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Seventeen patients with moderately active SLE participated in a double-blind, crossover study on the effect of MaxEPA, using olive oil as the control substance. During the first 3 months, 8/17 on Max EPA but only 2/17 on the control substance clinically and serologically improved (p = 0.05), but at 6 months there was no difference. The beneficial effect (if any) of MaxEPA on the disease was short-lived.
100 consecutive Chinese patients with SLE were recruited for study of HLA-A, B and DR antigen. Clinical and serological parameters were analysed with respect to the HLA antigens. B5 was associated with presence of other autoimmune diseases (thyrotoxicosis, myasthenia gravis, diabetes mellitus, corrected p less than 0.025); absence of malar rash (corrected p less than 0.025); B35, with male sex (corrected p less than 0.025); DR2 with anti-Ro (anti-SSA) antibody (p less than 0.05). Previous study of association with B13, B17 was not present in our cohort. Except for malar rash, subclassification of disease status with respect to HLA antigen did not reveal significant association.
When normal polymorphonuclear leukocytes (PMN) were incubated with sera from patients with active systemic lupus erythematosus (SLE), a significantly increased cytotoxicity against human cultured vascular endothelial cells (EC), compared with normal control sera, was demonstrated by the standard 51Cr release method. The degree of this cytotoxicity was correlated with the immune complex level in each serum. The cytotoxicity did not correlate with the presence of anti-EC antibody. An absorption study with C1q-Sepharose 4B further suggested that the immune complexes are the factor which induce cytotoxicity. A gel fractionation study, however, indicated the heterogenity of the cytotoxic activity, and suggested the possible contribution of other substances including anti-EC, at least in some of the patients. This type of cytotoxicity may initiate the inflammatory process including vascular damage of the disease.
One hundred and fifty six Chinese patients with Systemic Lupus Erythematosus (SLE) were studied prospectively over 50 months. The patients in the retrospective group (Group I) were diagnosed before and in the prospective group (Group II), at the time of entry into the study. The overall female to male ratio was 25:1 with mean age at onset (+/- SD) of 26 +/- 9.9 years. Neurological manifestation as the presenting feature was rare (3%), and none of the untreated patients presented with infection. Anti-nuclear antibody (ANA) was positive in 94% and anti double stranded-DNA antibody (anti DNA) 65%. New manifestations developed in 34 patients (26%) and 218 episodes of relapses occurred in 100 patients with a rate of 0.042 relapse per patient month. Five patients died during the study period with a 5 year survival of 97% and 10 year survival of 94% in the cohort. There was no significant difference in survival between Group I and Group II patients at 50 months (p = 0.72).
A patient with RA who developed anti-Sm antibodies, a false positive serological test for syphilis (FPSTS), pericardial effusion, and leukopenia, 19-year after the onset of classical RA, is described. This case indicates a possible clinical association between the development of specific autoantibodies and clinical symptoms of SLE.
We describe a case of disseminated strongyloidiasis involving a female patient with active systemic erythematosus (SLE). The cause of death was massive pulmonary hemorrhage induced by a filariform larvae infection. This was initially diagnosed during examination of the bronchoalveolar lavage fluid just 2 days before her death. The case indicated that immunosuppressed individuals would be paid attention to possible parasitic infection prior to starting therapy even in non-endemic areas as well as other microorganisms.
Kienbock's disease, or radiologic avascular necrosis (AVN) of the carpal lunate, is an uncommon disease of young adults. The precise etiological mechanisms are uncertain although multiple mechanical, anatomical, and vascular factors are thought to be involved. A patient with systemic lupus erythematosus (SLE) who developed bilateral Kienbock's disease during the course of her illness was reported. A vasculopathy related to active vasculitis or the antiphospholipid antibodies was thought to be responsible.
Current investigations into the role of CD8+ T cells and their derived cytokine, interleukin (IL)-16, in the induction of CD4+ T cell abnormalities in systemic lupus erythematosus (SLE) were reviewed and discussed on the basis of results mainly obtained in our laboratory.
Autoantibodies in the sera of patients with systemic lupus erythematosus were examined with respect to their specificity for proteolytic fragments of histone H1 that retain, or do not retain, DNA-binding domains. 16 of 31 sera contained IgG and IgM antibodies to histone H1. IgM antibodies to H1 in 8 sera (50%) were directed at 18 kD and 20 kD alpha-chymotrypic H1 fragments that bore binding sites for DNA, as identified by staining immunoblots containing the fragments with ssDNA plus 6/0, a mouse monoclonal antibody against ssDNA, IgM with this type of histone H1 specificity did not react with comparably-sized V8 protease fragments of H1. IgM antibodies to H1 in the other patients were directed against entirely different epitopes which were preserved in V8 protease digests of H1. In serial studies of three patients during different phase of their SLE, the level of antibodies against the 18 kD and 20 kD histone H1 fragments varied in parallel with the level of anti-ssDNA antibodies in one and varied inversely in the other two. The data suggest that a significant proportion of autoantibodies to histone H1 are directed at a limited number of epitopes localized to H1 fragments containing DNA-binding sites.
To investigate the specificity of anti H1 antibodies peptides from the N- and C-domain of H1 and the synthetic oligonucleotide (AT)6 were complexed. Circular dichroism (CD) spectroscopy indicated that the free peptides H1(1-16), H1(204-218) and C(121-210) in low salt buffer assume a random structure but become helical when bound to the oligonucleotide. The structured and unstructured H1 fragments were then analyzed by enzyme linked immunosorbent assay (ELISA) with anti-H1 antibodies in sera from patients with systemic lupus erythematosis (SLE) and with the monoclonal anti-H1 antibody MRA-12 derived from MLR lpr/lpr autoimmune mice. Binding of these antibodies to H1(204-218) and C was inhibited to a level of 50% when these H1 peptides were complexed with (AT)6. When the same antibody was tested with H1 fragment GC(34-210), attachment to oligonucleotide (AT)6 did not influence antibody binding. Competition studies with liquid phase GC and C antigen against solid phase GC and C indicated that liquid phase GC was more efficient in displacing antibody binding reactivity than liquid phase C. The displacement effect of both liquid phase antigens was greatest against solid phase C. We conclude that anti-H1 autoantibodies are directed against an epitope located near the junction of the G- and C-domain which is exposed and not masked when H1 is bound to DNA.
Our studies of anti-DNA antibodies in systemic lupus erythematosus have demonstrated a preferential use of the V kappa I family to encode light chains of antibodies that express the anti-DNA associated 3I idiotype. This idiotype is present on a high percentage of anti-DNA antibodies in approximately 80% of SLE patients1,2. In this study, we employed PCR to obtain V kappa I germline genes from a lupus patient in order to address the following questions: Do the V kappa I germline genes of an individual with autoimmune disease differ from those of healthy individuals? What V kappa I genes are used to encode autoantibodies and are they used to encode protective antibodies also? Does the V kappa I gene family display peculiarities in V gene segment rearrangement or somatic mutation? Our analysis shows that the coding region sequences of germline genes of an autoimmune individual are highly homologous to those of non-autoimmune individuals. In addition, the same germline genes can be utilized to encode antibodies to both exogenous and self antigens. While rearranged V kappa genes are ordinarily derived from the J kappa proximal region of the V kappa locus, V kappa I genes encoding autoantibodies derive primarily from the J kappa distal region. It is not yet clear if this applies equally to V kappa I encoded antibodies directed to foreign antigen.
A 51-year-old woman was admitted to our hospital complaining of fever and general fatigue. Physical examination revealed butterfly-like erythema in face, facial edema and diffuse purpura all over her body. Laboratory data showed renal dysfunction, nephrotic syndrome and active phase of SLE. She was administered first methylprednisolone (1g/day/3 days by intravenous drip) then prednisolone (60 mg/day/month, orally) and had immune adsorption therapy for eight times. However, 14 days after the last session of immune adsorption, she developed fever of 39 degrees C and mild headache, and then 3 days later, she gradually became unconscious. Brain CT showed hydrocephalus. We diagnosed her as having tuberculous meningitis based on the detection of acid-fast bacillus in cerebrospinal fluid, and began treatment with antituberculous agents. We suspected that tuberculous meningitis had caused hydrocephalus. We tried percutaneous drainage of the left ventricle for hydrocephalus. Brain MRI showed a tuberculoma depicted as a mass of low intensity in the right cerebellum on the T1-weighted image, and of high intensity on the T2-weighted image, and the meninx in the basal cistern was enhanced. After treatment with antituberculous agents, we performed serial brain MRI and examined cerebrospinal adenosine deaminase activity (ADA). Despite treatment with antituberculous agents, new intracerebral tuberculomas had developed in some areas, whereas they had disappeared in other areas. After treatment for 4 months, the level of cerebrospinal ADA became normal, and the patient recovered consciousness despite the presence of multiple tuberculomas. Both the cell counts and the level of ADA in cerebrospinal fluid are the good indicators of the activity of tuberculous meningitis and reflected its clinical course. Furthermore, the level of ADA in cerebrospinal fluid changed with brain MRI image. Serial brain MRI and examination of ADA in cerebrospinal fluid were useful to know the activity of tuberculous meningitis and to evaluate the response to treatment.
A 70 year old woman developed a sensory-motor polyneuropathy 12 years after almost continuous treatment with hydrochloroquine for SLE. Sural nerve biopsy disclosed abundant lipid inclusions in schwann cells and vessels against a background of axonal degeneration. After cessation of therapy the patient improved moderately. This case underscores the usefulness of nerve biopsy in the study of management of patients with peripheral neuropathy associated with systemic illnesses.
A 23-year-old woman with a nine-month history of SLE, uncontrolled with high daily doses of steroids, was treated with the T-cell immunostimulant drug, levamisole. Following a single oral three-day course of therapy with this agent her immunologic parameters and clinical manifestations underwent marked regression. Continuous two-weekly course of this drug at three days per course have allowed rapid reduction of her steroid and resulted in complete remission of her symptoms. The theoretical considerations for the use of levamisole dovetailed perfectly with the observed response to this agent.
Sera from 18 of 56 individuals working in SLE laboratories bound more than 30 per cent of 0.1 mug of 125-I denatured calf thymus DNA, in an ammonium sulfate precipitation assay. Only two of 58 normal non-laboratory personnel and four of 40 sera from routine hospital laboratory personnel bound more than 30 per cent. Statistical analysis of these results with the Kolmogorov-Smirnov nonparametric test indicated this was a very significant difference (p less than .001). Using native DNA as a test antigen a similar pattern was seen, but it was not as clear cut. Part of this increased reactivity is heat labile. Further studies must be carried out before an adequate interpretation of these findings is possible.
From January, 1979 to December, 1990, 105 pregnancies of the 87 mothers with systemic lupus erythematosus (SLE) were studied. There were 15 (14.29%) fetal losses. Among the 90 livebirths, 23 (25.5%) were moderately premature; and 1 (1.1%), was extremely premature. All but 2 (2.2%) had an Apgar score more than 7 at 1 minute. There was no neonatal death. Significantly lower birth body weights were noted compared with the matched control group (p = 0.0001). Birth body length and head circumference were not different. Only 1 of the 13 newborns who had been small for gestational age at birth had body weight and length less than the 3rd percentile during follow-up. Three (3.3%) newborns presented as congenital complete atrioventricular block (CCAVB). Their mothers were all positive for SSA (Ro) antibody. One of them obligatorily needed pacemaker implantation. ECG abnormalities including multiple ventricular premature contractions, wandering atrial pacemaker, sinus arrhythmia, and first degree A-V block were detected in another six newborns. Congenital cardiac defect with secundum type atrial septal defect was noted in two newborns (2.2%). Among the 59 mothers who had been tested for SSA antibody, 29 (49.1%) were positive. The incidence of complete A-V block was significantly higher in newborns of mothers with SSA antibody (p < 0.001). On the contrary, the frequency of fetal loss has higher in newborns of mothers without SSA antibody (p = 0.0043).
This short report describes a possible beneficial effect of dapsone in the treatment of chronic unresponsive muco-cutaneous lesions of systemic lupus erythematosus (SLE) without any serious side effects.
A 23-year-old woman with SLE was admitted because of severe psychosis manifested by depression, delusions and the inability to perform minimal daily activities. The patient refused treatment with steroids, but was later convinced to try treatment with intravenous immunoglobulin (IVIG). Following treatment with IVIG a marked improvement was noted in her mental status and she was discharged. During a follow-up period of 18 months she resumed normal life; she does not receive any drugs currently and no psychiatric abnormalities have been noted. It is suggested that IVIG may be considered in the treatment of lupus cerebritis, especially when serious complications develop and other treatment modalities are ineffective.