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Biomedical subjects

A Isdale

Publications and source records attributed to A Isdale.

8 recordsLinked to original sources

Direct erosion of lumbar spine by an abdominal aortic aneurysm, resulting in paraparesis: unusual presentation. Case report.

Abdominal aortic aneurysm is a condition affecting nearly 4% of the elderly population. It has a potential for producing a wide range of symptoms, including abdominal pain and back pain. The latter is particularly difficult to interpret in patients with chronic rheumatological conditions, and delayed diagnosis may be associated with a poor outcome. We present a patient with rheumatoid arthritis and chronic low back pain, who developed bilateral leg weakness and hesitancy of micturition, due to an abdominal aortic aneurysm invading the spine.

Aged↗

The effect of non-steroidal anti-inflammatory drugs on faecal flora and bacterial antibody levels in rheumatoid arthritis.

The faecal flora and bacterial antibody levels of 22 patients with active rheumatoid arthritis (RA) were compared with those of 26 patients with osteoarthritis (OA) undergoing comparable treatment with non-steroidal anti-inflammatory drugs (NSAIDs), and a further 22 patients with OA who were not receiving NSAIDs. Faecal counts of Clostridium perfringens were significantly higher in the RA patient group and in those OA patients receiving NSAIDs, compared with those OA patients not taking NSAIDs (P = 0.032, P = 0.0004 respectively). Total aerobic and anaerobic counts were, however, identical in all three groups. Levels of serum IgA antibody to the alpha toxin of Cl. perfringens were higher in the RA group and in the OA group taking NSAIDs than in OA patients not taking NSAIDs (P = 0.011, P = 0.055). Serum IgG antibody to alpha toxin was higher in the RA group than in OA patients both on and off NSAIDs (P = 0.019, P = 0.0072) and also a group of normal controls (P = 0.032). These results suggest that the increased faecal counts of Cl. perfringens together with the associated increased antibody levels seen in this and previous studies are more likely to result from NSAID therapy used to treat the disease than from a disease specific change in bowel flora.

Adult↗

Human nocturnal blood melatonin and liver acetylation status.

The human dark phase melatonin concentrations exhibit a wide range of values. In an attempt to explain this variation, we measured 2250-2305 h melatonin levels by radioimmune assay in eleven fast and eleven slow acetylator phenotypes. No statistical difference between the two groups existed, suggesting therefore that such variations are not due to acetylator status. The study revealed a negative relationship between body weight or area and nocturnal melatonin concentration. No correlation was found between dark phase melatonin levels and age, anxiety, depression, or sleep rating.

Acetylation↗

Seronegative arthritis and the bowel.

In this chapter we have outlined the seronegative spondarthritides associated with bowel disease, excluding those discussed in separate chapters. Although, traditionally, Crohn's disease and ulcerative colitis have been dealt with separately in any discussion of seronegative arthritides, they have been discussed together here for the following reasons. Despite being pathologically distinct they show remarkable similarity in extraintestinal manifestations including any associated arthritis. Any observed differences in prevalence rates of arthritis may be secondary to the relative difficulty in diagnosing Crohn's disease, and most of the important prevalence studies were done before the more sophisticated techniques to investigate the bowel became available. This may in part explain the dramatic increase in the world-wide incidence of Crohn's disease seen in the last 30 years, particularly through the 1970s, but which has fallen off recently (Miller et al, 1974). It would seem that the body has a limited means of expressing disease processes. The final common pathway of a number of quite distinct disease entities is the concept of the seronegative spondarthritides. Exactly how the microbiological, immunogenetic and molecular factors interact to produce a particular disease end-point is currently not clearly defined, but with the increasingly sophisticated means to investigate the body at a cellular level the explanations may soon be at hand. Further controlled family studies are also needed to define the genetic relationships more precisely. We may then be able to piece the jigsaw puzzle together.

Arthritis↗