Two cases of acquired toxoplasmosis in asymptomatic Malaysian patients are described. In both instances the diagnosis was first made on the finding of the Piringer-Kuchinka reaction in excised lymph nodes from these patients and serological studies further confirmed the presence of hihg toxoplasmic antibody titres. The characteristic histological features of toxoplasmic lymphadenitis are discussed. Diagnosis and management of the disease are briefly reviewed with emphasis that the importance of diagnosing this disease goes beyond the establishment of a mostly self-limiting, clinically unimportant protozoan infection.
The first living patient with a Schistosoma japonicum-type infection who presented with the nephrotic syndrome is reported in detail. It is not clear whether the nephrotic syndrome was due to the schistosome infection or to the deposition of hepatitis B antigen and antibody complexes. This is the tenth case of schistosomiasis reported from aborigines in Malaysia and a sylvatic source of infection is suggested.
One hundred and forty-eight patients over the age of 12 years seen from July 1972 through December 1980 were accepted for this review of minimal change glomerular disease (MCGD). The diagnosis was based on a typical clinical presentation, and renal biopsy findings. MCGD forms 43.5 per cent of our patients with idiopathic nephrotic syndrome. The patients were predominantly young adults (82 per cent) and the onset of nephrotic syndrome (NS) occurred below the age of 30 years. Most patients had severe oedema and hypoalbuminaemia. Few patients recovered spontaneously. One hundred and thirty patients were given long-term alternate-day steroid (LASt) therapy. Four had cyclophosphamide alone, 21 patients had cyclophosphamide after a trial of LASt. Eighty-four patients (62.7 per cent) were initial responders: 17 of these after cyclophosphamide, 26 (19.4 per cent) were initial non-responders: five cyclophosphamide, 19 were late responders. Nine patients were partial responders, six were non-responders and one went into renal failure. Forty-one patients defaulted, emigrated or were seen only locally at the time of study. Ninety-nine patients were followed for three to 102 months (mean 23 . 3 months). Thirty-seven patients were followed for 36 to 102 months. Relapses were infrequent but occurred as late as 60 months.
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.
During a 6 yr period, 105 (69%) of 153 patients in whom a histological diagnosis of minimal change glomerular disease was made had renal biopsy tissue suitable for immunofluorescence examination. Thirty seven (35%) patients showed glomerular mesangial deposits of IgM. All the patients presented with the nephrotic syndrome. We found no significant difference in age and sex prevalence, presentation, response to therapy and glomerular morphology between IgM positive and IgM negative groups. This study suggests that there is no necessity to categorize IgM positive minimal change glomerular disease as a separate entity.
Two hundred and five healthy Malaysian adults were scanned for the length of their kidneys and the cortical thickness by both the sector real time and linear array static B-scan diagnostic ultrasound. The length of the left kidney was found to measure 105 (98-111) mm for males, and 100 (94-106) mm for females on average from the sector scan and the static B-scan. The right renal length was 102 (96-119) mm for males, and 98 (92-103) mm for females on the average from readings of both scans. The left kidney is longer in length than the right kidney in males and females on both scans. The cortical thickness at the equator of the kidneys of males and females ranges from 12-14 mm. In both sexes, the lengths of the kidneys may be estimated by the distance between the first to the fourth lumbar transverse processes when there is no scoliosis.
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.
In the 10-year period from October 1977 to July 1987, 149 cases of primary IgA nephropathy were histologically confirmed through renal biopsies in the Department of Pathology, University Hospital, Kuala Lumpur. The ages of these patients ranged from 5 to 72 years, with the majority in the 20-30 year age group. There was no sex preponderance. The ethnic distribution showed a significant predominance of Chinese with 107 (71.8%) Chinese, 24 (16.1%) Malays, 15 (10.1%) Indians and 3 others. A wide range of renal glomerular pathology was seen, the commonest being diffuse mesangioproliferative glomerulonephritis (59.1%). Focal proliferative glomerulonephritis (14.1%) followed by minimal change glomerulonephritis (10.7%) were next in order of frequency. Immunofluorescence studies consistently demonstrated heavy and predominant IgA deposition in the mesangium. Weak deposition of C3, IgG and IgM were also observed in various combinations.
An association of idiopathic systemic lupus erythematosus (ISLE) with genetically determined N-acetylation polymorphism has been suspected from previous studies, mainly on Caucasian populations in which there is an approximate incidence of 50% of slow and rapid acetylators. The present study is of the incidence of ISLE and acetylator status in a mixed population of Malaysia. The results did not support an association between ISLE and acetylator status: the frequencies of slow acetylators in the ISLE patients who were Malaysian Chinese and Malay were 13 and 38% respectively. This did not differ significantly from the respective healthy groups (20 and 29%). The small number of Indians in the survey did not allow a valid comparison, but the figures did suggest a lack of association between ISLE and acetylator status.
Systemic lupus erythematosus (SLE) is highly prevalent in Malaysia, which has a mixed population of Malays, Chinese, and Indians. A quantitative enzyme linked immunosorbent assay (ELISA) was used to determine anticardiolipin antibody (aCL) levels (total immunoglobulin, IgG, and IgM) in 200 patients with SLE (164 Chinese, 26 Malay, and 10 Indian) attending the University Hospital of Kuala Lumpur, Malaysia, and 103 matched controls. Only 33 (16.5%) of the patients had raised aCL levels; 26 had raised IgG aCL, five IgM aCL, and two both IgG and IgM aCL. There was a low prevalence of raised levels of aCL in the population studied, which was seen in conjunction with a rare occurrence of thrombosis. The classical association of high aCL levels with thrombocytopenia and recurrent abortions was noted, though not with cerebral disease. The low prevalence of aCL in this study population of mixed racial origin contrasts with findings in European patients with SLE and lends support to the influence of local factors, be they genetic or environmental, on the clinical manifestations of this disease.
We conducted a prospective longitudinal study to determine the nature and prevalence of cardiac abnormalities in systemic lupus erythematosus and to study their natural history and relationship with disease activity. Forty consecutive inpatients with systemic lupus erythematosus were studied during their admission and subsequently 6 to 12 months later. On each occasion a clinical cardiovascular examination was carried out, disease activity was scored using the "Lupus Activity Criteria Count" and a Doppler echocardiographic examination was carried out. 72.5% of patients had an abnormal echocardiogram in the first study while 51.7% were abnormal during the follow-up study. Valvar disease occurred in 37.5% of patients. The mitral valve was most commonly affected. Libman-Sacks endocarditis was rare (2.5%). Pericardial effusions were seen in 36.2% of echocardiograms. The majority (76.0%) of these were associated with hypoalbuminaemia. 80.0% of patients had active disease during the first examination and 41.4% at follow-up. There was no correlation between activity of disease and prevalence of cardiac abnormalities at either examination. We conclude that cardiac disease is common in systemic lupus erythematosus. Prevalence of cardiac abnormality did not correlate with disease activity.
At the University Hospital, Kuala Lumpur, Malaysia, nine patients with systemic lupus erythematosus (SLE) were treated for Pneumocystis carinii pneumonia (PCP) between January 1987 and December 1988. When they developed PCP all the patients' SLE disease course was active and eight of them were on prednisolone. Four of these eight patients were also receiving cyclophosphamide. Patients who were on more intensive immunosuppressive therapy were found to develop more severe PCP. All the patients except one were treated with high-dose cotrimoxazole. Four patients responded to antipneumocystis treatment and survived, while PCP was responsible for the death of the five non-survivors.
Systemic lupus erythematosus (SLE) and gout have been associated infrequently. We describe 3 young adults with SLE who developed tophaceous gout relatively early in the course of their disease. All were underexcretors of uric acid but were studied after the development of renal disease; 2 were treated with diuretics. In 2 cases, gout became obvious while lupus was quiescent.
We report a significantly increased prevalence of antiribosomal P protein antibodies in Malaysian Chinese patients (38%) with SLE compared to white Caucasian (13%) and Afro-Caribbean (20%) patients. The increased prevalence was not due to a generalized increase in autoantibody production because anti-dsDNA and anti-SSA antibodies were present in comparable frequencies in the three ethnic groups while anti-Sm and anti-SSB antibodies were rarely found in the Malaysian Chinese patients.
Cerebral infarction in the young is likely to be non-atheromatous. While in previous studies no cause has been found in 40% to 50% of patients, an increasing role for haemorheological factors is becoming apparent. Among these, an association between antiphospholipid antibodies (aPLs) and ischaemic cerebrovascular disease is now well-recognised. This entity has not been previously reported in Malaysian patients. In a study of 80 patients with stroke below the age of 50 years who were seen at the University Hospital, Kuala Lumpur, between January 1982 and May 1992, 3 patients with ischaemic cerebral infarction were found to have aPLs. aPLs was detected using ELISA method for anticardiolipin antibodies (aCLs), and presence of lupus anticoagulant (LA) was established by kaolin clotting time, thromboplastin inhibition test and platelet neutralisation procedure. Only 1 patient had active systemic lupus erythematous. Cerebrovascular events were recurrent in one of the 2 non-lupus patients. aPL-related stroke should be considered in young patients who have cerebral ischaemia occurring without obvious cause. More cases are likely to emerge in Malaysia with active screening.