Occasional Series—Lupus Around the World Systemic lupus erythematosus in India

Abstract

The first case of systemic lupus erythematosus (SLE) was reported from India in 1995 followed by two more case reports and further, a series of eight cases, till 1969. Since the establishment of a clinical immunology laboratory at a major teaching institution in New Delhi in 1968, SLE was extensively studied and reported from that centre. From mid-1980 onwards several other centres in different regions in India including Chennai (old name Madras), Mumbai (old name Bombay), Calcutta and Hydrabad, also published their regional experience on SLE. Based on these data, the present report describes the clinical and laboratory characteristics of 1366 SLE patients seen in different regions of India. Arthritis, rash, photosensitivity, seizures and psychosis were seen in comparable proportions to other racial groups. Similarly, ANA and anti-DNA antibody positivity was also within the range seen in other racial groups. When compared with other series, however, alopecia, renal lupus, oral ulcers and neurological involvement was seen in higher proportions, reaching statistically significant figures in comparison to some racial groups. In contrast, haematological manifestations were seen in significantly less proportions in comparison to some of the racial groups. Serositis and discoid lesions were also seen in lower proportions than in most of other races. The proportion of those with anti-Sm antibodies was in between two extremes of highest among Africans and Israelis and lowest among Chinese and Europeans. Other manifestations were comparable to most other racial groups. Compared to North American and European reports, significantly low 5 and 10 year survival was observed among patients from India. This could be related to the general public health situation in the country including less than optimal management facilities in hospitals, delay in diagnosis due to lack of awareness of the disease, referral bias where only serious patients reach major city hospitals, or a truly severe disease among Indians, or a combination of these genetic, environmental and/or sociocultural factors. The Main causes of death were irreversible renal damage, infections and neurological involvement. Despite a comparable prevalence of anticardiolipin antibodies (aCL) and lupus anticoagulants (LAC), clinical antiphospholipid syndrome was significantly less common. Genetic studies showed appreciable increase of HLA DR4 (37.5%) among patients compared with controls (18%). Additionally the haplotype B8-DR3 was encountered frequently in the patient group.

Antiphospholipid syndrome in Asians: clinical manifestations, serological markers and outcome of the National University of Singapore/National University Hospital antiphospholipid cohort

“…Among other Asian populations, the frequency of aPL varies between 13% to 71% (Table 9). 34–42 This was similar to Western SLE cohorts which reported positive aPL in 25–50% of their SLE patients, and thrombosis in 40–50% of those with aPL 43 . In the Asian studies, the frequency of SAPS in SLE appears to be much lower in the Far‐eastern patients (< 10%), while among the Middle‐eastern population, particularly in Kuwait, it was high (> 20%) 41,42 .…”

Clinical picture of lupus nephritis in patients with systemic lupus erythematosus (SLE): Results of a large survey

“…The overall prevalence rate of lupus nephritis was higher in the current study compared to notable surveys [22,23]. It is noteworthy that previous studies have suggested that the highest rate of renal involvement in the world (73%) was found in Indo-Asians [16,24].…”

Mannose binding lectin: a biomarker of systemic lupus erythematosus disease activity

“…There are limited studies on Indian SLE patients. Although the prevalence of SLE in India is rare (3/100,000) [3], the survival rates of these patients (70% at 5 years, 50% at 10 years) are very low compared to Western cohorts [4,5]. Several factors are thought to be responsible for poor survival rates, the most important being delayed diagnosis [6].…”