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PubMed2002

Clinical and laboratory features of systemic lupus erythematosus (SLE) in Pakistani patients.

OBJECTIVES: To study the clinico-pathological features of systemic lupus erythematosus (SLE) in Pakistani patients at the time of presentation in the four teaching hospitals of Rawalpindi-Islamabad area. SETTINGS: Department of Immunology, Armed Forces Institute of Pathology (AFIP), Rawalpindi, Military Hospital (MH), Rawalpindi, Armed Forces Institute of Urology (AFIU), Rawalpindi, Combined Military Hospital (CMH), Rawalpindi, Department of Rheumatology, Pakistan Institute of Medical Sciences (PIMS), Islamabad. SUBJECTS: Patients suffering from SLE, diagnosed on the basis of the ARA criteria. MAIN OUTCOME MEASURES: Clinico-pathological features at the time of presentation. RESULTS: Twelve male patients in age range 5-30 years (mean 21.6 years) and 38 female patients in age range 8-37 years (mean 22.2 years) were included in the study, showing a female to male ratio of 3:1. Fever was the most common presenting feature (100%), followed by arthralgias/arthritis (98%), malar rash (64%) and oral ulcers (58%). Laboratory results showed antinuclear antibody to be positive in all patients followed by anti double stranded DNA antibodies (anti DNA antibodies: 64%), anti extractable nuclear antigen antibodies (anti ENA antibodies: 64%) and evidence of complement consumption in 64% of the patients. Erythrocyte Sedimentation Rate (ESR) was found to be increased with a mean of 64 mm first hour fall in males and a mean of 87 mm first hour fall in the female patients. The C reactive protein was detected to be normal or marginally increased inspite of the increased ESR with mean of 7 mg/l for male patients and 5 mg/1 for the females. CONCLUSION: The subject patient population presented almost universally with fever and arthralgias or arthritis in combination with malar rash or oral ulcers and in some patients a combination of all of the above was observed. A combination of positive anti nuclear antibody test, evidence for consumption of the complement in form of low C4 and C3, increased ESR and low C reactive protein were found to be a sensitive and cost effective set of laboratory findings for the diagnosis of patients suffering from SLE. The above mentioned set of clinical and laboratory features would help in the correct and early diagnosis of patients suffering from SLE, a relatively rare disease, in the busy medical out patient departments in our set up.

Adult↗

PubMed2002

[Lung involvement in systemic lupus erythematosus (SLE)--own experience].

Pulmonary disorders in systemic lupus erythematosus are frequent and sometimes they are the first symptoms of the disease. SLE may cause a variety of clinical presentations and pathologic patterns, which can be difficult to diagnose. We observed 11 patients (9 women and 2 men) with pulmonary manifestations of SLE during last 18 years in our department. Mean age of patients was 47.7 +/- 13.4 years. There were no patients with drug induced SLE. Interstitial lung diseases (7/11) acute or chronic and pleural involvement (5/11) were the most frequent clinical presentation. In three cases airway disease presented as reduction of FEV1%VC index was detected. In one case "shrinking lung" syndrome was confirmed by muscle function (diaphragm relaxation time) and lung function tests. Pulmonary hypertension confirmed by echocardiography, was associated with interstitial lung disease or vasculitis. Six cases representing different lung involvement pattern of SLE were described in details.

Adult↗

PubMed1992

[Prevalence of lupus anticoagulant, autoimmune hemolysis, thrombocytopenia and disorders of platelet function in unselected patients with SLE].

Prevalence of lupus anticoagulant (LA) in patients with systemic lupus erythematosus (SLE) and clinical manifestations vary widely between different clinical series. We investigated the relation between LA, autoimmune hemolytic anemia (AIHA), thrombocytopenia and platelet dysfunction in 80 unselected patients with SLE. AIHA was found in 6 patients (7.5%) and thrombocytopenia in 10 patients (12.5%), which was not related to platelet aggregation abnormalities. Compared to controls, patients with SLE showed significantly prolonged aPTT and kaolin clotting time (KCT), but platelet aggregation induced by both collagen and thrombin was not impaired. LA activity as defined by Rosner et al. (index for LA/ICA) was found in 15 patients (18.9%). Only 7 of these patients showed a positive platelet neutralization test (Triplett) and 9a positive tissue thromboplastin inhibition test (Schleider). In our SLE patients 23.7% have suffered from at least one thrombotic complication. In patients with LA activity thromboembolic complications were increased (p < 0.05). Thrombocytopenia was found in 6% of LA-negative but in 20% of LA-positive patients.

Abortion, Spontaneous↗

PubMed2005

Mapping autoimmune disease genes in humans: lessons from IBD and SLE.

The inflammatory bowel diseases (IBD) and systemic lupus erythematosus (SLE) are common autoimmune diseases that affect 2-3 million people in the USA alone. Crohn's disease (CD) and ulcerative colitis (UC), the inflammatory bowel diseases, are idiopathic, chronic inflammatory disorders of the gastrointestinal tract. SLE is a chronic, multi-system autoimmune disease that generally presents in women of childbearing age as fatigue, arthralgia and rash. Although the aetiology of these two diseases is not fully known, it is believed that genetic, hormonal and environmental influences contribute to susceptibility. Genomewide linkage scans in IBD have revealed significant loci that, upon comprehensive association mapping strategies, yield what are believed to be causal susceptibility alleles. Human linkage studies performed to date in SLE have not been as informative, although genetic mapping in mouse models of SLE as well as candidate gene approaches have provided important clues to the genetic susceptibility in humans. We will examine how some of the recent advances in our understanding of genetic variation in the human genome are greatly improving our ability to map autoimmune disease genes in humans.

Autoimmune Diseases↗

PubMedDate not supplied

[SLE: Extra-renal clinical manifestations and lupus nephritis].

Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease affecting multiple organ systems, skin and joints the most involved. Lupus Nephritis occurs in Approximately 50% of patients, sometimes it may be the first manifestation of SLE. Clinical features range from asymptomatic urinary abnormalities to full-blown nephrotic syndrome or rapidly progressive renal failure. Because of the heterogeneity of clinical renal manifestations, renal biopsy plays an important role in the management of patients with SLE: it provides information about the class, severity, activity and chronicity of the renal disease that cannot be accurately predicted on the basis of clinical parameters. The complexity of protean renal manifestation of SLE can be approached using the original WHO classification (1982), recently revised (2004).

Humans↗

PubMed1991

Major histocompatibility complex (MHC) complement deficiency, ancestral haplotypes and systemic lupus erythematosus (SLE): C4 deficiency explains some but not all of the influence of the MHC.

In 1982 we reported that among Caucasians with systemic lupus erythematosus (SLE) there is an increased frequency of C4A null. As this allele occurs on the HLA-A1,B8,BfS, C4AQO,B1,DR3 (8.1) supratype, we suggested this accounted for the reported association of B8 and DR3. Since then we have shown that many supratypes including 8.1 identify unique segments of DNA conserved from a common but remote ancestor. Many of these ancestral haplotypes (AH), including 8.1, carry disease genes and some bear C4 null. We have therefore tested the hypothesis that in SLE C4 null alleles are directly involved by examining (1) whether all or only some AH bearing C4 null alleles are increased, (2) whether C4 null is increased in all racial groups examined, and (3) whether C4 null is associated with the presence of antinuclear antibodies (ANA) in the absence of SLE. We performed HLA and complement allotyping on 62 Australian Caucasians and 9 Australian aborigines with SLE and on the 10 out of 133 healthy individuals with 7 or more international units of ANA. Our data confirm an association of C4A null in Australian Caucasians (gene frequency 0.30 versus 0.15 in controls) and show an increased frequency of C4B null in Australian aborigines (gene frequency 0.33 versus 0.22). A review of an extensive literature shows C4A and/or C4B null are increased in all racial groups examined. On the other hand, the HLA-A3,B7,BfS,C4A3,B1,DR2 (7.1) AH rather than C4 null is associated with ANA in health. Our data indicate that while C4 nulls contribute to MHC susceptibility, other genes are likely to be involved.

Alleles↗

PubMed1991

SLE in Zimbabwean patients: a review of clinical and serologic features and evaluation of criteria for classification.

The clinical and serologic features have been reviewed in a group of 18 black Zimbabwean patients with SLE, a rare condition in this racial group. The relative merits of the preliminary and revised criteria for the classification of the SLE have been assessed. The prevalence of individual clinical criteria was essentially similar in this group when compared to a larger North American cohort. Minor variations were attributable to racial and environmental differences. Serologic tests were identified. The revised criteria had greater sensitivity for SLE than the preliminary criteria although this was not the case if individual serologic items were omitted. Clinically, SLE is a uniform condition when our cases are compared with those in other areas. In areas where the technology does not exist to perform specific serologic testing, the preliminary criteria with their greater dependence on clinical features still have a useful role when compared to the revised criteria with their greater dependence on serologic testing.

Humans↗

PubMed1991

[Evaluation of the past history of chilblain in cases of systemic lupus erythematosus (SLE) and its similar diseases].

We sent out a questionnaire to 47 patients of SLE and its similar diseases as to their past histories of chilblain. The results of the patients were compared to those of 141 cases of control. Although the percentage of cases who had revealed chilblain frequently (40.0%) and the age of chilblain onset (mean: 10.8 years old) in SLE group were not significantly different from those of control (28.4% and 12.4 years old, respectively), the chilblain which SLE patients developed had some characteristics compared to that of control, (1) higher incidence of chilblain episodes, (2) longer duration until cure, (3) more liability that chilblain leads to erosion or ulceration and (4) frequent occurrence of chilblain in the other seasons than winter. Especially SLE patients with the characteristic of (4) had higher association rates of Raynaud's phenomena, chilblain LE and livedo, suggesting disorder of peripheral circulation. It was also revealed that females are generally more liable to develop chilblain than males (females: 40.0%, males: 13.1%). Those results suggest some important relationship between chilblain and LE lesions. It is supposed that chilblain with the characteristics described above may possibly be transformed into LE lesions.

Adolescent↗

PubMed1991

Mononuclear phagocyte system dysfunction in murine SLE: abnormal clearance kinetics precede clinical disease.

Although several studies have reported abnormal immune clearance in murine models of systemic lupus erythematosus (SLE), a consistent defect in mononuclear phagocyte function in SLE-prone mice has not been described. To evaluate the mechanism(s) of immune clearance in murine SLE, we applied the technique of kinetic analysis to clearance studies of radiolabeled, immunoglobulin-sensitized red blood cells in normal BALB/c and autoimmune BXSB, MRL-lpr/lpr, New Zealand black (NZB) and New Zealand black/white (NZB/W) mice. Clearance studies were performed in 4-week-old to 18-month-old mice with a complement-fixing rabbit IgG antimouse red blood cell antibody. Four clearance rate constants governing complement- and Fc-mediated clearance function were evaluated: complement-mediated sequestration (k1), C3b deactivation and release (k2), complement-dependent phagocytosis (k4), and Fc-mediated sequestration and phagocytosis (k3). BXSB male, MRL-lpr/lpr female and male, NZB female, and NZB/W female and male mice all had significantly decreased Fc-mediated clearance function (k3) when compared with control BALB/c mice (p less than 0.0001). This defect in Fc-mediated clearance was present in all four strains of autoimmune mice by 6 months of age and preceded the onset of serologic and clinical disease activity in NZB mice. Abnormal complement-mediated clearance was detected in MRL-lpr/lpr female and male mice, NZB female, and NZB/W female and male mice, but not in BXSB mice. In MRL-lpr/lpr mice decreased complement-mediated sequestration (k1, p less than 0.0001) and complement-dependent phagocytosis (k4, p less than 0.0001) were present as early as 4 weeks of age. In contrast, the change in complement-mediated clearance in NZB and NZB/W mice was characterized by decreased C3b deactivation and release (k2, p less than 0.001) and resulted in an enhanced early phase of clearance. Decreased k2 values in New Zealand mice occurred as early as 2 months of age, preceding serologic and clinical disease activity as well as decreased Fc receptor function. These studies demonstrated an early, progressive, and uniform defect in Fc-mediated clearance in the four murine strains of SLE studied. Complement-mediated clearance, however, varied considerably in lupus-prone mice, ranging from severe impairment in MRL-lpr/lpr to normal function in BXSB and accelerated clearance in NZB and NZB/W mice. Accelerated clearance in New Zealand mice was characterized by decreased C3b deactivation and release of antibody sensitized cells, which in turn led to increased phagocytosis of sensitized cells sequestered by complement-dependent processes.

Animals↗

PubMed1990

[Clinical features of male SLE patients--summary of our 22 cases].

We investigated clinical features of our 22 male SLE patients with main respect to 11 articles of ARA criteria for diagnosis of SLE (1982). As for skin lesions, 14 cases (64%) manifested wide spread discoid lupus erythematosus as their first symptoms, however, rather rare lesions could be seen as follows: 3 cases with nodular cutaneous lupus mucinosis, 1 with vesiculobullous LE. As to visceral manifestations, renal involvements could be seen in 11 cases (50%), among which 6 showed nephrotic syndromes. In immunological examinations, 1 case revealed C4A deficiency. The clinical tendency of male SLE cases has not been settled by now, for the disease is uncommon in men. Each of our 22 cases manifested a variety of features respectively, indicating that rather atypical cases as SLE can be more often seen in males than females. In addition, many of our cases showed remarkable changes clinically during their courses, which suggests that we should follow them carefully from now.

Adolescent↗

PubMed1990

Serological studies of an SLE-associated antigen-antibody system discovered as a precipitation reaction in agarose gel: the HAKATA antigen-antibody system.

Current population studies indicate that the HAKATA antigen is one of the normal plasma proteins not yet completely characterized. The frequency of Japanese donor, patients and Swedish patients was 100%, 99.99% and 99.98%, respectively. Anti-HAKATA antibody production was found in three patients, all with systemic lupus erythematosus (SLE). Transient HAKATA antigen deficiency was found in 13 patients and appeared to be strongly associated with SLE (11 out of 13). None of the 14 SLE patients had a history of transfusion. It is therefore concluded that anti-HAKATA antibody is produced as one of the autoantibodies in SLE.

Antibody Formation↗

PubMed1990

[A new autoantibody, anti-210kDa microtubule associated protein antibody, detected in the serum of patients with various liver diseases and SLE].

A new autoantibody to 210kDa microtubule associated protein (MAP) obtained from rabbit liver excrude was detected in the serum with various liver diseases and SLE. As there were no reports concerning autoantibodies to MAPs in animals and human, it may say that anti-210kDa MAP autoantibody we detected was a new cytoskeleton antibody. Using western blotting method, the anti-210kDa MAP autoantibody was frequently found in the patients with alcoholic liver diseases (52.5%), PBC (55.6%), autoimmune hepatitis (83.3%), SLE (71.4%) but rarely in the patients with viral liver diseases (26.4%) and none in normal controls at a serum dilution of 1:10. In addition, at a serum dilution of 1:100, the anti-210kDa MAP autoantibody was found in the patients with alcoholic liver diseases (22.5%), PBC (44.4%), autoimmune hepatitis (66.7%), SLE (71.4%), viral liver diseases (17.0%) and none in normal controls. It was confirmed that the anti-210kDa MAP autoantibody was frequently detected in cases of alcoholic liver diseases, PBC, autoimmune hepatitis and SLE than in those of viral liver diseases and normal control.

Autoantibodies↗

PubMed1989

Antibody binding of macromolecular DNA and RNA in the plasma of SLE patients.

Plasmapheresis fluids from 20 patients with clinically active SLE, from three patients with Waldenstrom's disease, from three patients with rheumatoid arthritis, two patients with myasthenia gravis and other diseases including active systemic disorders were precipitated using polyethylene glycol 6000 (PEG). By applying ethidium bromide staining, plasma nucleic acids (PNA) could be demonstrated in PEG-precipitates of SLE patients exclusively. Purified immunoglobulins of SLE plasma precipitates were shown to form antigen-antibody complexes with PNA as demonstrated by electronmicroscopy. Further characterization of PNA by agarose gel electrophoresis revealed a molecular weight up to 20 kbp. Cesium chloride buoyant density gradients showed non-homogeneous molecules, excluding pure microbial origin. In spite of RNase digestion, the PNA contained RNA with 30-70% riboguanosine as shown by nucleoside analysis. The high amount of guanosine-rich RNA was further supported by similarities between PNA and polyriboguanylic acid in hyperchrome shifting due to thermic denaturation. HPLC analysis showed a molecular weight of ribonucleic acids of more than 60 b thus excluding mere oligonucleotides. In contrast to B-type dsDNA, PNA from SLE patients were immunogenic. Antibodies against PNA could be induced in rabbits by subcutaneous injection. The antisera thus obtained showed crossreactivity with polyriboguanylic acid and dsDNA preparations.

Antibodies, Antinuclear↗

PubMed1989

[Effect of acoustic stress on immunoregulatory cells in female patients with systemic lupus erythematodes (SLE), patients with sarcoidosis and normal comparative subjects].

14 patients with systemic lupus erythematosus (SLE), 12 with sarcoidosis and two age- and sex-matched groups of healthy subjects were exposed to a 10-minute acoustic stress test. Healthy subjects and patients with sarcoidosis showed significant increases in leukocyte and lymphocyte counts (p less than 0.01), relative elevations of B and Tsc lymphocytes (p less than 0.01) and a relative reduction of Th lymphocytes (p less than 0.01). Patients with SLE showed the same characteristic alterations (p less than 0.01) but the degree of this cell mobilization was significantly less pronounced as compared with the healthy subjects (p less than 0.01). No dependence was found between corticosteroid therapy or disease activity and the cellular reaction in SLE patients. In SLE patients there thus seemed to be an attenuated immune response due to stress which may play an etiopathogenetic role in this disease.

Acoustic Stimulation↗

PubMedDate not supplied

Anti-histone antibodies in SLE and other autoimmune diseases.

The frequency of IgG and IgM anti-total histones and anti-histone subfractions were studied in 63 patients with SLE and 257 patients with other autoimmune conditions employing the ELISA. IgG anti-histone antibodies were found in 17 of 63 (25%) sera of lupus patients and in only 16 of 257 (6%) sera of patients with other autoimmune conditions. The latter incidence did not differ statistically from that of 115 healthy control subjects. Furthermore, the concomitant appearance of both IgG and IgM anti-histone antibodies was observed only in SLE patients. Anti-histone subfraction (H1, H2A, H2B, H3, H4) activity was determined in sera containing anti-total histone antibodies. There was a higher preponderance for antibodies to H1, H2A, H2B in SLE. We conclude that anti-histone antibodies seem to be a marker for lupus and its variants (e.g. drug induced lupus) and should be routinely looked for in SLE patients.

Antibodies↗

PubMed1988

The rate of loss of CR1 from ageing erythrocytes in vivo in normal subjects and SLE patients: no correlation with structural or numerical polymorphisms.

The stability of CR1 (complement receptor type 1) on ageing erythrocytes in vivo was examined in a group of normal subjects who had been genotyped using a restriction fragment length polymorphism (detected using a cDNA probe for CR1) that correlates with the numerical expression of CR1 on normal erythrocytes (H = allele correlating with high expression, L = low). Erythrocytes were separated into 5 fractions of increasing age on discontinuous Percoll gradients. Mean CR1 numbers on erythrocytes fell from 636 molecules per cell in the first fraction to 384 in the fifth in the HH group and from 478 to 315 in the LL group. There was no difference in the rate of decline of CR1 numbers between the groups. A group of nine SLE patients was also studied in the same way; their genotypes were HH (four) and HL (five). Mean CR1 numbers amongst all of these patients fell from 477 to 232, a faster rate of decline than in a genotypically matched group of normal subjects. There was no difference in the prevalence of the different structural allotypes amongst 30 SLE patients compared with 21 normal subjects. These data provide further evidence that there are enhanced extracellular mechanisms for the removal of CR1 from erythrocytes of SLE patients and do not support the hypothesis that inherited variation in CR1 expression on erythrocytes increases disease susceptibility to SLE.

Cell Separation↗

PubMedDate not supplied

Random locomotion and phagocytosis of monocytes in undiluted normal serum and in undiluted SLE serum.

Time-lapse filming was performed with normal monocytes in normal serum and in SLE serum, with and without yeast cell phagocytosis. Undiluted sera were used. After incubation of the monocytes with SLE serum we found a decreased velocity of random movement and a change of morphology to more condensed, rounded-up and un-spread cells with a decreased yeast cell phagocytosis. No obvious correlation was found between the SLE serum induced impairment of monocyte function and disease activity, complement levels or the presence of immune complexes. We conclude that monocyte in vitro membrane functions, such as random motility, spreading and yeast cell phagocytosis, are impaired in the presence of undiluted SLE serum.

Adult↗

PubMed1988

Expression of an interspecies idiotype in sera of SLE patients and their first-degree relatives.

Sera from 29 SLE patients and 81 first-degree healthy family members were tested for quantitative expression of a cross-reactive idiotype present on a murine monoclonal anti-Sm autoantibody (Y2). Forty-one percent of SLE patients and 27% of all relatives showed increased serum levels of the Y2 idiotype compared to 6% in a normal, unrelated control group. In addition, female relatives of SLE patients showed slightly increased levels of anti-Sm antibodies compared to male relatives (15% vs 3%). In one of the 28 families and three unrelated SLE patients studied, there was a significant correlation between the Y2 idiotype expression and expression of another idiotype present on anti-DNA antibodies (1341d). Affinity column absorption studies showed that these two idiotypes were present on different antibody molecules. This study demonstrates: (1) a genetic predisposition for an anti-Sm antibody idiotype expression in humans; and (2) that two different idiotypes may be under parallel or coordinate regulation.

Antibodies, Antinuclear↗