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Gallbladder and biliary dyskinesia are conditions that are becoming increasingly recognized due to improved technology. They are motility disorders that affect the gallbladder and sphincter of Oddi (SO), respectively. Gallbladder dyskinesia presents with typical biliary pain in the absence of gallstones. Work-up includes laboratory tests and imaging to rule out gallstones. Further investigation leads to a functional radionuclide study to investigate gallbladder ejection fraction. An ejection fraction of less than 40% is considered abnormal, and patients should be referred for cholecystectomy. Symptom relief after the procedure has been seen in 94% to 98% of patients. The term sphincter of Oddi dysfunction (SOD) describes a collection of pain syndromes that are attributed to a motility disorder of the SO. SOD can be further subdivided into biliary and pancreatic SOD. Patients typically have had a prior cholecystectomy and present with episodic biliary pain. The initial work-up includes laboratory tests and imaging to rule out other structural causes of abdominal pain, such as retained gallstones. Imaging and laboratory studies further subdivide patients into types of SOD. SO manometry (SOM) is the gold standard for assessing biliary dyskinesia and can help stratify patients into one of two groups: SO stenosis versus SO dyskinesia. Those with stenosis (type I SOD) are the most likely to respond to treatment with endoscopic biliary sphincterotomy (EBS). As the vast majority of type I patients (>/= 90%) benefit from EBS, SOM is not necessary. Pancreatic SOD patients can be similarly divided into one of three groups. These patients present with recurrent bouts of abdominal pain and/or pancreatitis in the absence of gallstones or other structural abnormalities. Pancreatic sphincter manometry can help distinguish which patients would benefit from endoscopic pancreatic sphincterotomy. Recurrent stenosis of the opening after endoscopic treatment in these patients may necessitate a surgical (open) approach.

SUMMARY HMG CoA reductase inhibition suppresses in vitro HCV replication through depletion of cellular sterol proteins such as geranylgeraniol. Our aims were to prospectively evaluate the changes in serum and lipid fraction HCV RNA with Rosuvastatin in non-responder (NR) patients with CHC. A total of 11 patients with CHC genotype-1 received Rosuvastatin at 20 mg qd (weeks 0–4), 40 mg qd (weeks 5–12), with 4 week follow up. Lipid fractions were separated by a sucrose density gradient ultracentrifugation, HCV RNA determined at wks 0, 2, 4, 8, 12, 16 in serum, and in selected very low- (VLDF) to high-density (HDF) lipid fractions. A reduction in LDL and total cholesterol (TC) was not accompanied by significant decline in HCV RNA. At baseline, there was an inverse correlation between HDL and HCV RNA (ρ = −0.45, P = 0.036). At 20 mg, there was correlation between change (Δ) in TG and Δ HCV RNA (ρ = 0.75, P = 0.007), Δ ALT and Δ TC (ρ = −0.64, P = 0.03) and Δ LDL (ρ = −0.67, P = 0.02). At 40 mg, Δ TG maintained a positive correlation with Δ HCV RNA (ρ = 0.65, P = 0.03). There was a group difference for HCV RNA in relation to lipid fractions (P = 0.04) but not study time intervals (P = 0.17); mean log HCV RNA was greater in VLDF compared to HDF (5.81 ± 0.59 vs 5.06 ± 0.67, P = 0.0002) with no other differences to study time intervals (P = 0.099). Short-term Rosuvastatin monotherapy is not associated with significant changes in serum or lipid fraction HCV RNA in NR patients. HCV co-localizes with the lowest density lipid fractions in serum.

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