Over the past year, many reports have been published on a variety of clinical manifestations related to antiphospholipid antibodies. The low prevalence of anticardiolipin antibodies with the rare occurrence of thrombosis and a low rate of fetal loss in studies in Malaysia and China showed a potential role for local factors. A study of cross-reactive idiotype of the anticardiolipin antibody suggested that anticardiolipin antibodies are derived from a set of natural autoreactive clones. Regarding the pathogenic role of the antiphospholipid antibody, evidence has been presented that the epitopes formed between cardiolipin and beta 2 glycoprotein I are the targets of the antiphospholipid antibody. Complement activation, abnormalities of natural anticoagulants such as protein S deficiency, and genetic association with DR4, DR7, and DRw53 have also been studied.
The association between HLA-B27 and the spondyloarthropathies (SpAs) is so strong that it is supposed that the HLA-B27 molecule plays a pathogenetic role. In whites and Indonesians, the frequency of HLA-B27 is about 10%; in Chinese it is about 8%; and in Japanese it is only about 1%. The prevalence of SpA in the Chinese is at least 0.2%, but in native Indonesians, Philippinos, and Malaysians, SpA is rarely seen. Twenty-three subtypes (B*2701-B*2723) have been distinguished. These subtypes are not equally distributed over the world. In most countries the distribution of the subtypes among HLA-B27 SpA patients is the same as that among the normal HLA-B27-positive population. In China, the subtype B*2704 is frequent and the prevalence of SpA is high. Native Indonesians, however, mostly have subtype B*2706, and SpA is rarely seen in this population. It was shown that B*2706, probably like B*2709 in Sardinia, is not associated with SpA. The difference between the SpA-associated and non-SpA-associated subtypes is limited to only two amino acid residues (114 and 116) at the bottom of the peptide-binding groove of HLA-B27. This small difference between health and disease rewards studies for different peptide-binding capacities and may help us characterize the peptides that are involved in the pathogenesis of SpA. The differences in disease associations in these countries also have clinical implications. In Southeast Asia, HLA-B27 typing without subtyping has less clinical usefulness than in parts of the world where B*2706 is rarely seen. When native Indonesians, Malaysians, or Philippinos are suspected of having ankylosing spondylitis or a related SpA, it is worth asking if they had white or Chinese ancestors. If native HLA-B27-positive Indonesians (with subtypes other than B*2706) develop SpA, the clinical features are not different from those in other parts of the world. In the Chinese population on the mainland and in Taiwan, juvenile SpA is frequently seen. The onset is often a peripheral arthritis or enthesitis.
Eosinophilia is occasionally a feature of rheumatic disease. The differential diagnosis of eosinophilia includes parasitic infection, systemic vasculitides, eosinophilic arthritis, and myopathies, together with the idiopathic hypereosinophilic syndrome and malignancy. Careful evaluation of the patient should enable an accurate diagnosis to be made. Parasitic infection is the commonest cause of eosinophilia worldwide and can cause systemic disease, as illustrated by the report of Sarcocystis myositis in a group of military personnel in Malaysia. A persistent arthropathy associated with eosinophilia, but not with parasitic infection, has been reported from the far East. Drugs may also cause eosinophilia, and there has recently been much discussion of the relation between Churg-Strauss syndrome and the leukotriene antagonist zafirlukast. The present view is that reduction of steroid dose allows unmasking of previously undiagnosed Churg-Strauss syndrome. The idiopathic hypereosinophilic syndrome may represent a lymphoproliferative process; evidence for this comes from the demonstration that many patients have a clonally expanded population of aberrant T cells.