Immunohistological studies of the kidney in systemic lupus erythematosus and systemic sclerosis using antisera to IgG, C3, fibrin, and human renal glomeruli.
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[A case of fulminant hepatic failure in Wilson's disease combined with systemic lupus erythematosus].
Patients with systemic lupus erythematosus (SLE) have a chance of developing liver involvement in their lifetime. The main cause of liver involvement in SLE patients is previous treatment with hepatotoxic drugs or hepatotropic viral hepatitis. Wilson's disease is a hereditary disorder and is usually diagnosed in patients presenting either neuropsychiatric disorders or manifestations related to chronic liver disease. Fulminant hepatic failure as the initial manifestation of Wilson's disease is rare. The relationship between systemic lupus erythematosus and Wilson's disease has not been established. We report a case of a 12-year-old girl with SLE who presented fulminant hepatic failure as an initial manifestation of Wilson's disease. The diagnosis was established with decreased serum ceruloplasmin level and the presence of Kayser-Fleischer ring. We treated with repeated plasma exchange. Despite repeated plasma exchange she died of multi-organ failure on the 16th hospital day. Considering this case, Wilson's disease should be considered as a cause of fulminant hepatic failure, especially in juvenile age cases.
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Pemphigus erythematosus: a unique association with systemic lupus erythematosus.
An association between pemphigus erythematosus and systemic lupus erythematosus is well recognized. However, most reports strongly imply that the clinical manifestations of lupus erythematosus are usually minimal or only serologically significant. We describe the case of a 27-year-old black woman who experienced life-threatening systemic lupus erythematosus while recovering from pemphigus erythematosus. Unique histopathologic findings show the presence of both disorders in the same lesion.
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Dyslipoproteinemia in pediatric systemic lupus erythematosus.
Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoproteinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.
Adolescent↗
Recurrent lupus nephritis in the second allograft of a patient with systemic lupus erythematosus.
Lupus glomerulonephritis is a common and serious complication of systemic lupus erythematosus (SLE) affecting up to 50% of lupus patients. Recurrent lupus nephritis is rare, complicating as low as 1% of the lupus transplant population according to some authors. However, it may be underreported with more realistic recurrent rates oscillating from 2.8 to 8.7%. We report the case of a patient with SLE who lost her first allograft 4 years after transplantation with a diagnosis of de novo fibrillary glomerulopathy. She underwent a second renal transplantation and her renal function was stable for the past 5 years. She now presented with skin rash, arthralgias and positive lupus serologies. Her creatinine was slightly elevated and proteinuria was also noted. A renal biopsy performed revealed a recurrent focal proliferative lupus nephritis (WHO III). Retrospectively, we believe that her first allograft was also lost to recurrent lupus nephritis. This is a unique case of recurrent lupus nephritis in the second allograft of a patient with SLE.
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Depressive symptoms in patients with systemic lupus erythematosus: association with central nervous system lupus and Sjögren's syndrome.
OBJECTIVE: To determine if patients with systemic lupus erythematosus (SLE) with depressive symptoms differ in regard to organ involvement and serological activity from other patients with SLE. METHODS: Disease manifestations were compared between 71 patients with SLE with a history of depressive symptoms and 278 patients without a history of depressive symptoms by univariate analysis and multiple logistic regression. RESULTS: Both univariate and logistic regression analysis revealed an association of depressive symptoms with neuropsychiatric lupus and secondary Sjögren's syndrome (SS). Patients with neuropsychiatric lupus had an adjusted odds ratio of 3.43 (95% CI 2.55, 4.63; p = 0.00005), and patients with secondary SS had an adjusted odds ratio of 2.97 (95% CI 2.08, 4.25; p = 0.0006) for depressive symptoms. No other organ involvement or serological abnormality was associated with depressed mood. CONCLUSION: These discrete associations of depressive symptoms with neuropsychiatric lupus and secondary SS suggest that depression does not occur purely as a response to social stresses, and may be a manifestation of autoimmune disease in some patients.
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Neurologic symptoms in children with systemic lupus erythematosus.
Neurologic complications of systemic lupus cerebritis are not as well known in children as in adults. Twenty-five children with neurologic complications were identified after reviewing the hospital medical records of 86 children with systemic lupus erythematosus. Seven children (28%) had neurologic symptoms at the time of initial diagnosis of systemic lupus erythematosus; median time between diagnosis of systemic lupus erythematosus and onset of neurologic complications was 1 month (range 0-5 years). Seizures were the most common neurologic symptoms overall, but headaches were the most frequent neurologic manifestation in children without a previous diagnosis of systemic lupus erythematosus. Sixteen children had seizures, and 12 children had seizures as the initial central nervous system involvement. Almost all children who developed seizures had an established diagnosis of systemic lupus erythematosus; only one child had seizures that led to the diagnosis of systemic lupus erythematosus. No patient had status epilepticus, and, in general, seizures were not difficult to control. In six children, headache was the initial symptom of central nervous system involvement. Five children had lupus cerebritis, three children had stroke, and two had isolated cranial neuropathies. Chorea was seen in only two cases, and three children had pseudotumor cerebri. Treatment with high-dose intravenous methylprednisolone led to a good response in 18 children; cyclophosphamide was required in 6 patients and plasmapheresis in 1 child. Outcome was generally good, although one child developed fulminant cerebritis with intracranial hypertension and died.
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Raynaud's phenomenon with oral manifestation in systemic lupus erythematosus.
A 24-year-old woman with discoid lupus erythematosus developed systemic lupus erythematosus after 6 years. One of the clinical features was Raynaud's phenomenon in the fingers and toes, and furthermore Raynaud's phenomenon appeared in the tongue when exposed to cold and windy weather.
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Antimalarial drugs, systemic lupus erythematosus and pregnancy.
Antimalarial drugs containing the 4-amino quinoline radical are used to help control disease activity in discoid lupus erythematosus and systemic lupus erythematosus (SLE). Many patients with these complaints are young women, some of whom will become pregnant. The use of these substituted 4-amino quinoline compounds in pregnancy is controversial. We studied the full obstetric histories of 8 women with SLE who had taken either chloroquine phosphate or hydroxychloroquine sulphate (Plaquenil) throughout the entire length of at least 1 pregnancy. These 8 women had 14 pregnancies while receiving antimalarial drugs. Fetal wastage was high in these patients, regardless of antimalarial therapy, and was almost 100% in patients who were clinically active. Six normal full term spontaneous deliveries resulted from these pregnancies with clinically healthy normal babies born despite exposure to antimalarial therapy throughout the pregnancies.
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[Psychiatric manifestations of lupus erythematosus systemic and Sjogren's syndrome].
UNLABELLED: We present one case of Sjögren's syndrome (SS) secondary to systemic lupus erythematosus (SLE) with predominant psychiatric manifestations, treated with success by cyclophosphamide. From this case, we review the psychiatric aspects of these two autoimmune diseases as described in the literature and we present the etiopathogenic hypothesis and treatment of the psychiatric disorders. Case report--In August 1996, a 38 year old man was admitted in our psychiatric department for agitation. Primary SS had been diagnosed in July 1996. He had previously attempted to suicide but was never hospitalized in a psychiatric department. During the hospitalization in our department, the patient had auditive hallucinations and felt persecuted. He received loxapine 400 mg/day and was remitted in a few days. He was discharged to a convalescent home with the diagnosis of brief psychotic disorder. In October 1996, he was readmitted to our department for agitation. He had shown agitated behavior and aggression in the convalescent home. There were no hallucinations and no affective disorders. He became calm rapidly and was discharged home a few days later. In November 1996, he was found in a coma by a neighbor. He was admitted to an intensive care unit. The lumbar punction revealed blood cells. Cerebral computer tomography showed subarachnoid hemorrhage. The diagnosis was meningeal hemorrhage due to vasculitis. After regaining consciousness, the patient complained of reduced visual acuity. This was believed to be due to retrobulbar neuritis and the patient's vision improved slightly with corticosteroids. The third hospitalization in our department occurred in February 1997 for depression. The patient had shut himself away for days in his apartment. He had suicidal ideas. His mood improved progressively under fluoxetine 40 mg/day. He was discharged to a convalescent home with the diagnosis of major depressive disorder. The fourth and last admission in our department occurred in June 1997. There were disturbances of memory and orientation. He felt sad and guilty about accusation of sexual abuse on his daughter. He presented typical histrionic symptoms: he had catatonic attitudes only in public areas such as the corridors. Cerebral computer tomography and electroencephalogram were normal. There was no biological abnormality. Signs of confusion rapidly disappeared. He felt better after reintroduction of fluoxetine 40 mg/day. Diagnosis was non-specified depressive disorder, but this episode could be retrospectively seen as delirium. After being hospitalized on these four occasions in one year in our psychiatric department, the diagnosis of his systemic disease was revised by rheumatologists. The patient was diagnosed as suffering from systemic lupus erythematosus associated with secondary Sjögren's syndrome. From September 1997, he received cyclophosphamide 2 g intraveinously per month during 6 months. His vision improved dramatically. His ocular dryness became milder. His mood is now stable. He has not suffered from hallucinations or delusion since. Psychiatric disorders in SLE--During the course of SLE, the occurrence of psychiatric manifestations varies widely from 5 to 83%. They include psychotic disorders, major depressive disorders, subtle cognitive disorders and personality disorders of histrionic type. Etiopathogenic hypothesis are: direct activity of the disease on the central nervous system by autoantibodies (antiphospholipide and antiribosome P autoantibodies) (18, 19) or cytokines (interleukin 2, interleukin 6, alpha interferon) (38, 59), side-effects of glucocorticosteroids and hydroxychloroquine (16) or anxious reaction to a chronic and potentially lethal illness (43, 54). Nevertheless, immunologic and cerebral imagery research suggests that psychiatric disorders are related to vasculitis and non-inflammatory vasculopathy of the small cerebral blood vessels. The management of the patients should include treatment of the disease itself and specific psychotropic treatment. Glucocorticosteroids and especially intravenous infusions of immunosuppressive agents, such as cyclophosphamide, are effective. Psychotropic drugs must be used, making sure to avoid SLE-inducing drugs, like chlorpromazine, carbamazepine and lithium carbonate (19, 20, 45). In addition, psychologic care is essential. Psychiatric disorders in SS--During the course of the primary SS, the occurrence of psychiatric disorders is large as well: from 20 to 70% (47, 61, 62). They are mainly major depressive disorders, anxiety disorders, cognitive disorders and dementia. Brief psychotic disorders and delirium are rare. Etiopathogenic hypotheses are similar as those in SLE, with some differences: antiphospholipide and antiribosome P autoantibodies are not usually found in SS and anti-Ro (SSA) autoantibodies in serum are associated with psychiatric disorders (3-11, 61). According to Drosos et al. (29, 30), psychiatric disorders are explained by psychological distress. This slowly progressive fluctuating disease creates constant discomfort from dysphagia, dyspareunia and functional disability. Some of these manifestations can be treated by corticosteroids and psychotropic drugs. Drugs with anticholinergic side-effects, like phenothiazines, tricyclic antidepressants and hydroxyzine which can enhance the oral dryness have to be avoided. Social and psychological support is important too. DISCUSSION: The diversity of psychiatric morbidity in SLE and SS may be due to differences in patient selection and a lack of uniform clinical criteria. Studies which use standardized diagnostic criteria and control groups don't allow one to come to a conclusion about the relative prevalence of the psychiatric disorders in these autoimmune diseases. This will probably be resolved thanks to the recently published "American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes" (1). Finally, we can ask ourselves if there is a significant number of undiagnosed SLE and SS in psychiatric departments. Two studies report systematic search for SLE in psychiatric patients. In 1992, Hopkinson et al. (39) searched for several autoantibodies in serum samples of nearly 300 hospitalized psychiatric patients. In 1993, Van Dam et al. (65) did the same with more than 2,000 patients admitted to a psychiatric hospital. Hopkinson et al. found 1% undiagnosed SLE, which is much higher than in general population, and recommended to search SLE in every patient with a high erythrocyte sedimentation rate in psychiatric services. Results of the Van Dam et al. study suggest on the contrary, that SLE is not a common cause of admission to psychiatric hospitals. There is no study which report systematic search of Sjögren's syndrome in a psychiatric department. This is probably because most of patients receive or have recently received psychotropics with anticholinergic side-effects which is an exclusion criteria of SS. CONCLUSION: Psychiatrists should keep in mind that SLE and primary SS are potential causes of psychiatric manifestations when examining patients with multiple unexplained somatic complaints and psychiatric symptoms. They should then search for autoantibodies in the serum after careful physical examination. Diagnosis of SLE or SS could lead to a better adapted prescription of corticosteroids and/or immunosuppressive drugs and specific psychotropic drugs, making sure to avoid lupus-inducing drugs in SLE and drugs with anticholinergic effects in SS. The existence of psychiatric manifestations in SLE and SS constitutes an indisputable clinical reality that each practitioner must be able to recognize and treat.
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[Neuropsychiatric lupus and lupus nephritis as a clinical manifestations of systemic lupus erythematosus].
Neuropsychiatric (NP) lupus and lupus nephritis are one of the most profound manifestations of the Systemic lupus erythematosus (SLE), with wide variety of clinical manifestations. Especially NP lupus is the most poorly understood subset of the disease, and the most difficult therapeutic problem. We present case report of female SLE patient with the associated difficult and different clinical manifestations of central and peripheral nervous system disease end renal involvement. Agressive treatment option with intermittent pulsed intravenous cyclophosphamide and corticosteroids after the second month of treatment brought to complete remission of nephrotic syndrome. Improving of life-threating clinical manifestations of NP lupus was obtained after six months treatment by this immunosupressive therapy and included intravenous immunoglobulin 400 mg/kg body weight during five days monthly.
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Reliability and validity of six systems for the clinical assessment of disease activity in systemic lupus erythematosus.
Six systems for defining and evaluating disease activity in patients with systemic lupus erythematosus (SLE) (the Ropes system, the National Institutes of Health [NIH] system, the New York Hospital for Special Surgery system, the British Isles Lupus Assessment Group [BILAG] scale, the University of Toronto SLE Disease Activity Index [SLE-DAI], and the Systemic Lupus Activity Measure [SLAM]) were tested on 25 SLE patients who were selected to represent a range of disease activity. The patients were evaluated independently by 2 physicians on 2 occasions approximately 1 month apart. Differences between patients demonstrated the largest source of variation in scores, accounting for 56-84% of the total variance, depending on the instrument. Differences between physicians (i.e., error) showed the next largest variation, 11-28% of the total variance, and differences between visits made up 5-16% of the total. The BILAG, SLE-DAI, and SLAM had the best inter-visit and inter-rater reliability. Convergent validity was shown by the strong correlations of scores among the different instruments (r = 0.81-0.97). All instruments correlated highly with the physicians' clinical impression of disease but less well with their evaluation of disease severity. The number of American Rheumatism Association criteria for SLE that were met by the patients correlated poorly with the physicians' global evaluation and with the scores of the instruments. The patients' self-reported disease activity scores correlated highly with the physicians' assessments of disease activity (r = 0.85-0.91), and the mean values from self-reports and from physicians' assessments were nearly equal. In contrast, severity scores correlated less well between self-reports and physician assessments (r = 0.49-0.69), and mean self-reported severity values were lower than the means from physicians. The BILAG, SLE-DAI, and SLAM systems appear to have better psychometric properties than the others for clinical research.
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Predictors of neuropsychiatric damage in systemic lupus erythematosus: data from the Maryland lupus cohort.
OBJECTIVE: To identify factors predictive of significant neuropsychiatric (NP) damage in systemic lupus erythematosus (SLE). METHODS: One hundred and thirty patients with SLE were followed at the University of Maryland Lupus Clinic from 1992 until 2003. NP manifestations were defined according to the revised American College of Rheumatology (ACR) nomenclature and case definitions for NP-SLE syndromes. Disease activity was measured using the SLE Disease Activity Index (SLEDAI), organ damage using the Systemic Lupus International Collaborating Clinics Damage Index SLICC/ACR (SDI); NP damage (NPDI) was measured with the corresponding domain of the SDI. At end of study period, 64 patients exhibited no NP damage (NPDI = 0) and 66 patients developed significant NP damage (defined as NPDI > or =1). The baseline features for these two patient groups were compared, and variables found to be significantly different were examined by multivariable analyses to determine their contribution to NP damage. RESULTS: Significant NP damage is common in SLE; mortality is infrequent and the cause of death is unrelated to NP damage. Independent predictors of significant NP damage were disease activity, Caucasian ethnicity and the presence of antiphospholipid antibodies and anti-Ro/SSA antibody. Certain clinical features at baseline predicted specific NP damage. For example, higher disease activity at baseline was predictive of psychosis and cognitive impairment, anti-dsDNA was predictive of polyneuropathy, and antiphospholipid antibodies were predictive of seizures and cerebrovascular accidents. CONCLUSIONS: In this longitudinal SLE cohort, significant cumulative NP damage occurred. Early aggressive therapy targeted towards NP manifestations may prevent the occurrence of NP damage.
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Major histocompatibility complex genes and susceptibility to systemic lupus erythematosus.
Susceptibility to systemic lupus erythematosus is associated with major histocompatibility complex (MHC)--encoded genes. We have used nucleotide sequence analysis to better define the disease-associated MHC alleles. HLA-DR2, DQw1, and especially the rare allele DQ beta 1. AZH confer high relative risk (RR = 14) for lupus nephritis in a Caucasian population of patients. Pilot studies using historical controls suggest that these genes also confer a high risk in non-Caucasian ethnic groups (RR = 24-78). We have found that DR4 is significantly decreased in patients with lupus nephritis. Fifty percent of the patients with lupus nephritis had either the DQ beta 1.1, the DQ beta 1.AZH, or the DQ beta 1.9 alleles. These alleles share amino acid residues that have been predicted to be the contact points for antigen and the T cell receptor. These HLA alleles appear to have a direct role in the predisposition to lupus nephritis, whereas DR4 may have a "protective" effect.
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An unusual case of systemic lupus erythematosus, lupus nephritis, and transient monoclonal gammopathy.
A 23-year-old female patient suffering from active systemic lupus erythematosus (SLE) was treated with azathioprine (2 mg/kg per day) and prednisone. Lupus nephritis class III with increasing proteinuria developed 28 months after disease onset. Treatment was switched to monthly pulse cyclophosphamide administered intravenously for 6 months (total dose 6.3 g), followed by oral azathioprine and low-dose prednisone to maintain partial remission. Eight months later, the patient developed an acute exacerbation of SLE with fever, proteinuria of 9.1 g/day, pancytopenia, and cerebral involvement with cephalgias and a grand mal seizure. She responded well to high-dose corticosteroids (500 mg prednisolone pulses over 3 days, i.v.) and was azathioprine switched from to methotrexate (12.5-15 mg per week). Under this treatment, lupus activity gradually decreased and the patient felt well again. Five years after the initial diagnosis of SLE, a rapidly increasing immunoglobulin G-kappa type (IgG-kappa) monoclonal gammopathy developed, reaching a maximal serum paraprotein concentration of 73.5 g/l. Bone marrow biopsy revealed 15% of moderately abnormal, highly differentiated plasma cells arranged in small clusters and expressing IgG-kappa. No bony lesions were detectable on skeletal radiographs. Pulses of dexamethasone (40 mg) were administered and led to a transient decrease of paraproteinemia to a minimum of 31.9 g/l, followed by an increase to 62 g/l. At that point, high-dose chemotherapy supported by autologous stem cell transplantation was considered. Due to an intermittent pneumococcal septicemia, methotrexate was discontinued and dexamethasone was replaced by 5-10 mg cloprednol. At this point, totally unexpectedly, the paraprotein decreased spontaneously without any further cytostatic treatment and was no longer detectable 1 year later. Concomitantly, plasma cell counts in bone marrow biopsies fell to below 5%. As SLE remained inactive, the patient became pregnant and gave birth to a healthy child. During late pregnancy, SLE activity flared up with rising proteinuria and blood pressure. Therefore, after delivery, cyclophosphamide (100 mg/day, orally) was readministered for 4 months, resulting in an improvement of kidney function with stable proteinuria of 1-2 g/l to date. Paraproteins are no longer detectable. In conclusion, this case report documents the rare event of transient paraproteinemia in a patient with SLE. A self-limiting regulatory defect in the control of a terminally differentiated B-cell clone may be the origin of this phenomenon.
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The use of the British Isles Lupus Assessment Group (BILAG) index as a valid tool in assessing disease activity in childhood-onset systemic lupus erythematosus.
OBJECTIVES: The British Isles Lupus Assessment Group (BILAG) index is a standardized systemic lupus erythematosus (SLE) disease activity assessment. The main aim of this study was to correlate the BILAG index with laboratory measures of disease activity in childhood-onset SLE with and without biopsy-proven lupus nephritis. METHOD: Prospective observational comparison study of the BILAG index in 21 SLE patients under 18 yr of age over a 12-month period in a tertiary referral paediatric outpatient clinic. RESULTS: Eleven patients with lupus non-nephritis and 10 patients with lupus nephritis were reviewed. The lupus nephritis patients had significantly (P<0.001) more admissions over a similar time interval since diagnosis. The renal BILAG disease activity scores were significantly greater (P = 0.013) in the lupus nephritis group (range 1-9, median 3.0, compared with 0-3 and 1.0 in the lupus non-nephritis group). The total BILAG scores and patient visual analogue scores (VAS) were higher in the lupus nephritis groups, unlike the lower physician VAS, but these differences were not statistically significant compared with other laboratory indices of disease activity. CONCLUSIONS: The BILAG index is a useful tool in monitoring disease activity in children and adolescents with SLE. The data collected for the BILAG index can be used serially and effectively by different clinicians over time to enable recording of disease status at sequential assessments. The lower patient VAS in the lupus non-nephritis group was not significant and may reflect the patients' own perception of lethargy at times of increased disease activity.
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Long-term outcome in systemic lupus erythematosus membranous glomerulonephritis. Lupus Nephritis Collaborative Study Group.
The pathology of membranous glomerulonephritis (MGN) in patients with systemic lupus erythematosus (SLE) may be complicated by superimposed glomerular inflammation and/or necrosis. This retrospective study examined whether various histologic patterns of glomerulonephritis (GN) seen on renal biopsy impact upon the prognosis of these patients. Clinical parameters at the time of biopsy were also studied, to determine which might serve as risk factors associated with renal and patient outcome. On the basis of renal biopsy findings, patients were stratified into three pathological study groups by using the World Health Organization (WHO) classification (11). Thirty-six patients had "pure' SLE MGN without (WHO Va) or with (WHO Vb) mesangial hypercellularity. Fifteen patients had SLE MGN with segmental endocapillary proliferation and/or necrosis in < 50% of glomeruli (WHO Vc < 50%). Twenty-eight patients had SLE MGN with endocapillary proliferation and/or necrosis in > or = 50% of glomeruli (MGN with segmental proliferation and/or necrosis in > 50%, WHO Vc > or = 50%, or MGN with superimposed diffuse endocapillary proliferation, WHO Vd). There were no significant differences in sex, age, or race among patients in the three study groups. There was a trend for increasing serum creatinine concentration, urine protein excretion, and diastolic blood pressure, and decreasing the third component of serum complement (C3) to be associated with increasing glomerular inflammation, and these differences were significant when Vc > or = 50% and Vd was compared with Va and Vb (P < 0.05). The 5- and 10-yr actuarial survival rates without reaching the study outcomes of death or renal replacement therapy for the three study groups were 86, 72, and 49% and 72, 48, and 20% respectively, and the differences between Va and Vb and Vc > 50% and Vd were significant (P < 0.05). SLE MGN has a heterogeneous course and outcome, and this variability is related to the extent and degree of glomerulonephritis seen on renal biopsy. The only clinical factor with an independent risk of reaching a study outcome was elevation of the initial serum creatinine concentration (Cox regression analysis). This predictive value appears to apply only to patients with the most severe forms of glomerulonephritis, suggesting that they may have a different natural history and/or a response to therapy than SLE MGN with less widespread glomerular inflammation and/or necrosis.
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Anti-chromatin antibodies in systemic lupus erythematosus: a useful marker for lupus nephropathy.
BACKGROUND: Anti-chromatin antibodies have recently been described in patients with systemic lupus erythematosus (SLE) and it has been suggested that their presence is associated with lupus nephritis. OBJECTIVE: To assess the prevalence and clinical associations of these antibodies in SLE. METHODS: The presence of anti-chromatin antibodies in 100 patients with SLE was investigated by an enzyme linked immunosorbent assay (ELISA). To determine the specificity of these antibodies, 100 patients with primary Sjögren's syndrome, 30 with primary antiphospholipid syndrome (APS), 10 with systemic sclerosis, and 100 normal controls were also tested. RESULTS: Positive levels were detected in 69/100 (69%) patients with SLE. In contrast, they were found in only 8/100 (8%) of those with primary Sjögren's syndrome, in 1/10 (10%) with systemic sclerosis, in 2/30 (7%) with primary APS, and in none of the 100 healthy controls. Patients with anti-chromatin antibodies had a twofold higher prevalence of lupus nephropathy than those without these antibodies (58% v 29%, p<0.01). A significant correlation was found between the levels of anti-chromatin antibodies and disease activity score as measured by the European Consensus Lupus Activity Measurement (ECLAM; p=0.011). CONCLUSIONS: The measurement of anti-chromatin antibodies appears to be a useful addition to the laboratory tests that can help in the diagnosis and treatment of SLE. These antibodies are both sensitive and specific for SLE, and are a useful marker for an increased risk of lupus nephritis.
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