Iron deficiency anaemia in patients with rheumatic disease receiving non-steroidal anti-inflammatory drugs: the role of upper gastrointestinal lesions

Article Abstract:

Arthritis patients who take non-steroidal anti-inflammatory drugs (NSAIDs, including aspirin and ibuprofen) often develop anemia, a deficiency of red blood cells. Impaired metabolism of iron or iron deficiency may be the cause. It has been thought that blood loss from upper gastrointestinal (stomach and upper intestine) lesions associated with NSAID treatment may cause iron deficiency. However, recent studies have shown that lesions also occur in the lower intestine and colon. The relationship between healing of upper gastrointestinal (GI) lesions and iron deficiency was studied in 104 patients with rheumatic disease and iron deficiency, to determine if there was a cause-and-effect relationship. In the records studied, half of the patients had upper GI lesions, indicating that the significance of these lesions in anemia may be overestimated. Healing was studied by endoscopy in half of these patients, and anemia improved in 56 percent of the healed patients. Other factors besides healing may have been associated with improvement of anemia. Neither indigestion nor a positive fecal occult blood test was associated with upper GI lesions. Further investigation of the lesions in the small intestine and of other factors is needed to establish the cause of iron-deficiency anemia in rheumatoid diseases. (Consumer Summary produced by Reliance Medical Information, Inc.)

Gastrointestinal mucosa, Rheumatic diseases, Iron deficiency anemia

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Effect on gastric and duodenal mucosal prostaglandins of repeated intake of therapeutic doses of naproxen and etodolac in rheumatoid arthritis

Article Abstract:

Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, indomethacin, and ibuprofen, decrease the inflammation of arthritis, but can damage the gastric mucosa (stomach lining). The damage is considered to be due to suppression of stomach prostaglandins, which are hormones manufactured and acting locally in many tissues. Etodolac is a new type of NSAID that is reported to have fewer gastric side effects. Its effects were compared with those of naproxen (another NSAID) in 27 patients with rheumatoid arthritis. Naproxen suppressed gastric levels of prostaglandin E2 and duodenal (intestinal) levels of prostaglandin E2 and I2, while etodolac did not. Naproxen patients had somewhat higher levels of thromboxane B2 (a derivative of prostaglandins) than etodolac patients. Naproxen and etodolac had similar anti-inflammatory effects, so that morning stiffness and joint flexibility were enhanced by treatment. Both drugs caused gastritis (inflammation of the stomach mucosal lining), although it was less frequent in etodolac-treated patients. There was no correlation between prostaglandin levels and mucosal damage. The results show that not all NSAIDs suppress prostaglandins in the digestive tract, but other factors associated with NSAIDS may lead to gastric disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Prostaglandins, Naproxen

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Effect of cyclosporin A on interleukin-6 and soluble interleukin-2 receptor in patients with rheumatoid arthritis

Article Abstract:

Cyclosporin A may reduce concentrations of inflammatory promotion factors circulating in the blood of patients with rheumatoid arthritis (RA). Blood plasma samples were collected and analyzed from 24 RA patients with active disease before and after 16 weeks treatment with cyclosporin A. Average levels of interleukin-6, an inflammatory factor produced in diseased joints by white blood cells and connective tissue forming cells, decreased from 165 IU ml to 71 IU ml. Average levels of soluble interleukin-2 receptor, a marker of lymphocyte (a type of white blood cell) activation, decreased from 665 U ml to 570 U ml. The decrease correlated with improvement in morning stiffness and score on the Ritchie articular index and a decrease in the number of swollen joints. Pain assessment scores did not improve.

Physiological aspects, Cyclosporine, Cyclosporins, Interleukin-2, Interleukin-6, Drug receptors

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