHA on lymphocytes were reduced. PAHA stimulated interleukin-1 production by adherent cells at 25 mumol/L but had no effect at lower concentrations. Superoxide anion release was unaffected by PAHA in "resting" adherent cells. Pretreatment with PAHA (2 mumol/L) diminished superoxide release in response to stimulation by phorbol myristate acetate (PMA) or latex bead phagocytosis but augmented superoxide release when coincubated with PMA or latex. These observations indicate that PAHA produces complex, concentration-dependent interactions with human immunoregulatory cells, and they suggest that the effects of PAHA on lymphocyte function may result from the further oxidation of PAHA by hemoglobin, perhaps to the nitroso form.
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PMID:Immunomodulatory effects of procainamide metabolites: their implications in drug-related lupus. 253 20

Serum samples (n = 137) from 47 wild wolves (Canis lupus; 21 pups and 26 adults) were evaluated from 1975 to 1985 for antibodies against canine parvovirus, using the hemagglutination inhibition (HI) test. In addition, several blood samples (n = 35) from 14 of these wolves (6 pups and 8 adults) were evaluated simultaneously for erythrocyte and leukocyte counts, and for hemoglobin and blood urea nitrogen concentrations. Sixty-nine (50%) of the serum samples (35 wolves) had HI titers of greater than or equal to 256, whereas 68 (50%) of the samples (16 wolves) had HI titers of less than or equal to 128. Significant differences in the geometric mean titers were not found between pups and adults or between males and females. Of the 47 wolves evaluated, 12 (25%) developed a greater than or equal to fourfold increase in antibody titers during the 11-year period, with 2 wolves developing serologic conversions in 1976. The data indicate that canine parvovirus may have begun infecting wolves before or at the same time that it began infecting the dog population in the United States.
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PMID:Antibodies against canine parvovirus in wolves of Minnesota: a serologic study from 1975 through 1985. 285 72

A lupus-like disease characterized by a severe immune complex glomerulonephritis and IgG autoantibody production was induced in (C57BL/6 X DBA/2)F1 mice by injection of parental DBA/2 lymphoid cells. The ensuing graft-vs-host (GVH) reaction resulted in a 10- and a 100-fold increase in serum IgG antibody levels to denatured DNA and total histones, respectively, compared with that in F1----F1 control mice. The level of anti-DNA antibodies peaked 2 wk after injection of DBA/2 cells and preceded peak anti-histone levels by approximately 2 wk. Anti-histone antibodies were generated predominantly to histones H1, H2A, and H2B, a profile different from that observed in NZB/NZW and MRL-lpr/lpr mice. The marked increase in IgG antinuclear antibodies did not correlate with increases in total IgG serum levels and was not associated with comparable increases in antibodies to transferrin, hemoglobin, fibrinogen, or thyroglobulin. Selective autoantibody production was also observed in vitro, wherein GVH spleen cells produced high levels of IgG antibodies to total histones and denatured DNA but not to these non-nuclear protein antigens. In contrast, spleen cells stimulated in vitro with lipopolysaccharide produced equivalent amounts of antibodies to all antigens tested. Our results are in agreement with those of other investigators and collectively suggest that IgG autoantibodies in GVH disease, and possibly in spontaneous lupus-like disease, are not secondary to a generalized B cell activation, but may be selectively generated in response to self antigens with unique configurational properties.
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PMID:Autoimmunization in murine graft-vs-host disease. I. Selective production of antibodies to histones and DNA. 387 58

We describe 12 patients with systemic lupus erythematosus (SLE) who developed massive pulmonary hemorrhage with very active disease. Other causes of pulmonary bleeding were excluded. Eleven of the 12 patients died, but only 4 had hemoptysis. Massive pulmonary hemorrhage should be suspected, even in the absence of hemoptysis, in severely ill patients with lupus who develop acute respiratory distress with bilateral pulmonary infiltrates and a drop in hemoglobin of 3 or more g/dl. Because of the deadly nature of this complication of SLE, when it is suspected, intensive corticosteroid and immunosuppressive treatment should be instituted.
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PMID:Fatal pulmonary hemorrhage in systemic lupus erythematosus. Occurrence without hemoptysis. 404 53


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