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)
Plaque reduction neutralization tests, using five group A arboviruses (chikungunya, Ross River, Getah, Bebaru and Sindbis), were done on sera from human populations in 44 Southeast Asia and Pacific island localities. Specificity of the plaque neutralization test was determined by examining convalescent sera from patients with known alphavirus infections. Chikungunya-specific neutralizing antibodies were demonstrated in sera of persons living in South Vietnam, Northern Malaysia, Indonesia (Kalimantan and Sulawesi), as well as Luzon, Marinduque, Cebu and Mindanao islands in the Philippines. Evidence of Ross River virus infection was found among populations living in West New Guinea and Papua New Guinea mainland, the Bismark Archipelago, Rossel Island and the Solomon Islands. There appeared to be no geographic overlap in the distribution of chikungunya and Ross River viruses, with the separation in their distribution corresponding with Weber's line in the Pacific. Sindbis neutralizing antibodies were found in 7 of 21 populations sampled, but in general the prevalence of infection was low. Four sera, from Vietnam, Malaysia and Mindanao gave monospecific reactions with Getah virus. No evidence of specific Bebaru virus infection was detected. The epidemiology of these five alphaviruses in Southeast Asia and the Pacific islands is discussed.
Twenty-one patients with rheumatoid arthritis (RA) were investigated for various immunological parameters, both humoral and cellular. IgG concentration was 1673+/-266 mg/dl, IgM 259+/-108 mg/dl and IgA 302 +/-7 mg/dl. Enumeration of T lymphocytes in peripheral blood revealed a value of 66% with a B cell count of 10%. Additionally, IgG levels, in 5 selected patients, appeared to fall to normal levels in the course of treatament with D-penicillamine. The significance of these findings are discussed.
Two children with Juvenile Rheumatoid Arthritis (JRA) and severe growth suppression from corticosteroid therapy are described. Prolonged 'tailing-off' of steroids occurred during outpatients follow-up and this may be related to the high turnover of doctors involved. Suggestions for improving such follow-ups and caution against the continuous use of steroids are made.
Study site: Queen Elizabeth Hospital, Kota Kinabalu, Sabah, Malaysia
410 cases of psoriasis [282 males (68%) and 127 females (31%)] were interviewed and examined to study the nail changes. The prevalence of nail changes was 78.0% (males = females). Common changes were pitting (67.5%) and onycholysis (67.2%). Dystrophy of varying degrees occurred in 35.0%, subungual hyperkeratosis in 24.7%, discoloration in 18.4%, loss of nails in 2.8% and pustulation in 1.3%. Pitting and onycholysis was the most common combination (45.6%). Nail changes were significantly more common in patients who have moderate to severe psoriasis as compared with patients with mild psoriasis; in patients who have psoriasis for greater than 5 years as compared with patients who have psoriasis for less than 5 years; and in patients older than age 50 as compared with those aged less than 50. A definite correlation was found between the prevalence of nail changes and the presence of scalp and periungual psoriasis, and the presence of joint involvement.
Cerebral involvement associated with juvenile rheumatoid arthritis is rare. It is not influenced by treatment and the presentation can be varied. We describe a case of cerebral infarction secondary to vasculitis in a child with juvenile rheumatoid arthritis.
We report a patient with hyperosmolar non-ketotic hyperglycaemia who presented with chorea and septic arthritis on his knee. The chorea resolved completely and quickly with correction of the metabolic disturbance, only to return just as quickly when his metabolic disturbance subsequently deteriorated as a result of overwhelming septicaemia, suggesting coexisting cerebral ischaemia, although the basis of focal neurological sign in non-ketotic hyperglycaemia remains controversial.
Components of kallikrein-kininogen-kinin are activated in response to noxious stimuli (chemical, physical or bacterial), which may lead to excessive release of kinins in the synovial joints that may produce inflammatory joint disease. The inflammatory changes observed in synovial tissue may be due to activation of B2 receptors. Kinins also stimulate the synthesis of other pro-inflammatory agents (PGs, LTs, histamine, EDRF, PGI2 and PAF) in the inflamed joint. B2 receptor antagonists may provide valuable new analgesic drugs. The mode of excessive kinin release in inflamed synovial joints leads to stimulation of pro-inflammatory actions of B2 kinin receptors. These properties could be antagonized by novel B2 receptor antagonists (see Fig. 4). Further, it is suggested that substances directed to reduce the activation of KKS may provide a pharmacological basis for the synthesis of novel antirheumatic or anti-inflammatory drugs.
Components of the kallikrein-kininogen-kinin are activated in response to noxious stimuli (chemical, physical or bacterial), which may lead to excessive release of kinins in the synovial joints that may produce inflammatory joint disease. The inflammatory changes observed in synovial tissue may be due to activation of B2 receptors. Kinins also stimulate the synthesis of other pro-inflammatory agents (PGs, LTs, histamine, EDRF, PGI2 and PAF) in the inflamed joint. B2 receptor antagonists may provide valuable agents as new analgesic drugs. Further, it is suggested that substances directed to reduce the activation of KKS may provide a pharmacological basis for the synthesis of novel anti-rheumatic or anti-inflammatory drugs.
The mechanisms causing inflammation in rheumatoid arthritis (RA) are not yet clearly known. They may be associated with different types of inflammatory cells and probably numerous mediators (SHARMA and MOHSIN 1990). Nowadays, the platelet activating factor (PAF) is discussed as an important mediator in RA.
Kinins are potent mediators of rheumatoid inflammation. The components of the kinin-forming system are hyperactive in RA. Excessive release of kinins in the synovial fluid can produce oedema, pain and loss of functions due to activation of B1 and B2 receptors. These receptors could be stimulated via injury, trauma, coagulation pathways (Hageman factor and thrombin) and immune complexes. The activated B1 and B2 receptors might cause release of other powerful non-cytokines and cytokines mediators of inflammation, for example, PGE2, PGI2, LTs, histamine, PAF, IL-1 and TNF derived mainly from polymorphonuclear leukocytes, macrophages, endothelial cells and synovial tissue. These mediators are capable of inducing bone and cartilage damage, hypertrophic synovitis, vessels proliferation, inflammatory cells migration, and possibly angiogenesis in pannus formation. These pathological changes, however, are not yet defined in human model of chronic inflammation (RA). Hence, the role of kinin and its interacting inflammatory mediators would soon start to clarify the detailed questions they revealed in clinical and experimental models of chronic inflammatory joint diseases. Several B1 and B2 receptor antagonists are being synthesized in an attempt to study the molecular functions of kinins in inflammatory processes (RA, periodontitis and osteomyelitis), and they represent and important area for continued research in rheumatology. Future development of specific, potent and stable B1 and B2 receptor antagonists or combined B1 and B2 antagonists with y-IFN might serve as pharmacological basis of more effective rationally-based therapies for RA. This may lead to significant advances in our knowledge of the mechanisms and therapeutics of rheumatic diseases.
Fourteen cases of sarcoidosis consisting of 7 male and 7 female patients with a mean age of 42.4 years were seen at the University Hospital from 1972 to 1990. There were 10 Indians, 2 Malays, and 2 Chinese. Twelve patients had thoracic involvement. The other common disease manifestations included weight loss, arthralgia, hepatomegaly, erythema nodosum, peripheral lymphadenopathy, and hypercalcaemia. At initial presentation, the disease was in radiographic stage I, II, and III in 8, 3 and one patient respectively. The Kveim test was positive in 7 out of 9 patients. Eight patients required steroid therapy.
Seventy consecutive patients with definite or classical RA attending a University Hospital Rheumatology Clinic in Malaysia, were compared with an age, sex, disease duration matched group of RA patients seen in a British University Hospital. There were no differences in measures of disease activity, overall functional status or serological status in the two groups. However significant differences were seen in both the articular and extra-articular manifestations of the disease in the two countries. British patients had more severe disease in the feet, and a higher prevalence of nodules, vasculitis and pulmonary fibrosis. The Malaysian population had fewer erosions, more frequent involvement of the wrists and cervical spine, and a much higher incidence of secondary sicca syndrome. Radiographic changes were generally milder in Malaysian patients. Possible reasons for these differences in the expression of RA in the two countries are discussed.