Positive LE Cell Tests Research Articles

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  The incidence of Systemic Lupus Erythematosus (SLE) in Thailand is not well described. Here, we report the prevalence of a positive LE cell test and anti-dDNA latex agglutination test among a sample of Thai adolescents. Of 80 Thai young adolescent subjected to a positive LE cell test and anti-dDNA latex test was found one case having clinical presentations from mild to moderate symptoms, giving the prevalence equal of 1.25%.   Key words: SLE, Thai adolescent, prevalence

Drugs recently associated with lupus syndromes.

A number of drugs have recently been implicated in a syndrome that resembles systemic lupus erythematosus. One of the difficulties in many of these patients is that the signs, symptoms and serological abnormalities reported in these patients may be a natural consequence of the primary diseases rather than the incriminated drug. A second problem with the studies is a lack of uniform reporting of the techniques used to detect autoantibodies. For example, a patient that has a highly positive ANA with a homogeneous pattern of staining or a positive LE cell test usually has antibodies directed against chromatin components (DNA, histones, high mobility group (HMG) proteins). The discrepancies in clinical criteria and the serological techniques in many of these reports, emphasize the importance of using guidelines for the diagnosis of drug-induced or drug-related lupus. In the future, it appears that the increased use of biological response modifiers such as interferon-alpha and other cytokines may prompt more reports of lupus syndromes associated with their use.

Coexistent gout and systemic lupus erythematosus

We are unaware of any previous report concerning the coexistence of gout and systemic lupus erythematosus (SLE). Since gout is a relatively common disease affecting over 500,000 Americans (l), it seems likely that it would occur in some patients with SLE. In fact, on the basis of disease prevalence data (2), approximately 100 cases of coexistent gout and SLE might be expected in the United States (Table 1). This report documents the first known case of coexistent gout and SLE, and the various factors that may contribute to the lack of association between these diseases are discussed. Case Report. The patient was a 48-year-old white man who was first seen at the Ann Arbor Veterans Administration Medical Center in November 1979 with nephrotic syndrome. He had a 10-year history of intermittent arthralgia of the ankles, feet, hands, and elbows, a 15-year history of intermittent urticaria, a positive LE cell test, and hypocomplementemia. The patient had been treated with 5-10 mg prednisone per day for 5 years. In 1978 he developed hypertension, 10-pound weight gain, and proteinuria. The serum uric acid was 13 mg/100 ml. He was placed on diuretics and continued on low dose prednisone, but by 1979 severe peripheral edema and fatigue developed. The patient denied a history of Raynaud's phenomenon, mucosal ulcerations, alopecia, and photosensitivity. The physical examination was remarkable for a blood pressure of 215/105 and 4+ pitting edema up to the knees. Laboratory data included hemoglobin 1 1.3 gm/ 100 ml, hematocrit 3 1.7%, white blood count 5,300, platelets 220,000, BUN 25 mg/100 ml, creatinine 1.9 mg/100 ml, uric acid 11 mg/100 ml, creatinine clear-

Membranous lupus nephropathy: a clinicopathologic study.

Twenty-eight patients with SLE and distinct, well-defined renal morphologic lesions of membranous nephropathy were followed up for 4 years. These patients comprised approximately 8% of the patients evaluated for SLE during a 12-year period. The patients with membranous lupus nephropathy had typical systemic features of SLE, and most of them had positive LE cell tests and ANA, low serum complement concentrations, and mildly elevated serum antinative DNA levels. Proteniuria and microscopic hematuria were usually discovered years after systemic symptoms of SLE had developed, Only two patients had slowly progressive renal failure, and most patients continued to have proteinuria. Prednisone treatment did not influence either proteinuria or renal function. In only one patient, the renal character of the disease changed drastically, demonstrating membranoproliferative glomerulonephritis. Six patients died (21%); most of these died of cardiovascular illnesses. The relatively benign and stable renal course of membranous lupus nephropathy in patients with otherwise typical SLE suggests that the renal pathogenesis is different from that of proliferative lupus nephritis.

Transmission of autoimmune disease by thymus transplantation in mice

A previous study demonstrated the development of autoimmune disease in CBA/H-T 6 T 6 (CBA-T 6 ) mice following neonatal thymectomy and replacement grafting from newborn NZB X NZW F 1 hybrid mice, animals which spontaneously develop autoimmune renal disease. The grafted mice developed glomerular disease with additional immunopathological markers such as positive antiglobulin, LE cell and latex nucleoprotein tests. These animals died prematurely in renal failure with uraemia. To extend these findings, a series of similarly thymectomized and grafted mice was studied in an elective killing programme, the criterion for inclusion being apparent good health. The present report concerns the results of immunofluorescent testing for antinuclear antibody (ANA) in 101 male and 92 female mice. The overall prevalence of ANA was 51% in the male and relatively constant throughout life. In the female, the prevalence was 59% with maxima at 3 and 7 mth. The incidence of ANA in ungrafted CBA-T 6 mice was close to zero. Additional findings included an increased prevalence of positive antiglobulin tests and of nucleoprotein antibody. Body weight and blood urea did not differ from controls, as expected in such an elective killing programme. However, histological study showed early glomerular changes. These results support the view that autoimmune disease has been transmitted by thymus transplantation from an autoimmune to a normal inbred strain of mice.

C-type viruses in systemic lupus erythematosus.

VIRUSES have been implicated as the agents of systemic lupus erythematosus (SLE) expressed by dogs1 and mice2. We have shown that cell-free filtrates prepared from the spleens of dogs with positive LE cell tests induced anti-nuclear and anti-double-stranded DNA antibodies in CAF1 mice. The canine filtrate also induced lymphoid tumours in some recipient mice1. One of these neoplasms, SP 104, produces a monoclonal antibody against double-stranded DNA. Cultured SP 104 cells produce, in addition to the anti-DNA antibody, C-type RNA viruses that induce anti-nuclear antibodies when inoculated into normal mice (R.M.L., W.T., C.S., and R.S.S., unpublished). Here we present preliminary evidence linking the SP 104 virus to SLE in humans. Our results suggest that antigenic determinants related to the SP 104 virus are present on the lymphocytes of patients with SLE.

SLE Latex Test Kit

To the Editor.— In answer to the comment on our data concerning the Lederle Diagnostics Systemic Lupus Erythematosus (SLE) Latex Test Kit for detection of SLE by the latex agglutination slide method (225:637, 1973), Wolfe noted that only 38.8% of our 121 patients with SLE had positive LE cell tests compared with 70% in most series (226:357, 1973). All of these patients had documented SLE and met the American Rheumatism Association diagnostic criteria 1 ; we studied both treated and untreated patients which explains the lower incidence of positive LE cell tests. It helps to use patients with varying degrees of SLE activity in such an investigation, because the presence of classic LE cells is as diagnostically important as a strongly positive preparation. Furthermore, the 70% finding of LE cells in SLE is cumulative and refers to the total incidence of LE cells in a patient over the span of many

Clofibrate-Induced Antinuclear Factor and Lupus-like Syndrome

To the Editor.— Clofibrate is widely used for lowering the serum cholesterol level. The case reported here suggests strongly an association between the drug clofibrate and the development of a systemic lupus-like reaction with antinuclear factor. There is no similar case published previously, although an unpublished case limited to dermatitis with a positive LE cell test result in a patient taking clofibrate was reported to the Ayerst Laboratory. Several other drugs have been implicated in the induction of a lupuslike syndrome, commonly hydralazine, procaine, sulfonamides, and occasionally chlorpromazine, isoniazid, diphenylhydantoin, penicillin, tetracycline, quinidine, and penicillamine (references on request). This syndrome may be indistinguishable from idiopathic systemic lupus erythematosus with fever, arthritis, rash, polyserositis, hematologic abnormalities, and autoimmune reactions. Report of a Case.— A 66-year-old woman was seen from December 1972 through March 1973, with complaints of weight loss, anorexia, photophobia, malaise, arthralgias, and daily fevers to 38.3 C. Before the

Comparison of LE Cell Tests

To the Editor.— Lederle Diagnostics recently introduced the Systemic Lupus Erythematosus (SLE) Latex Test Kit for detection of SLE by the latex agglutination slide method. The reagent consists of polystyrene latex particles coated with deoxyribonucleoprotein (DNP) extracted from fetal calf thymus. The test is similar to the Test Kit 1 marketed by Hyland Laboratories in 1961. We compared the results of the Lederle test in 230 patients with various diseases with a rotary LE cell test 2 (performed in all cases), a rotatedwashed clot LE cell test 2 (in 171 cases), and an antinuclear antibody (ANA) determination, utilizing a leukocyte substrate 3 (in 132 cases). The latex test was quite specific as shown in the Table. No false positives were seen. Twenty-one of 121 known SLE patients with varying degrees of disease activity had positive latex tests; 16 of these 21 had positive rotary LE cell tests while three

Hereditary C2 Deficiency with Some Manifestations of Systemic Lupus Erythematosus

Summary A family with hereditary C2 deficiency was studied. The proposita, homozygous for this trait, showed certain clinical and serologic manifestations of systemic lupus erythematosus which included a widespread skin rash and a positive LE cell test.

Hepatitis, arthritis and lupus cell phenomena caused by methyldopa.

A patient is described who developed hepatocellular jaundice after methyldopa was administered. When the drug was again prescribed, hepatitis recurred. This exacerbation, along with transient arthritis, antinuclear antibodies and positive LE cell tests, document this as a case of hepatotoxicity due to methyldopa.

Chronic Active and Lupoid Hepatitis Caused by a Laxative, Oxyphenisatin

Abstract In six patients with chronic constipation, chronic active liver disease developed after one to two years of daily ingestion of laxative preparations containing oxyphenisatin; in a seventh liver disease occurred after ingestion of laxatives of unknown composition. Clinical features were jaundice, fatigue, firm hepatomegaly and, occasionally, spider angiomas and splenomegaly. Laboratory abnormalities included an increase in transaminase activity of 10 to 40 times, decreased prothrombin, depressed serum albumin and raised globulin. Two patients had positive LE-cell tests, two others had antinuclear antibody and three had smooth-muscle antibody; none had hepatitis-associated antigen. Liver biopsies showed areas of collapse and fibrosis, with stromal lymphocytic infiltrate and focal areas of hepatocytolysis. All patients improved after changing laxatives. Challenge with oxyphenisatin in three patients caused abrupt rises in transaminase activity. A toxic etiology should be considered, therefore, in al...

Canine systemic lupus erythematosus. Genetic analysis of an established breeding colony.

Three breeding lines, originating from dogs with SLE, have been established. Two lines were initiated by mating a female with SLE with a normal male. The third line resulted from a mating of two affected dogs. Brother-to-sister matings have reached the third generation in each line. In addition, backcross and outcross matings were carried out. More than one-third of the autopsied dogs had thymic abnormalities. The commonest lesion was a lymphoid follicle; the thymus of one dog contained multiple granulomas, and in one animal a reticulum cell sarcoma of the thymus was found. Multiple serological abnormalities, including positive LE cell tests, anti-nuclear antibodies (ANA), and rheumatoid factor, were found in the progeny. The development of ANA appeared unrelated to the incidence of positive LE cell tests. About 10% of the animals had rheumatoid factor in their serum. Control populations of dogs; including house pets; two other, unrelated lines of inbred dogs; and normal dogs housed in the same facility as the SLE colony did not have these abnormalities. The incidence of positive LE cell tests in the inbred, backcross, and outcross matings was not consistent with any conventional genetic mechanism of inheritance. It is conceivable that the results can be explained by vertical transmission of an infectious agent in a genetically susceptible individual.

Liver Pathophysiology: Its Revelance to Human Disease

Relating high serum levels of fetoglobulin to hepatoma, Australia antigen to serum hepatitis, and lithocholate to alcoholic hepatitis and cirrhosis, Dr. Davidson details recent concepts of the liver's responses to injury and disease. The test for fetoglobulin, he notes, facilitates curative resection of solitary hepatomas. Finding the Australia antigen identifies acute, and perhaps chronic, serum hepatitis. And reducing lithocholate formation and absorption, with antibiotics and cholestyramine, may benefit cirrhotic patients. Nor does Davidson slight the long-established tests for hepatic injury. He considers the cephalin flocculation and thymol turbidity tests valuable indicators of hepatocellular disease and discusses the autoimmune phenomena distinguishing primary biliary cirrhosis and chronic hepatitis. High concentrations of γ-globulin (where most antibodies reside), frequently positive LE cell tests, and antibodies to tissues including liver, denote altered immune mechanisms. However, he finds that suppressing the immune responses of patients with chronic hepatitis (with adrenal steroids, azathioprine, and mercaptopurine) is temporarily

Procainamide-induced serologic changes in asymptomatic patients.

AbstractSerologic findings in cardiac patients who had no manifestations of drug‐induced lupus and who had been taking procainamide for 6 weeks or more were compared to a similar group receiving quinidine, and a series of age‐ and sex‐matched controls. Significant changes occurred only in the group of 22 patients treated with procainamide (p < 0.01). LE cell tests were positive in 12 (55 per cent). Antidesoxyribonucleoprotein (anti‐DNP) tests were positive in 15 (68 per cent) and anti‐DNA in 8 (36 per cent). A positive LE cell test, anti‐DNP, or anti‐DNA reaction was found in 17 (77 per cent).

The coincidence of Klinefelter's syndrome and systemic lupus erythematosus.

AbstractThe clinical features of 3 patients with Klinefelter's syndrome who had manifestations of systemic lupus erythematosus are reported. Two of them, young men with XXY karyotype, developed fever, arthritis, proteinuria, and positive LE cell tests; one of the two also had pleurisy with effusion, and the other, treated intermittently with diphenylhydantoin, developed a hemolytic anemia. The third patient, also with XXY karyotype, developed the nephrotic syndrome and was found to have a proliferative glomerulonephritis and a positive antinuclear factor test. The possible relationship of these patients to the “autoimmune” phenomena observed in chromosomal aberrations is discussed.

Studies in myasthenia gravis: Part 2. The relation of some clinical and immunological data

The clinical and serological findings in 125 patients with myasthenia gravis are compared. The patients were classified according to their age, sex, type and gravity of their myasthenia and to the presence or absence of a thymoma. The sera of patients and matched controls were studied for the presence of antibodies against skeletal muscle, thymus, thyroid, gastric mucosa, adrenocortex and for the rheumatoid factor, the antinuclear factor and positive LE-cell test and immunoelectrophoretic aberrations. No definite relationship could be established between the clinical condition and the presence of antibodies. However all patients with thymomas had antibodies reacting with skeletal muscle and thymus. They also exceeded the patients without thymomas in the production of antinuclear factor. No influence on the frequency of serological abnormalities could be found according to sex or the duration of the disease; some antibodies and the total antibody production increased with age. Antibodies reacting with muscle were present in nearly 40% of the patients; antibodies reacting with epithelial cells of the thymus were demonstrated in 26%. One or more antibodies occurred in 68% of the patients in contrast to 19% of the controls. Although multiple antibody formation and some clinical traits place myasthenia gravis in the group of idiopathic autoimmune diseases, this provides no causal relationship with the observed defect of acetylcholine metabolism at the neuromuscular junction.

Immunopathologic studies of systemic lupus erythematosus (SLE). I. Tissue-bound immunoglobulins in relation to serum antinuclear immunoglobulins in systemic lupus and in chronic liver disease with LE cell factor.

We studied the composition of tissue-bound immunoglobulins and of antinuclear factors by immunofluorescent techniques in five patients with systemic lupus and two with chronic liver disease associated with positive LE cell tests. Renal glomeruli in all seven demonstrated deposits of bound gammaG-globulin and complement, although the presence of gammaA- and gammaM-immunoglobulins was variable. Blood vessel walls contained primarily gammaG-globulin and complement in the systemic lupus patients, but such deposits were absent from vessels in the two with chronic liver disease. We observed antinuclear factors, demonstrated by immunofluorescence, in all three immunoglobulin classes. In six of the seven patients, evidence was obtained of a correspondence between the classes of bound immunoglobulins in glomeruli and vessels and the serum titers of antinuclear immunoglobulins. These observations are consistent with the concept that immunoglobulin deposits in tissues may be derived at least in part from antinuclear factors. Neither bound immunoglobulins nor complement was observed in liver parenchyma of the two patients with chronic liver disease or in two patients with systemic lupus and liver pathology. It thus seems doubtful that serum antibodies play a primary role in the pathogenesis of forms of chronic liver disease associated with positive LE cell tests.

Lupoid Hepatitis.

s1 October 1964Lupoid Hepatitis.T. B. Reynolds, M.D., F.A.C.P., Hugh A. Edmondson, M.D., F.A.C.P.T. B. Reynolds, M.D., F.A.C.P.Search for more papers by this author, Hugh A. Edmondson, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-4-804_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn 13 patients with chronic liver disease and positive LE cell tests, liver disease was usually insidious in onset and often far advanced when first discovered. Twelve of the patients were women, seven of whom were over 50 years of age. Characteristic laboratory findings were those of chronic liver disease, that is, albumin/globulin reversal, prothrombin depression, and marked transaminase elevation during episodes of jaundice.During the earlier stages of the disease, liver biopsies showed active focal liver necrosis, diffuse intralobular round cell infiltration, and connective tissue and round cell increase in the portal triads. In the later stages a coarsely... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: T. B. Reynolds, M.D., F.A.C.P.; Hugh A. Edmondson, M.D., F.A.C.P.Affiliations: Los Angeles, Calif. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1964Volume 61, Issue 4Page: 804-804KeywordsBiopsyChronic liver diseaseConnective tissueConnective tissue diseasesHepatitisLiverLiver diseasesNecrosisNeutrophilsResearch laboratories ePublished: 1 December 2008 Issue Published: 1 October 1964 PDF downloadLoading ...