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Clinical research on heroin in cancer pain control

American Journal of Hospice & Palliative Care Volume 17, Number 1, January/February 2000 In the 1980s, a debate raged over the use of heroin in cancer pain. Sides were drawn, studies were performed, and in the end the conclusion seemed to be “the relative efficacy of heroin and morphine in the relief of chronic cancer pain remains unknown.”1 Since then, very few studies have been published on heroin versus other opioids. In fact, a Medline search using the terms “heroin AND neoplasms AND pain” (MeSH terms) generated only two hits in the last five years. Reaching back 10 years yielded eight citations, but 20 years generated 37. One argument against the use of heroin (diacetylmorphine) is that it offers nothing over the opioids that we already have at our disposal, and introducing yet another potentially troublesome drug to the marketplace would therefore be a mistake. Interestingly, there is mounting evidence that opioids have immune response and tumor growth rate modulating activities. A study from Ohio State University showed that the opioid antagonist naltrexone reduced the overall size of mammary tumors in rats over a 25-day period. Tumor regression occurred in 75 percent of rats who were given naltrexone orally, and those tumors were primarily estrogen and progesterone receptor positive.2 Human breast cancer cells have been shown to have opioid peptide immunoreactivity, and, in one study from Denmark, 56 percent of the invasive ductal carcinomas from 61 premenopausal women were found to have cells expressing opioid reactivity.3 The endogenous opiate dynorphin has been shown to increase the growth of a prostatic carcinoma cell line, an effect blocked by naloxone and thought to be due to stimulation of the kappa opioid receptor.4 Naloxone had a starring role in a Japanese study involving human ovarian carcinoma cells. Nude mice were inoculated with growth culture cells derived from a human ovarian cancer cell line. The mice were either pretreated or post-treated with naloxone. The study showed that “in comparison to a median survival time of 38 days for untreated controls, the naloxone preand post-treated groups showed increases of 26 to 71 percent in median survival.”5 Morphine was actually shown to increase metastatic tumor growth of a certain carcinosarcoma cell line in a 1986 study. Rats were inoculated with the tumor cells and then morphine was administered. There was a significant increase in subpulmonic metastases in the morphine group, with blockade of this effect by pretreatment with naloxone. Contrary to expectation, naloxone alone did not influence the number of metastases. Co-administration of pentazocine (an agonist to kappa receptors, but imperfectly antagonistic of receptors) partially blocked the enhancing effects of morphine.6 The mechanism of morphine’s enhancement of the growth of certain tumors is suggested in a Japanese study from 1993. Morphine-treated mice showed decreased Tand B-cell Clinical research on heroin in cancer pain control