LETTER
Astemizole in the Treatment of Granulocyte Colony-Stimulating Factor-Induced Bone Pain
Rajashree Gudi;
Muthuswamy Krishnamurthy; and
Bruce R. Pachter
1 August 1995 | Volume 123 Issue 3 | Pages 236-237
TO THE EDITOR:
Granulocyte colony-stimulating factor (G-CSF) is commonly used to stimulate the production of granulocytes. A major side effect of G-CSF is bone and generalized muscle pain, which can last for 10 or more days. The pain may be severe enough to require narcotic analgesics [1]. It has been suggested that G-CSF may potentiate the inflammatory reaction by causing distinct cellular signaling and by increasing the histamine release [2]. An increase in histamine levels has been shown to cause nociceptive c-fiber-mediated pain and neuropathic pain [3]. Bennett [4] suggested that high levels of histamine can increase edema formation within bone; the increased pressure leads to pain. Investigators have observed that antihistamines such as terfenadine and astemizole have anti-inflammatory properties in addition to their potency as histamine-1 antagonists [5].
We report a case in which G-CSF-induced bone pain and generalized myalgia resolved with an oral antihistamine (astemizole).
A 59-year-old woman with bilateral breast cancer was treated every month with taxol, 390 mg, by intravenous infusion over 24 hours. Granulocyte colony-stimulating factor was administered for 10 days after taxol treatment. The patient reported generalized myalgia and bone pain that was not relieved by Tylenol (McNeil Consumer Products Company, Fort Washington, Pennsylvania) during her previous chemotherapy cycles. During her last cycle of chemotherapy, astemizole was given concurrently with G-CSF as follows: 30 mg once on day 1; 20 mg once on day 2, and 10 mg once a day on days 3 to 10. Pain completely resolved during this full chemotherapeutic cycle.
Taxol-induced bone and muscle pain, which usually lasts for 24 to 72 hours, has been reported to be relieved by terfenadine [5]. Our patient had continuous pain that lasted for 10 days, suggesting that G-CSF was responsible. Oral antihistamine therapy appears to be effective in resolving G-CSF-induced pain.
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Author and Article Information
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New York Methodist Hospital; Brooklyn, NY 11215.
1. Weaver CH, Buckner CD, Longin K, Appelbaum FR, Rowley S, Lilleby K, et al. Syngeneic transplantation with peripheral blood mononuclear cells collected after the administration of recombinant human granulocyte colony-stimulating factor. Blood. 1993; 82:1981-4.
2. Konig B, Konig W. Effect of growth factors on Escherichia coli 
-hemolysin-induced mediator release from human inflammatory cells. Involvement of the signal transduction pathway. Infect Immun. 1994; 62:2085-93.
3. Baron R, Saguer M. Postherpetic neuralgia. Are c-nociceptors involved in signaling and maintenance of tactile allodynia? Brain. 1993; 116:1477-96.
4. Bennett A. The role of biochemical mediators in peripheral nociception and bone pain. Cancer Surv. 1988; 7:55-67.
5. Martoni A, Zamagni C, Gheka A, Pannuti F. Antihistamines in the treatment of taxol-induced paroxystic pain syndrome. J Natl Cancer Inst. 1993; 85:676.
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