Improvement in hepatopulmonary syndrome after methadone withdrawal: A case report with implications for disease mechanism

Abstract

Spontaneous resolution of hepatopulmonary syndrome (HPS) without liver transplantation or improvement in the underlying liver disease has rarely been reported in the literature. Increased endogenous production of nitric oxide has been implicated in the pathogenesis of HPS. We report the case of a 50-year-old man with hepatitis C cirrhosis who demonstrated dramatic improvement in HPS after withdrawal from chronic methadone therapy. We speculate on the potential role of opiate receptors in the pulmonary vasculature and their effect on nitric oxide signaling as a potential mechanism accounting for the patient's clinical improvement. Liver Transpl 16:870-873,

Systematic Review: Treatment for Addictive Disorder in Transplant Patients

“…Methadone is poorly removed by hemodialysis, 117 so it is unlikely to be prescribed in patients with end‐stage renal disease; however, methadone has been used successfully in liver transplant recipients 79 . Methadone treatment, while effective for addictive disorders, may require certain precautions when used in medically ill: one case report describes spontaneous resolution of hepatic pulmonary syndrome in a patient with liver cirrhosis that occurred after withdrawal of chronic methadone therapy 118 . Liver transplant recipients who were on methadone maintenance are reported to require greater amounts of intraoperative anesthesia, postoperative analgesia, and an adjustment of the methadone dose after transplantation 76 .…”

Hepatopulmonary syndrome: A recent review of the literature

“…Yet, results of small uncontrolled studies in human HPS with pentoxifylline are conflicting 41 . Extra interventions have included inhaled prostacyclin derivatives to improve ventilationperfusion matching 43 and withdrawal of chronic methadone 44 . The administration of supplemental oxygen to maintain O 2 saturations above 88% is advised based on experience in treating non specific pulmonary vascular and parenchymal disorders 33 .…”

The hepatopulmonary syndrome

“…The authors hypothesize a role for opiate receptors in modulating NO signaling and release as the pathophysiologic mechanism for the effects [82,83]. Both patients had hepatitis C as the cause for their underlying liver disease; one of them achieved sustained virologic response after interferon and ribavirin therapy, 3 years prior to the resolution of the syndrome.…”