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BackgroundSymptomatic cholelithiasis is a common surgical disease and accounts for half of the over one million cholecystectomies performed in the USA annually. Despite its prevalence, only one prior systematic review has examined the evidence around treatment strategies and it contained a narrow scope. The goal of this systematic review was to analyze the clinical effectiveness of treatment options for symptomatic cholelithiasis, including surgery, non-surgical therapies, and ED pain management strategies.MethodsLiterature search was performed from January 2000 through June 2020, and a narrative analysis was performed as studies were heterogeneous.ResultsWe identified 12 publications reporting on 10 trials (9 randomized controlled trials and 1 observational study) comparing treatment methods. The studies assessed surgery, observation, lithotripsy, ursodeoxycholic acid, electro-acupuncture, and pain-management strategies in the emergency department. Only one compared surgery to observation.ConclusionThis work presents the existing data and underscores the current gap in knowledge regarding treatment for patients with symptomatic cholelithiasis. We use these results to suggest how future trials may guide comparisons between the timing of surgery and watchful waiting to create a set of standardized guidelines. Providing appropriate and timely treatment for symptomatic cholelithiasis is important to streamline care for a costly and prevalent disease.Trial registrationPROSPERO Protocol Number: CRD42020153153.

Background: Varicella zoster virus presents clinically as primary (chickenpox) or secondary (herpes zoster) infection. Cutaneous and extracutaneous dissemination may occur, usually in immunocompromised patients. VZV hepatitis that progresses to fulminant hepatic failure is very rare and fatal. To the best of our knowledge, 9 cases have been reported to date, of which 7 were in immunocompromised adults, and only one patient was on short duration steroid therapy. Presentation of case: We present a 26-year old man who was admitted initially with acute abdomen as query persistent biliary colic. Later, he showed clinical and laboratory findings of VZV hepatitis that progressed rapidly despite maximal medical ICU support and he expired on day 3 of admission. Conclusions: Acute VZV infection may present as fulminant hepatitis. The presentation may initially be challenging for the diagnosis and should be considered if the patient has been in contact with a sick case. Low dose corticosteroid could carry a risk for fatal VZV fulminant hepatitis and should be used very cautiously especially with VZV patients’ contacts. Further causative relationships remain to be established.

Background: Varicella zoster virus presents clinically as primary (chickenpox) or secondary (herpes zoster) infection. Cutaneous and extracutaneous dissemination may occur, usually in immunocompromised patients. VZV hepatitis that progresses to fulminant hepatic failure is very rare and fatal. To the best of our knowledge, 9 cases have been reported to date, of which 7 were in immunocompromised adults, and only one patient was on short duration steroid therapy. Presentation of case: We present a 26-year old man who was admitted initially with acute abdomen as query persistent biliary colic. Later, he showed clinical and laboratory findings of VZV hepatitis that progressed rapidly despite maximal medical ICU support and he expired on day 3 of admission. Conclusions: Acute VZV infection may present as fulminant hepatitis. The presentation may initially be challenging for the diagnosis and should be considered if the patient has been in contact with a sick case. Low dose corticosteroid could carry a risk for fatal VZV fulminant hepatitis and should be used very cautiously especially with VZV patients’ contacts. Further causative relationships remain to be established.

Background: Varicella zoster virus presents clinically as primary (chickenpox) or secondary (herpes zoster) infection. Cutaneous and extracutaneous dissemination may occur, usually in immunocompromised patients. VZV hepatitis that progresses to fulminant hepatic failure is very rare and fatal. To the best of our knowledge, 9 cases have been reported to date, of which 7 were in immunocompromised adults, and only one patient was on short duration steroid therapy. Presentation of case: We present a 26-year old man who was admitted initially with acute abdomen as query persistent biliary colic. Later, he showed clinical and laboratory findings of VZV hepatitis that progressed rapidly despite maximal medical ICU support and he expired on day 3 of admission. Conclusions: Acute VZV infection may present as fulminant hepatitis. The presentation may initially be challenging for the diagnosis and should be considered if the patient has been in contact with a sick case. Low dose corticosteroid could carry a risk for fatal VZV fulminant hepatitis and should be used very cautiously especially with VZV patients’ contacts. Further causative relationships remain to be established.

Background: Varicella zoster virus presents clinically as primary (chickenpox) or secondary (herpes zoster) infection. Cutaneous and extracutaneous dissemination may occur, usually in immunocompromised patients. VZV hepatitis that progresses to fulminant hepatic failure is very rare and fatal. To the best of our knowledge, 9 cases have been reported to date, of which 7 were in immunocompromised adults, and only one patient was on short duration steroid therapy. Presentation of case: We present a 26-year old man who was admitted initially with acute abdomen as query persistent biliary colic. Later, he showed clinical and laboratory findings of VZV hepatitis that progressed rapidly despite maximal medical ICU support and he expired on day 3 of admission. Conclusions: Acute VZV infection may present as fulminant hepatitis. The presentation may initially be challenging for the diagnosis and should be considered if the patient has been in contact with a sick case. Low dose corticosteroid could carry a risk for fatal VZV fulminant hepatitis and should be used very cautiously especially with VZV patients’ contacts. Further causative relationships remain to be established.

Background: Varicella zoster virus presents clinically as primary (chickenpox) or secondary (herpes zoster) infection. Cutaneous and extracutaneous dissemination may occur, usually in immunocompromised patients. VZV hepatitis that progresses to fulminant hepatic failure is very rare and fatal. To the best of our knowledge, 9 cases have been reported to date, of which 7 were in immunocompromised adults, and only one patient was on short duration steroid therapy. Presentation of case: We present a 26-year old man who was admitted initially with acute abdomen as query persistent biliary colic. Later, he showed clinical and laboratory findings of VZV hepatitis that progressed rapidly despite maximal medical ICU support and he expired on day 3 of admission. Conclusions: Acute VZV infection may present as fulminant hepatitis. The presentation may initially be challenging for the diagnosis and should be considered if the patient has been in contact with a sick case. Low dose corticosteroid could carry a risk for fatal VZV fulminant hepatitis and should be used very cautiously especially with VZV patients’ contacts. Further causative relationships remain to be established.

The sphincter of Oddi (SO) is a smooth muscle valve regulating the flow of biliary and pancreatic secretions into the duodenum, initially described in 1887 by the Italian anatomist, Ruggero Oddi. SO dysfunction (SOD) is a broad term referring to numerous biliary, pancreatic, and hepatic disorders resulting from spasms, strictures, and relaxation of this valve at inappropriate times. This review brings attention to various factors that may increase the risk of SOD, including but not limited to: cholecystectomy, opiates, and alcohol. Lack of proper recognition and treatment of SOD may be associated with clinical events, including pancreatitis and biliary symptoms with hepatic enzyme elevation. Pharmacologic and non-pharmacologic approaches are discussed to help recognize, prevent, and treat SOD. Future studies are needed to assess the treatment benefit of agents such as calcium-channel blockers, glyceryl trinitrate, or tricyclic antidepressants in patients with SOD.

The sphincter of Oddi (SO) is a smooth muscle valve regulating the flow of biliary and pancreatic secretions into the duodenum, initially described in 1887 by the Italian anatomist, Ruggero Oddi. SO dysfunction (SOD) is a broad term referring to numerous biliary, pancreatic, and hepatic disorders resulting from spasms, strictures, and relaxation of this valve at inappropriate times. This review brings attention to various factors that may increase the risk of SOD, including but not limited to: cholecystectomy, opiates, and alcohol. Lack of proper recognition and treatment of SOD may be associated with clinical events, including pancreatitis and biliary symptoms with hepatic enzyme elevation. Pharmacologic and non-pharmacologic approaches are discussed to help recognize, prevent, and treat SOD. Future studies are needed to assess the treatment benefit of agents such as calcium-channel blockers, glyceryl trinitrate, or tricyclic antidepressants in patients with SOD.

Background and aims: C219 (NCT01054573) was an open-label, single-arm, rollover study that examined telaprevir (TVR)-based therapy in patients with chronic HCV genotype 1 infection who failed to achieve a sustained virologic response (SVR) following peginterferon/ribavirin (PR) alone in the REALIZE study, or with >=1 dose of TVR in Phase I studies. We present data from patients previously treated with PR alone in the REALIZE study. Method(s): Patients received TVR 750 mg q8h plus PR at standard doses (180 mug once-weekly and 1000 or 1200 mg/day, respectively) for 12 weeks, followed by PR alone for 36 weeks. HCV RNA levels were evaluated using the COBAS TaqMan assay v2.0. The primary endpoint was SVR24, defined as having HCV RNA '<25 IU/mL, target not detected' 24 weeks after last medication intake. Result(s): Of the 81 patients who did not achieve SVR in the PR arm of the REALIZE study, 27 (33%) were relapsers, 22 (27%) partial responders, and 32 (40%) null responders. The study included 70% males, mostly Caucasian (93%) and median age 53 years. At baseline, an equal proportion of patients had genotype 1a/1b (50%/50%); 25% had cirrhosis. Median log10 HCV RNA was 6.62 IU/mL, with HCV RNA >=800,000 IU/mL in 83% of cases. 90% of patients completed TVR treatment, and 67% completed PR treatment. Overall, 81%, 73%, and 34% of prior relapsers, partial responders and null responders, respectively, achieved SVR (Table). Among patients with virologic failure, observed resistant variants were consistent with those previously described for TVR. The most frequent (>=30%) adverse events (AEs) occurring during TVR treatment phase were pruritus (42%), fatigue (41%), rash (36%), and anemia (32%), most of which were Grade 1/ 2. Serious AEs occurred in 5 (6%) patients in the TVR phase: anemia (4%), biliary colic and pyelonephritis (each 1%). TVR was permanently discontinued in 4 (5%) patients due to AEs. Conclusion(s): In this treatment-experienced population, the efficacy, safety and

Background and Aims: C219 (NCT01054573) was an open-label, single-arm, rollover study that examined telaprevir (TVR)-based therapy in patients with chronic HCV genotype 1 infection who failed to achieve a sustained virologic response (SVR) following peginterferon/ribavirin (PR) alone in the REALIZE study, or with >=1 dose of TVR in Phase I studies. We present data from patients previously treated with PR alone in the REALIZE study. Method(s): Patients received TVR 750mg q8h plus PR at standard doses (180 mg once-weekly and 1000 or 1200 mg/day, respectively) for 12 weeks, followed by PR alone for 36 weeks. HCVRNA levels were evaluated using the COBAS TaqMan assay v2.0. The primary endpoint was SVR24, defined as having HCVRNA '<25 IU/mL, target not detected' 24 weeks after last medication intake. (Table presented) Results: Of the 81 patients who did not achieve SVR in the PR arm of the REALIZE study, 27 (33%) were relapsers, 22 (27%) partial responders, and 32 (40%) null responders. The study included 70% males, mostly Caucasian (93%) and median age 53 years. At baseline, an equal proportion of patients had genotype 1a/1b (50%/50%); 25% had cirrhosis. Median log10 HCVRNA was 6.62 IU/mL, with HCVRNA >=800,000 IU/mL in 83% of cases. 90% of patients completed TVR treatment, and 67% completed PR treatment. Overall, 81%, 73%, and 34% of prior relapsers, partial responders and null responders, respectively, achieved SVR (Table). Among patients with virologic failure, observed resistant variants were consistent with those previously described for TVR. The most frequent (>=30%) adverse events (AEs) occurring during TVR treatment phase were pruritus (42%), fatigue (41%), rash (36%), and anemia (32%), most of which were Grade 1/2. Serious AEs occurred in 5 (6%) patients in the TVR phase: anemia (4%), biliary colic and pyelonephritis (each 1%). TVR was permanently discontinued in 4 (5%) patients due to AEs. Conclusion(s): In this treatment-experienced population, the efficacy, s

Background and aims: C219 (NCT01054573) was an open-label, single-arm, rollover study that examined telaprevir (TVR)-based therapy in patients with chronic HCV genotype 1 infection who failed to achieve a sustained virologic response (SVR) following peginterferon/ribavirin (PR) alone in the REALIZE study, or with >=1 dose of TVR in Phase I studies. We present data from patients previously treated with PR alone in the REALIZE study. Method(s): Patients received TVR 750 mg q8h plus PR at standard doses (180 mug once-weekly and 1000 or 1200 mg/day, respectively) for 12 weeks, followed by PR alone for 36 weeks. HCV RNA levels were evaluated using the COBAS TaqMan assay v2.0. The primary endpoint was SVR24, defined as having HCV RNA '<25 IU/mL, target not detected' 24 weeks after last medication intake. Result(s): Of the 81 patients who did not achieve SVR in the PR arm of the REALIZE study, 27 (33%) were relapsers, 22 (27%) partial responders, and 32 (40%) null responders. The study included 70% males, mostly Caucasian (93%) and median age 53 years. At baseline, an equal proportion of patients had genotype 1a/1b (50%/50%); 25% had cirrhosis. Median log10 HCV RNA was 6.62 IU/mL, with HCV RNA >=800,000 IU/mL in 83% of cases. 90% of patients completed TVR treatment, and 67% completed PR treatment. Overall, 81%, 73%, and 34% of prior relapsers, partial responders and null responders, respectively, achieved SVR (Table). Among patients with virologic failure, observed resistant variants were consistent with those previously described for TVR. The most frequent (>=30%) adverse events (AEs) occurring during TVR treatment phase were pruritus (42%), fatigue (41%), rash (36%), and anemia (32%), most of which were Grade 1/ 2. Serious AEs occurred in 5 (6%) patients in the TVR phase: anemia (4%), biliary colic and pyelonephritis (each 1%). TVR was permanently discontinued in 4 (5%) patients due to AEs. Conclusion(s): In this treatment-experienced population, the efficacy, safety and

Background and Aims: C219 (NCT01054573) was an open-label, single-arm, rollover study that examined telaprevir (TVR)-based therapy in patients with chronic HCV genotype 1 infection who failed to achieve a sustained virologic response (SVR) following peginterferon/ribavirin (PR) alone in the REALIZE study, or with >=1 dose of TVR in Phase I studies. We present data from patients previously treated with PR alone in the REALIZE study. Method(s): Patients received TVR 750mg q8h plus PR at standard doses (180 mg once-weekly and 1000 or 1200 mg/day, respectively) for 12 weeks, followed by PR alone for 36 weeks. HCVRNA levels were evaluated using the COBAS TaqMan assay v2.0. The primary endpoint was SVR24, defined as having HCVRNA '<25 IU/mL, target not detected' 24 weeks after last medication intake. (Table presented) Results: Of the 81 patients who did not achieve SVR in the PR arm of the REALIZE study, 27 (33%) were relapsers, 22 (27%) partial responders, and 32 (40%) null responders. The study included 70% males, mostly Caucasian (93%) and median age 53 years. At baseline, an equal proportion of patients had genotype 1a/1b (50%/50%); 25% had cirrhosis. Median log10 HCVRNA was 6.62 IU/mL, with HCVRNA >=800,000 IU/mL in 83% of cases. 90% of patients completed TVR treatment, and 67% completed PR treatment. Overall, 81%, 73%, and 34% of prior relapsers, partial responders and null responders, respectively, achieved SVR (Table). Among patients with virologic failure, observed resistant variants were consistent with those previously described for TVR. The most frequent (>=30%) adverse events (AEs) occurring during TVR treatment phase were pruritus (42%), fatigue (41%), rash (36%), and anemia (32%), most of which were Grade 1/2. Serious AEs occurred in 5 (6%) patients in the TVR phase: anemia (4%), biliary colic and pyelonephritis (each 1%). TVR was permanently discontinued in 4 (5%) patients due to AEs. Conclusion(s): In this treatment-experienced population, the efficacy, s