ABSTRACT
We present the case of a 31-year-old man who was admitted to our emergency department after injection of 10 mL of methadone into his penis. He had a history of drug abuse over the last 15 years and a background of 3 attempted suicidal episodes with a combination of at least 2 drugs over the past 12 months. The current suicide attempt had serious consequences: he suffered from acute renal and liver failure. One previously unreported side effect of methadone is erectile dysfunction following injection into the penis. In our case, the patient received vardenafil 10 mg once daily without any signs of functional improvement. Ten months after the event, there still was complete erectile dysfunction.
Subject(s)
Analgesics, Opioid/poisoning , Drug Users/psychology , Erectile Dysfunction/chemically induced , Methadone/poisoning , Opiate Substitution Treatment , Penile Erection/drug effects , Penis/drug effects , Substance Abuse, Intravenous/rehabilitation , Suicide, Attempted , Acute Kidney Injury/chemically induced , Adult , Analgesics, Opioid/administration & dosage , Chemical and Drug Induced Liver Injury/etiology , Erectile Dysfunction/drug therapy , Erectile Dysfunction/physiopathology , Humans , Imidazoles/administration & dosage , Injections , Liver Failure, Acute/chemically induced , Male , Methadone/administration & dosage , Penis/physiopathology , Phosphodiesterase 5 Inhibitors/administration & dosage , Piperazines/administration & dosage , Substance Abuse, Intravenous/psychology , Sulfones/administration & dosage , Triazines/administration & dosage , Vardenafil DihydrochlorideABSTRACT
BACKGROUND AND PURPOSE: Cerebral ischemia is ensued by a cellular immune depression syndrome. The postischemic functional capacity of T lymphocytes is controversial, and interactions between leukocyte subsets are largely unknown. Understanding the immunologic interplay between antigen-presenting cells and lymphocytes as well as between distinct lymphocyte subsets after stroke might be of clinical/therapeutic significance because animal data argue for a cerebroprotective effect of, for example, CD4+CD25+ regulatory T cells. METHODS: Ex vivo CD4+ T cell proliferation was analyzed in experimental and human stroke using fluorescence activated cell sorter analysis. To investigate suppressive effects of CD4+CD25+ regulatory T cells as well as the influence of costimulatory cells on CD4+ T cell proliferation, subsets were magnetically sorted before proliferation assay setup. RESULTS: After stroke: (1) proliferation of mouse and human CD4+ T cells on T cell receptor stimulation was unaltered; (2) the suppressive effect of CD4+CD25+ regulatory T cells in mouse and man was unaltered; and (3) efficacy of circulating costimulatory cells from stroke animals was reduced by a mean of 0.6 (SEM 0.1, P=0.001) CD4+ T cell division numbers compared with sham-treated animals. CONCLUSIONS: Reduced costimulatory efficacy of circulating costimulatory cells in mice is an important feature of stroke-induced immunodepression. Understanding the interplay of costimulatory cells and responder T cells (eg, CD4+ T cells or CD4+CD25+ regulatory T cells) after stroke may offer new insights into the prevention of secondary inflammatory damage to the brain and help to guide new therapeutic strategies.
