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Fosamax
First of all, please understand that we DO NOT suggest that people disregard the advice of their physician. Period. I have made remarks about Fosamax, including the observation that bone density increases in multinational tests have been less than thrilling (6-7%) and that the rate of increase appears to decline over time. Most important, recent clinical trials show that the drug does not decrease fracture risk! (see reference # 1 below). Considering the multiple drug interactions, contraindications and adverse side effects, how can one explain the fact that doctors are writing prescriptions for this drug so fast they get writers cramp?
I believe it has to do with TIME. To go over a woman's diet and lifestyle, to show her specific weight-bearing exercises that will be effective and get her to understand that Osteoporosis is a METABOLIC disorder and NOT merely a calcium deficiency... All of that takes TIME. You can write a prescription for Fosamax in about 30 seconds.
Of course, you then have to carefully warn the patient not to lay down after taking this drug because it will burn the heck out of their esophagus. But still.. prescribing Fosamax saves time... Even if evidence suggests that it does not reduce fracture risk. In a study just published in Gastroenterology (reference # 3 below) the incidence of gastric, esophageal and duodenal ulcer was 15% after only 2 weeks of Fosamax use.
I hope you're getting my point. People do not have osteoporosis due to a Fosamax deficiency. Research - the latest one being Baulieu's year-long study with DHEA replacement - shows that bone density can be increased by restoring anabolic metabolism - even without supplementing with calcium. Obviously, it is best to do both; restore anabolic drive (the repair signal) AND provide the raw materials for that repair.
Conclusion: It is not for us to go out and tell people to disregard the advice of their physicians but to involve everyone - researcher, physician and patient in a productive discussion that will result in the best care and the best outcome.
Sincerely,
Stephen Cherniske
REFERENCES:
1. Alendronic acid in primary prevention: new indication. No reduction in fracture risk. Prescrire Int 2000 Jun;9(47):70-2
(1) Alendronic acid at a dose of 5 mg/day is now licensed in France for primary prevention of postmenopausal fractures. (2) The clinical file is relatively bulky and methodologically adequate, but there are no comparisons with combined hormone replacement therapy or with raloxifen. (3) Three trials have shown that 5 mg/day alendronic acid slows postmenopausal bone loss. However, this effect disappears on treatment cessation, and mineral bone density is only one risk factor for postmenopausal fractures. (4) A placebo-controlled trial of primary prevention involving more than 4,000 patients showed no reduction in the risk of fracture after 4 years of treatment with alendronic acid (5 mg/day for 2 years, then 10 mg/day). (5) Alendronic acid increases the risk of oesophageal ulceration, necessitating strict precautions during ingestion.
2. Abraham SC, Cruz-Correa M, Lee LA, Yardley JH, Wu TT. Alendronate-associated esophageal injury: pathologic and endoscopic features. Mod Pathol 1999 Dec;12(12):1152-7
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2196, USA. sabraha@welchlink.welch.jhu.edu
Ingestion of alendronate sodium (Fosamax) by osteoporotic patients can be associated with esophagitis and esophageal ulcer. Alendronate can damage the esophagus both by toxicity from the medication itself and by nonspecific irritation secondary to contact between the pill and the esophageal mucosa, similar to other cases of "pill esophagitis." Despite its wide use, the histologic appearances of alendronate-associated esophageal ulceration have not been previously described in detail, nor is this type of medication-induced injury commonly appreciated by pathologists when evaluating biopsies from ulcer sites. We report a series of 10 patients who experienced erosive/ulcerative esophagitis while ingesting alendronate, and describe the associated endoscopic and pathologic features. Biopsies from all patients showed inflammatory exudate and inflamed granulation tissue as characteristic of any ulcer site. Polarizable crystalline foreign material was present in six of 10 biopsies (60%). Multinucleated giant cells within the inflammatory exudate were
present near this crystalline foreign material in three of 10 biopsies (30%) Adjacent squamous epithelium typically showed active inflammation and a reactive appearance with enlarged, hyperchromatic nuclei. Multinucleated squamous epithelial giant cells were present in two of 10 cases (20%). Microorganisms were unusual; scattered fungi and/or viral inclusions were present in only two of 10 biopsies (20%). Recognition of alendronate-associated erosive or ulcerative esophagitis, particularly in postmenopausal women, and communication of this possibility to the clinician can improve patient care.
3: Lanza FL, Hunt RH, Thomson AB, Provenza JM, Blank MA. Endoscopic comparison of esophageal and gastroduodenal effects of risedronate and alendronate in postmenopausal women. Gastroenterology 2000 Sep;119(3):631-8.
Houston Institute for Clinical Research, Houston, Texas 77074, USA.
BACKGROUND & AIMS: This study compared the incidence of gastric ulcers after treatment with risedronate, a pyridinyl bisphosphonate, and alendronate, a primary amino bisphosphonate. Esophageal and gastroduodenal injury assessed by endoscopy scores was a secondary endpoint. METHODS: Healthy, postmenopausal women (n = 515) received 5 mg risedronate (n = 255) or 10 mg alendronate (n = 260) for 2 weeks. At baseline and on days 8 and 15, subjects underwent endoscopy and evaluator-blinded assessment of the esophageal, gastric, and duodenal mucosa. RESULTS: Gastric ulcers were observed during the treatment period in 9 of 221 (4.1%) evaluable subjects in the risedronate group compared with 30 of 227 (13.2%) in the alendronate group . Mean gastric endoscopy scores for the risedronate group were lower than those for the alendronate group at days 8 and 15 (P </= 0.001). Mean esophageal and duodenal endoscopy scores were similar in the 2 groups at days 8 and 15. Esophageal ulcers were noted in 3 evaluable subjects in the alendronate group, compared with none
in the risedronate group, and duodenal ulcers were noted in 1 evaluable subject in the alendronate group and 2 in the risedronate group. CONCLUSIONS: At doses used for the treatment of osteoporosis, risedronate was associated with a significantly lower incidence of gastric ulcers than alendronate. These findings confirm that bisphosphonates differ in their potential to damage the gastroesophageal mucosa.
4. Baulieu EE, Thomas G, Legrain S, Lahlou N, Roger M, Debuire B, Faucounau V, Girard L, Hervy MP, Latour F, Leaud MC, Mokrane A, Pitti-Ferrandi H, Trivalle C, de Lacharriere O, Nouveau S, Rakoto-Arison B, Souberbielle JC, Raison J, Le Bouc Y, Raynaud A, Girerd X, Forette F Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: contribution of the DHEAge Study to a sociobiomedical issue. Proc Natl Acad Sci U S A 2000 Apr 11;97(8):4279-84
Institut National de la Sante et de la Recherche Medicale Unit 488 and College de France, 94276 Le Kremlin-Bicetre, France. baulieu@kb.inserm.fr
The secretion and the blood levels of the adrenal steroid dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) decrease profoundly with age, and the question is posed whether administration of the steroid to compensate for the decline counteracts defects associated with aging. Two hundred and eighty healthy individuals (women and men 60-79 years old) were given DHEA, 50 mg, or placebo, orally, daily for a year in a double-blind, placebo-controlled study. No potentially harmful accumulation of DHEAS and active steroids was recorded. Besides the reestablishment of a "young" concentration of DHEAS, a small increase of testosterone and estradiol was noted, particularly in women, and may be involved in the significantly demonstrated physiological-clinical manifestations here reported. Bone turnover improved selectively in women >70 years old, as assessed by the dual-energy x-ray absorptiometry (DEXA) technique and the decrease of osteoclastic activity. A significant increase in most libido parameters was also found in these older women.
Improvement of the skin status was observed, particularly in women, in terms of hydration, epidermal thickness, sebum production, and pigmentation. A number of biological indices confirmed the lack of harmful consequences of this 50 mg/day DHEA administration over one year, also indicating that this kind of replacement therapy normalized some effects of aging, but does not create "supermen/women".
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