Faculty Bibliography

Cannabinoid hyperemesis syndrome (CHS) is a rare constellation of clinical findings that includes a history of chronic heavy marijuana use, severe abdominal pain, unrelenting nausea, and intractable vomiting. A striking component of this history includes the use of hot showers or long baths that help to alleviate these symptoms. This is an underrecognized syndrome that can lead to expensive and unrevealing workups and can leave patients self-medicating their nausea and vomiting with the very substance that is causing their symptoms. Long-term treatment of CHS is abstinence from marijuana use-but the acute symptomatic treatment of CHS has been a struggle for many clinicians. Many standard medications used for the symptomatic treatment of CHS (including ondansetron, promethazine, and morphine) have repeatedly been shown to be ineffective. Here we present the use of lorazepam as an agent that successfully and safely treats the tenacious symptoms of CHS. Additionally, we build upon existing hypotheses for the pathogenesis of CHS to try to explain why a substance that has been used for thousands of years is only now beginning to cause this paradoxical hyperemesis syndrome.

AIM: To determine if natural killer T cell (NKT) populations are affected in nonalcoholic fatty liver disease (NAFLD). METHODS: Patients undergoing bariatric surgery underwent liver biopsy and blood sampling during surgery. The biopsy was assessed for steatosis and immunocyte infiltration. Intrahepatic lymphocytes (IHLs) were isolated from the remainder of the liver biopsy, and peripheral blood mononuclear cells (PBMCs) were isolated from the blood. Expression of surface proteins on both IHLs and PBMCs were quantified using flow cytometry. RESULTS: Twenty-seven subjects participated in this study. Subjects with moderate or severe steatosis had a higher percentage of intrahepatic CD3+/CD56+ NKT cells (38.6%) than did patients with mild steatosis (24.1%, P = 0.05) or those without steatosis (21.5%, P = 0.03). Patients with moderate to severe steatosis also had a higher percentage of NKT cells in the blood (12.3%) as compared to patients with mild steatosis (2.5% P = 0.02) and those without steatosis (5.1%, P = 0.05). CONCLUSION: NKT cells are significantly increased in the liver and blood of patients with moderate to severe steatosis and support the role of NKT cells in NAFLD.

Androgens provide survival signals to prostate epithelial cells, and androgen ablation induces apoptosis in the prostate gland. However, the molecular mechanisms of actions of the androgen-signaling pathway in these processes are not fully understood. Here, we report that androgens induced expression of the cellular FLIP (c-FLIP) gene, which is a potent inhibitor of Fas/FasL-mediated apoptosis. The androgen receptor (AR) was recruited to the promoter of the c-FLIP gene in the presence of androgens. We found that c-FLIP promoter contained multiple functional androgen response elements (AREs). In addition, we show that c-FLIP overexpression accelerated progression to androgen independence by inhibiting apoptosis in LNCaP prostate tumors implanted in nude mice. Our results suggest that AR affects survival and apoptosis of prostate cells through regulation of the c-FLIP gene in response to androgens