Low Dose Naltrexone and Lung Cancer: A Case Report and Discussion

Abstract

Low dose naltrexone (LDN) has been promising as a complementary medication for patients with a broad range of medical disorders. Although not a proven cure, evidence from clinical trials supports LDN as being a valuable adjunct for disorders in which the immune system plays a centralized role. Additionally, clinical trials have proposed a unique mechanism(s) allowing LDN to affect tumors including non-small cell lung cancer (NSCLC) at the cellular level by augmenting the immune system. We present a case of a 50-year-old male with a prolonged survival and a past medical history of prostate and lung cancer.

Impact of Opioid Use in Hematological Malignancies: Clinical, Immunological and Concomitant Aspects

“…Low-dose naltrexone (LDN) can be administered within the therapeutic range (when its plasma concentration would be between the minimum effective concentration for obtaining the desired immunomodulatory action and the minimum toxic concentration) as an immunoregulator in many autoimmune conditions and malignant neoplasms [ 61 ]. LDN’s ability to suppress opioid growth factor (OGF) activity, the inhibitory growth factor that stimulates p16 and/or p21 cyclin-dependent inhibitory kinases to slow cell replication, has been proven to be effective in a number of malignant tumors, including non-small cell lung cancer (NSCLC) [ 62 ], adenoid cystic carcinoma [ 63 ], ovarian cancer [ 64 ] and B-cell lymphoma [ 65 ]. LDN affects inter-cell signaling and cell cycle regulation and reduces tumor growth by blocking opioid growth factor receptors (OGFrs) and upregulating serum enkephalin levels [ 66 ].…”

Pharmacology Update: Low-Dose Naltrexone as a Possible Nonopioid Modality for Some Chronic, Nonmalignant Pain Syndromes

“…Naltrexone, 17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinan-6-one, is a long-acting opioid receptor antagonist that was initially approved by Food and Drug Administration (FDA) in 1984 for the treatment of opioid dependence, and is currently also FDA-approved for treatment of alcohol dependence. [3][4][5] Naltrexone has a great oral absorption, however it undergoes significant first-pass metabolism; it is metabolized by a noncytochrome dehydrogenase enzyme to its active metabolite, 6-b-naltrexol. Naltrexone is primarily renally excreted; however, dose adjustment is not needed with mild-renal impairment; dose adjustments in moderate to severe renal impairment have not been studied.…”

“…7,3 The standard dose of naltrexone at 50 to 150 mg also prevents inhibition of gamma-aminobutyric acid receptor as well as inhibition of dopamine release. 5 Initial off-label use of naltrexone in doses ranging from 1.5 mg to 3 mg appeared to have an immune-modulating effect in patients with acquired immune deficiency syndrome in 1990s. 8,3 Subsequently, it had gained popularity as an offlabel treatment for pain and inflammation in several autoimmune diseases including multiple sclerosis (MS) and Crohn disease, as well as fibromyalgia.…”

“…4 Evidence suggests that this rebound effect also prompts increased production of opioid receptors, thereby increasing the sensitivity of signaling in addition to increasing the production of endorphins, to compensate for the transient deficit. 5 Furthermore, increased production of endogenous opioids could inhibit the proliferation of B lymphocytes and T lymphocytes, thereby modulating the immune system. 6 Furthermore, intermittent blockade by naltrexone blocks the opioid growth factor (OGF) receptor resulting in biofeedback response that increases production of endogenous OGF, also known as [Met5]-enkephalin, with concomitant increase in m-opioid, delta-opioid, and OGF receptor expression, thereby facilitating interactions between OGF and opioid growth factor receptor (OGFr).…”

“…7,3 The standard dose of naltrexone at 50 to 150 mg also prevents inhibition of gamma-aminobutyric acid receptor as well as inhibition of dopamine release. 5…”