Three cases of myelosclerosis associated with systemic lupus erythematosus are described. The probable role of systemic lupus erythematosus in the initiation of myelonecrosis and subsequent myelosclerosis is discussed.
In West Malaysia RA appears to be less common than in temperate climates, but more common than in tropical Africa; furthermore, the incidence of gout and SLE is comparable. The clinical manifestations of RA are milder than those seen in more temperate climates. Subcutaneous rheumatoid nodules have not been observed. Positive serological tests for RF are significantly higher than in the general Malaysian population, but still lower than those reported for patients with RA in temperate climates. Of the three main ethnic groups, the highest incidence of positive results is found in the Chinese.
Study site: Arthritis Clinic, University Hospital, Kuala Lumpur (University Malaya Medical Centre, UMMC, Kuala Lumpur, Malaysia)
Following the opening of the University Hospital of the University of Malaya in 1967, over 126,000 patients (excluding obstetric patients) have been admitted. A retrospective review, run concurrently with a prospective study, of over 200 patients thought to have suffered from systemic lupus erythematosus (SLE) revealed that, up until the 31st December 1975, 175 patients fulfilled the criteria for the diagnosis of SLE. There was a highly significant increase in the diagnosis of SLE over this period among Chinese patients compared to all other races, and no significant differencein the diagnosis of SLE among Indian and Malay patients. A review of the literature revealed that SLE appears to be a worldwide disease, reported frequently from Chinese communities but infrequently from tropical Africa. It is concluded that SLE is more common in the Chinese from Peninsular Malaysia than the other races, and that a careful study of geographical and racial factors in SLE may contribute to further understanding of its pathogenesis.
In the first 9 years following the opening of the University Hospital in kuala Lumpur nearly 130,000 patients have been admitted (excluding obstetric patients), and, of these, 175 fulfilled the American Rheumatism Association criteria for the diagnosis of systemic lupus erythematosus. This diagnosis was made significantly more frequently in Chinese patients than in other races. SLE is more often reported from Chinese communities in Asia than from India and tropical Africa. There may be a lower susceptibility to autoimmune disease in black Africans than the suspected increased susceptibility to autoimmune disease in black Africans than the suspected increased susceptibility in their American Negro and West Indian descendants. A careful study of racial and geograhical factors in autoimmune disease should throw further light on the interaction between the host and his environment which results in autoimmune disease.
Adequately biopsied renal tissue received in the Department of Pathology, University Hospital, Kuala Lumpur from 1,000 consecutive Malaysian patients during an eleven year period between 1970 and 1981 was reviewed. The youngest patient was 6 days old and the oldest 80 years. Both sexes were equally represented. The majority of the patients were Chinese (71%) with Malays and Indians comprising most of the remainder. Over half the patients (50.4%) presented with the nephrotic syndrome. Other modes of presentation included systemic lupus erythematosus, proteinuria and haematuria separately or in combination and hypertension. Minimal change (25.7%) and proliferative glomerulonephritis (24.8%) were present in about equal numbers and together accounted for over half of the cases (50.5%). Lupus nephritis was the third most common diagnosis (18.4%). In addition, there were patients with focal glomerulonephritis (5.4%), membranous glomerulonephritis (5.5%), Berger's disease (5.8%), amyloidosis (0.6%) and end stage renal disease (4.0%).
A young Chinese female presented with severe bilateral chemosis without any other systemic evidence ofoedema or systemic lupus erythematosus (SLE). Investigations confirmed the diagnosis of SLE with early diffuse proliferative glomerulonephritis. The condition improved with steroid therapy.
In view of a high prevalence of hepatitis B virus infection in the Malaysian population, indirect immunofluorescence examination for hepatitis B surface antigen (HBsAg) was routinely performed on renal biopsy specimen at the University Hospital, Kuala Lumpur, over a 3-year period. Examination of renal tissue from 259 patients, including 47 with systemic lupus erythematosus (SLE), revealed 43 cases with HBsAg in glomerular immune complexes. A significantly high proportion (30/43) of these were SLE patients. The deposits were granular in nature, situated in both the capillary walls and mesangium and associated with immunoglobulin deposition. Morphological patterns of lupus nephritis involved were focal proliferative (one case), diffuse proliferative (23 cases) and membranous (six cases). None of these patients showed clinical evidence of liver disease. The significance of these findings remains uncertain, but the possibility exists that the hepatitis B virus may have a role in the pathogenesis of SLE in the tropics where both SLE and HBs antigenaemia are common.
Thirty-one patients with systemic lupus erythematosus had membranous lupus nephropathy (MLN). They were divided into two groups. Group I consisted of 13 patients who had pure MLN but the patients in Group 2 had segmental proliferation in up to 35 per cent of their glomeruli. The rest of the glomeruli had purely membranous change. The patients of Group 2 were no different from the other MLN patients in terms of age, sex and race. The extrarenal disease in both groups was extensive and severe. The renal disease was usually associated with the nephrotic syndrome or oedema but was asymptomatic throughout in one patient. Both renal and extrarenal features responded to treatment initially but relapses were frequent and often severe. Relapses often occurred as treatment was discontinued or medication reduced. Survival at six years in Group I was 62 per cent and in Group 2 was 50 per cent. Only one patient died with renal failure although five patients had impaired renal function at death. The chief causes of death were disease of the central nervous system and infection.
We report a case of systemic lupus erythematosus complicated by transverse myelopathy and hyperphagia. To our knowledge the latter has not been reported before.
Paraventricular calcification not previously reported in systemic lupus erythematosus was seen in cranial computed tomograms of two patients with this disorder.
Autoantibodies to the three extractable nuclear antigens (ENA), Anti-SSA (Ro), Anti-Sm, Anti-RNP and antinuclear antibodies were determined in 150 patients with SLE. Seventy patients (46.7%) had Anti-SSA (Ro), 40 (26.7%) Anti-Sm and 25 (16.7%) Anti-RNP antibodies. Ninety four percent patients had a positive Fluorescent anti-nuclear antibody (FANA) test. The commonest FANA pattern is the speckled pattern. Subclinical keratoconjunctivitis sicca (KCS) was present in 60% patients. No correlation could be demonstrated between the presence of ENA autoantibodies and the clinical features of patients.
Non-reactive SLE sera in an ELISA for anticardiolipin antibody (aCL) retested positive in the immunoassay when the sera were first heat-inactivated at 56 degrees C for 30 minutes. This was not a false positive phenomenon since the positive ELISA reactivity of the heated SLE sera was markedly reduced by inhibition with the cardiolipin antigen. Furthermore, the heat-potentiated ELISA reaction was abolished by prior IgG depletion of the SLE sera with Protein A preparation. The unmasked aCL in the heat-treated SLE sera also exhibited selective binding in ELISA to other negatively-charged phospholipids, namely phosphatidylserine and phosphatidic acid but not against either phosphatidylcholine or phosphatidyl-ethanolamine. The data strongly indicate an interaction between antiphospholipid antibodies and heat-sensitive serum component(s), a reduction of the latter resulting in the ELISA detection of the autoantibody.