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Biomedical subjects

E C Huskisson

Publications and source records attributed to E C Huskisson.

At least 55 records · Page 3Linked to original sources
PubMed1988

Low free testosterone levels in rheumatoid arthritis.

The androgen status of 25 male patients with rheumatoid arthritis (RA) was assessed and compared with that of age matched controls with osteoarthritis (OA). Significantly reduced levels of serum free testosterone were found in the RA group. Within that group free testosterone was unrelated to all indices of disease activity measured, though it was strongly related to latex positivity. These results support the hypothesis that male sex hormones may have a protective role in RA, though prospective studies would be necessary to determine whether the relation was one of cause or effect.

Adult↗
PubMed1988

Arthritis in Down's syndrome.

A 31 year old man with Down's syndrome presented with a 10 year history of an inflammatory polyarthritis resembling juvenile chronic arthritis. This case was similar to those already reported of an arthropathy associated with Down's syndrome but was eventually found to be gout. This emphasised the importance of serum uric acid estimation in patients with Down's syndrome and coexistent arthritis.

Adult↗
PubMed1988

Pharmacologic and non-drug therapies for osteoarthritis.

Many treatments have been shown to relieve symptoms in osteoarthritis but none have been found to influence the course of the disease. In the context of a symposium on cartilage changes in osteoarthritis, the major interest is in the possible action of non-steroidal anti-inflammatory drugs, either favourable or unfavourable, on the progression of cartilage destruction in this disease. On the one hand, there is experimental evidence that some anti-inflammatory drugs like indomethacin can adversely affect cartilage or interfere with repair mechanisms. Others like tiaprofenic acid do not have such effects. There is largely anecdotal evidence that indomethacin therapy can lead to rapid progression of hip disease in osteoarthritis. On the other hand, it is traditionally postulated that the process of inflammation with the release of enzymes and other noxious substances in diseases like rheumatoid arthritis, leads to cartilage damage. Anti-inflammatory drugs might be expected to inhibit such a process as they do in animal models. The long term actions of anti-inflammatory drugs are now being explored in a large scale prospective trial which should provide an answer to the question of whether anti-inflammatory drugs are good or bad for osteoarthritis. Meantime they remain the major symptomatic therapy for the disease.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

Milestones in anti-inflammatory therapy.

The anti-inflammatory era opened with aspirin, which for decades was the first-line treatment for rheumatoid arthritis. Striking advances have occurred in recent years with the introduction of propionic acid derivatives like ibuprofen and once-a-day drugs like piroxicam. The class now includes a range of drugs with properties suited to the range of clinical indications presented by rheumatic disorders. Anti-inflammatory drugs are now and will continue to be the mainstay of symptomatic therapy for arthritis.

Aged↗
PubMed1987

An in vitro system for studying cartilage degradation by macrophages.

Cartilage damage in inflammatory arthritis may be mediated by a number of cell types; the macrophage is one of them. To examine their role we developed a new macrophage-cartilage co-culture system on a microscale. This used macrophages derived from the peritoneal cavity of Balb/c mice together with cartilage slices from bovine nasal septa. We examined the effects of macrophages on cartilage proteoglycan loss measured colorimetrically. When chondrocytes were dead, cartilage released proteoglycan; macrophages increase the amount of proteoglycan loss; stimulating macrophages with zymosan further increased proteoglycan loss. With live chondrocytes the situation was different. Macrophages only gave a major increase in cartilage proteoglycan loss when stimulated by zymosan. These results show it is possible to establish a simple model of macrophage-induced cartilage degradation. In this a variety of effects given by macrophages can be demonstrated depending on the presence or absence of live chondrocytes.

Animals↗
PubMed1986

Rheumatoid inflammation and joint destruction: cause and effect or parallel phenomena?

Joint damage is a characteristic and important consequence of rheumatoid arthritis; it is usually considered to be a direct result of the inflammatory synovitis. This view implies that by treating actively the synovial inflammation subsequent joint damage will be reduced and the long-term outlook of patients with rheumatoid arthritis thus improved. However, there is relatively little clinical evidence that suppressing inflammation reduces rheumatoid joint damage. An alternative view is that the mechanisms causing inflammation and those leading to joint destruction are parallel processes related only indirectly. Considerable evidence supports such a concept. Clinical studies show radiological progression of the disease occurs despite improvements in measures of joint inflammation and a reduction in the levels of acute phase proteins. Damage can progress in either actively inflamed hot joints or cool swollen joints. Histopathologically the features of rheumatoid synovitis are non-specific, while the radiological pattern of joint damage is very characteristic. There is evidence that lymphocytic infiltration is not a poor prognostic finding, despite it being a typical feature of inflamed joints. Experimental studies also fail to show a close correlation between inflammation and cartilage damage: this is seen in experimental arthritis, coculture in vitro systems, and the air pouch model of cartilage damage. We suggest that attempts to improve the outcome of rheumatoid arthritis should not merely concentrate on controlling inflammation but should also seek to modify the associated connective tissue changes of the disease.

Anti-Inflammatory Agents↗
PubMed1985

Arthritis and coeliac disease.

We report six patients with coeliac disease in whom arthritis was prominent at diagnosis and who improved with dietary therapy. Joint pain preceded diagnosis by up to three years in five patients and 15 years in one patient. Joints most commonly involved were lumbar spine, hips, and knees (four cases). In three cases there were no bowel symptoms. All were seronegative. X-rays were abnormal in two cases. HLA-type A1, B8, DR3 was present in five and B27 in two patients. Circulating immune complexes showed no consistent pattern before or after treatment. Coeliac disease was diagnosed in all patients by jejunal biopsy, and joint symptoms in all responded to a gluten-free diet. Gluten challenge (for up to three weeks) failed to provoke arthritis in three patients tested. In a separate study of 160 treated coeliac patients attending regular follow up no arthritis attributable to coeliac disease and no ankylosing spondylitis was identified, though in a control group of 100 patients with Crohn's disease the expected incidence of seronegative polyarthritis (23%) and ankylosing spondylitis (5%) was found (p less than 0.01). Arthritis appears to be a rare manifestation of coeliac disease. This relationship may provide important clues to the role of gastrointestinal antigens in rheumatic diseases.

Adolescent↗
PubMed1984

The influence of D-penicillamine therapy on numbers of circulating immunoglobulin secreting cells in rheumatoid arthritis.

Higher numbers of plaque forming (immunoglobulin secreting) cells have been reported among peripheral blood mononuclear cells from patients with active rheumatoid arthritis than from patients with spontaneously inactive disease. Patients treated with D-penicillamine who showed a good clinical response were found to have lower numbers of circulating plaque forming cells than were detected in the active rheumatoid group. Similar numbers of plaque forming cells were detected in patients who showed a poor clinical response to D-penicillamine as in the active rheumatoid group (untreated with 'second line' drugs). Active rheumatoid arthritis is associated with increased numbers of plaque forming cells in the peripheral blood, changes in the numbers of these cells providing an index of disease activity.

Arthritis, Rheumatoid↗
PubMed1984

Increased numbers of active B cells in the circulation of patients with rheumatoid arthritis.

Increased numbers of cells secreting immunoglobulins of class G, M and A have been demonstrated in the peripheral blood of patients with active rheumatoid arthritis using the reverse haemolytic plaque assay. Lower numbers of secreting cells were detected in rheumatoid patients in spontaneous remission. Culture of the peripheral blood mononuclear cells was associated with a fall in the number of immunoglobulin secreting cells. Values for rheumatoid and normal cells did no differ significantly after 3 days of culture. The presence of an activating factor in th rheumatoid patients is postulated.

Aged↗
PubMed1984

Non-steroidal anti-inflammatory drugs. Current status and rational therapeutic use.

Aspirin (acetylsalicylic acid), the first of the NSAIDs (introduced in 1899), was initially never referred to as an anti-inflammatory agent. It was the advent of cortisone in 1949 that demonstrated dramatically that corticosteroids had anti-inflammatory properties and the term 'non-steroidal anti-inflammatory drug' was first used when phenylbutazone was introduced 3 years later. Since then, the NSAIDs have proliferated. There is to date no good evidence that they halt progression of rheumatoid disease, but by easing pain and diminishing swelling they make life much easier in osteoarthrosis, rheumatoid arthritis and many other types of arthritis, and are the drugs of first choice in acute gout. Their mode (or modes) of action are obscure and though inhibition of cyclo-oxygenase (prostaglandin synthetase) is clearly important, other mechanisms are also involved. The assessment of the anti-inflammatory action of these agents has received considerable attention in clinical trials because, whatever their action may be in experimental animal models, their action in inflamed joints in human patients must be ascertained, since there may be little parallel between the two. Different experimental animal models give different results with various agents and often bear little relation to their therapeutic action in man. No attempt has been made here to review in depth all the NSAIDs that have appeared since 1952. All have anti-inflammatory and analgesic activity and all can cause gastrointestinal side effects, though effectiveness and toxicity vary from drug to drug and patient to patient, there being very great interpatient variability. Non-reactors, patients who apparently fail to respond to certain agents, need further study, for it seems that these subjects may metabolise these agents differently from others. Considerable ingenuity has been shown not only in evolving new NSAIDs but in finding new ways of administering them. The number and variety of NSAIDs in their various forms varies greatly from country to country, depending largely on the regulatory bodies of those countries. In the meantime, the search for a better, less toxic compound continues with the hope that one may be found which has a deeper and more basic action on the underlying disease process.

Animals↗