The first case of systemic lupus erythematosus (SLE) was reported from
India in 1955 followed by two more case reports and further, a series
of eight cases, till 1969. Since the establishment of a clinical immu
nology 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 inclu
ding Chennai (old name Madras), Mumbai (old name Bombay), Calcutta and
Hydrabad, also published their regional experience on SLE. Based on t
hese data, the present report describes the clinical and laboratory ch
aracteristics of 1366 SLE patients seen in different regions of India.
Arthritis, rash, photosensitivity, seizures and psychosis were seen i
n comparable proportions to other racial groups. Similarly, ANA and an
ti-DNA antibody positivity was also within the range seen in other rac
ial groups. When compared with other series, however, alopecia, renal
lupus, oral ulcers and neurological involvement was seen in higher pro
portions, reaching statistically significant figures in comparison to
some racial groups. In contrast, haematological manifestations were se
en in significantly less proportions in comparison to some of the raci
al groups. Serositis and discoid lesions were also seen in lower propo
rtions than in most of other races. The proportion of those with anti-
Sm antibodies was in between two extremes of highest among Africans an
d Israelis and lowest among Chinese and Europeans. Other manifestation
s were comparable to most other racial groups. Compared to North Ameri
can and European reports, significantly low 5 and 10 year survival was
observed among patients from India. This could be related to the gene
ral 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 r
each major city hospitals, or a truly severe disease among Indians, or
a combination of these genetic, environmental and/or sociocultural fa
ctors. The Main causes of death were irreversible renal damage, infect
ions and neurological involvement. Despite a comparable prevalence of
anticardiolipin antibodies (aCL) and lupus anticoagulants (LAG), clini
cal antiphospholipid syndrome was significantly less common. Genetic s
tudies showed appreciable increase of HLA DR4 (37.5%) among patients c
ompared with controls (18%). Additionally the haplotype B8-DR3 was enc
ountered frequently in the patient group.