Battlefield acupuncture appears to be an effective therapy for pain management.

INTRODUCTION: The Department of Defense has been training primary care providers in battlefield acupuncture (BFA), a subtype of auricular acupuncture, as an adjunct therapy for pain management. METHODS: The objective of this study was to evaluate the effectiveness and safety of BFA for pain management in an outpatient Internal Medicine clinic staffed by resident physicians. The target population for this single-center prospective cohort study were military beneficiaries at a medical treatment facility located at the Wright-Patterson Air Force Base. Participants who met inclusion criteria were treated with BFA in addition to routine standard care for pain (n = 69). The control group was composed of participants who received routine standard care only without BFA (n = 27). Pain was assessed by a self-reported pain scale (0-10) at the time of encounter, immediately after BFA (for the intervention group), then at 24 and 48 h afterwards. RESULTS: Mean pain for the intervention group decreased from 5.45 before BFA to 3.29 immediately following BFA to 2.21 at 24 h and to 2.10 at 48 h (p < 0.001). Thus, at all three post-treatment time points, mean decrease in pain surpassed a two-point reduction, deemed to be a clinically important difference. The BFA group had a greater reduction in pain compared to the no intervention group at 24 h (3.14 vs 0.59, p < 0.001) and at 48 h (3.26 vs 0.96, p < 0.001). Four intervention group participants (6%) reported an adverse reaction (three with pain at the insertion site) or complication (one with superficial infection). CONCLUSION: BFA provided by Internal Medicine residents appears to be a safe and effective adjunct therapy for pain management in an outpatient setting, but requires further validation by randomized controlled trials.

Hepatic Abscess: A Rare Presentation of Sump Syndrome After Choledochojejunostomy.

Sump syndrome is a rare complication of choledochoenterotomy. Patients with sump syndrome often have abdominal pain, recurrent cholangitis, pancreatitis, malabsorption, fever, an abnormal liver function test, and, rarely, hepatic abscess. Roux-en-Y choledochojejunostomy or hepaticojejunostomy has been advocated to prevent sump syndrome. We report an 80-year-old man who presented with a hepatic abscess secondary to sump syndrome 26 years after a Roux-en-Y choledochojejunostomy for recurrent cholangitis. Sump syndrome should be considered for patients who underwent biliary diversion surgery, regardless of the type of procedure or time from surgery.

MET activation mediates resistance to lapatinib inhibition of HER2-amplified gastric cancer cells.

HER2 amplification is found in more than 15% of gastric cancers and is associated with poor clinical outcome. Lapatinib, a dual HER2 and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, has shown promising in vitro results in treating HER2(+) cancer cells. However, several studies have shown that activation of alternative receptor tyrosine kinases can mediate resistance to HER-targeted therapy. Here, we investigated whether activated MET can confer resistance to lapatinib inhibition of gastric cancer cells. A panel of gastric cancer cell lines was treated with lapatinib, and we observed that cell proliferation was reduced by 70% and that the degree of HER2 amplification corresponds to sensitivity to lapatinib. Immunoblotting analysis indicated that phosphorylation of HER2, EGFR, MET, AKT, and extracellular signal-regulated kinase was inhibited by lapatinib and presumably led to cell-cycle arrest as observed with flow cytometry. Hepatocyte growth factor (HGF) activation of MET receptors rescued cells from lapatinib-induced growth inhibition by restimulating the downstream pathways and restoring normal cell-cycle progression. This rescue effect could be abrogated by inhibiting MET with PHA-665752 (a highly specific MET inhibitor) or downregulating MET expression with short interfering RNA. No synergy in growth inhibition was observed when cells were treated with a combination of lapatinib and PHA-665752. Repeat studies using insulin-like growth factor 1 and fibroblast growth factor 3 could not uniformly rescue the lapatinib-treated gastric cancer cells. In conclusion, HGF/MET-mediated resistance to lapatinib is a novel mechanism of resistance to HER2-targeted agents in gastric cancer cells. Development of inhibitors targeting multiple receptors or common downstream signaling proteins merits further investigation.