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Cure Arthritis Naturally

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Beehrle DM and Evans D. A review of NSAID complications: Gastrointestinal and more. Prim Care Pract 1999;3:305-315.

Case JP. Old and new drugs used in rheumatoid arthritis: A historical perspective. Part 1: The older drugs. Am J Ther 2001;8:123-143.

Case JP. Old and new drugs used in rheumatoid arthritis: A historical perspective. Part 2: The newer drugs and drug strategies. Am J Ther 2001;8:163-179.

Kremer JM. Rational use of new and existing disease-modifying agents in rheumatoid arthritis. Ann Intern Med 2001;134:695-706.

Lee DM and Weinblatt ME. Rheumatoid arthritis. Lancet 2001;358:903-911.

McCarberg BH and Herr KA. Osteoarthritis: How to manage pain and improve patient function. Geriatrics 2001;56:14-17,20-22,24.

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Case Study A Visit to University Student

A21-year-old college student presented to her university's student health center with an acute exacerbation of asthma. Her respiratory rate was increased, and she was in obvious respiratory distress, with wheezes audible on both sides of the chest. The examination of the nasal passages revealed mucosal edema and a polyp on the right. There was marked swelling about the eyes, and her upper lip was swollen (angioedema). Her fingertips were slightly cyanotic. Her peak expiratory flow rate was 25% of the predicted normal value. Oxygen was given by face mask. She was given 1:1000 aqueous epinephrine 0.3 mL subcutaneously, diphenhydramine HCl 50 mg intramuscularly, and prednisone 40 mg by mouth. Subsequently she was given nebulized albuterol, and the peak flow rate improved to 75% of predicted. When questioned further, she said she had taken a friend's ibuprofen for menstrual cramps.

The case in context: Dysmenorrhea is a common condition caused by uterine contraction during menses. PGF2a may be the uterine contractant.


NSAIDs, such as ibuprofen, relieve dysmenorrhea by inhibiting the biosynthesis of PGF2a.This allows for enhanced production of the leukotrienes by a 5-lipoxygenase. The leukotrienes are potent bron-choconstrictors, and patients with asthma and nasal polyps are often much more sensitive to them than are other asthmatics and normal individuals. The logic of her therapy is as follows: Oxygen is needed in patients with peak flow rates less than 30% of their predicted value; epinephrine is a bronchodila-tor (p-adrenergic effect) and vasoconstrictor that prevents further angioedema (a-adrenergic effect); diphenhydramine is an H1 antihistamine; albuterol is a p2-adrenergic agonist; prednisone (a glucocorti-coid) is the most effective drug for asthma. Although its onset of action is slow (about 4 hours), many patients with an acute attack of asthma have a late response several hours later due to the influx and activation of lymphocytes, eosinophils, and perhaps neutrophils, which release further mediators of inflammation, such as the leukotriene-5. The patient should be warned to avoid NSAIDs in the future.

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