Assessing adherence to objective disease monitoring and outcomes with adalimumab in a real-world IBD cohort.

BACKGROUND: Data suggests that tight objective monitoring may improve clinical outcomes in IBD. AIM: To assess the adherence to serial tight objective monitoring(clinical and biomarkers) and its effect on clinical outcomes. METHODS: We retrospectively reviewed the chart of 428 consecutive IBD patients started on adalimumab between January 1,2015-January 1,2019 [338 Crohn's disease(CD), 90 ulcerative colitis(UC)]. Clinical symptoms(assessed by Harvey-Bradshaw-Index,partial Mayo),C-Reactive Protein(CRP), and fecal calprotectin(FCAL) assessments were captured at treatment initiation and at 3,6,9, and12 months. Dose optimization and drug sustainability curves were plotted by Kaplan-Meier method. RESULTS: Clinical evaluation was available in nearly all patients at 3(CD-UC:95-94%), 6(90-83%), 9(86-85%) and 12(96-89%) months. CRP testing frequency decreased in CD patients over time. Compliance to serial FCAL testing was low. Clinical remission at one-year was higher in patients adherent to early assessment visit at 3 months(p = 0.001 for CD and UC). Adherence to early follow-up resulted in earlier dose optimization in CD and UC patients(pLogrank=0.026 for UC & p = 0.09 for CD). Overall drug sustainability did not differ. CONCLUSION: Clinical & CRP, but not FCAL, were frequently assessed in patients starting adalimumab. Adherence to early objective combined follow-up visits resulted in earlier dose optimization, improved one-year clinical outcomes but did not change drug sustainability.

Randomised clinical trial: the efficacy of treatment, guided by a shorter duration of response, using peginterferon alfa-2a plus ribavirin for hepatitis C virus other than genotypes 2 or 3.

BACKGROUND: The efficacy of individualised antiviral treatment durations for chronic hepatitis C remains unclear. AIM: To evaluate treatment durations based on virological responses at week 4, 8 and 12 of peginterferon alfa-2a plus ribavirin therapy. METHODS: Previously untreated patients with HCV genotypes, other than 2 or 3, initiated therapy with peginterferon alfa-2a 180 µg/week plus ribavirin 1000-1400 mg/day. HCV-RNA-negative patients at week 4 rapid virological response (RVR) were randomised to 24 or 48 weeks of treatment; those negative at week 8 were randomised to 36 or 48 weeks; and those who were negative or had a ≥ 2-log drop at week 12 were randomised to 72 or 48 weeks. Sustained virological response (SVR) was defined as undetectable HCV-RNA after 24 weeks of follow-up. RESULTS: The study was terminated prematurely due to lagging enrollment. Of 236 patients who started treatment, 195 were randomised at week 4 (n = 50), 8 (n = 61) or 12 (n = 84). Ninety-five per cent of patients had genotype 1. SVR rates were not significantly different between patients randomised to 24 (84%) or 48 weeks (84%) at week 4, to 36 (73%) or 48 weeks (74%) at week 8, or to 48 (49%) or 72 weeks (40%) at week 12. CONCLUSIONS: In this predominantly genotype 1 cohort, shortening therapy to 24 weeks in patients with a week-4 response and 36 weeks in those with a week-8 response produced SVR rates that were similar to a 48-week regimen. Lengthening treatment to 72 weeks did not improve SVR rates. Genotype 1 patients with RVR can be treated for 24 weeks.

Does a rapid decline in the hematological and biochemical parameters induced by interferon and ribavirin combination therapy for the hepatitis C virus predict a sustained viral response?

BACKGROUND AND OBJECTIVES: To analyze whether rapid myelosuppression and a decrease in alanine aminotransferase (ALT) induced by standard interferon (IFN) and ribavirin (RBV) combination therapy predict a sustained viral response (SVR) in hepatitis C virus patients. PATIENTS AND METHODS: Data from 111 patients (mean age 48.1 years) with chronic hepatitis C virus were retrospectively analyzed. All patients were treated with the same initial doses of IFN and RBV combination therapy. The following laboratory values were measured at baseline, and then at weeks 2, 4, 8, 12 and 24 of treatment: hemoglobin, white blood cells (WBCs), neutrophils, platelets and ALT. A delta value was then calculated for each interval from baseline (baseline values minus two weeks, etc). The delta value of each variable was then compared between the responders and nonresponders using Wilcoxon's signed rank test. RESULTS: Sixty patients (54%) achieved an SVR. There were no significant differences between the responder and nonresponder groups for baseline variables. The delta value of ALT was the only significant marker in the prediction of an SVR. The mean +/- SD delta values for the ALT at week 2 of treatment were 71+/-92 U/L and 44+/-85 U/L for the responders and nonresponders, respectively (P<0.0046). At week 4, the values were 101+/-96 U/L and 84+/-100 U/L for the responders and nonresponders, respectively (P<0.0154). The decline was then calculated for the ALT as a percentage decrease from baseline: at weeks 2 and 4, the decreases were 64% and 66%, respectively, for the responders, and 43% and 41%, respectively, for the nonresponders. At week 2, the delta values for WBC count were found to be significant in predicting failure to achieve an SVR, with mean +/- SD delta values of 0.85 x 10(9)/L+/-1.48 x 10(9)/L and 1.53 x 10(9)/L+/-2.16 x 10(9)/L for the responders and nonresponders, respectively (P<0.0173). The same trend emerged at two weeks for neutrophils: 0.72 x 10(9)/L+/-1.33 x 10(9)/L for the responders and 1.02 x 10(9)/L+/-1.20 x 10(9)/L for the nonresponders (P<0.0150). The delta values were insignificant for hemoglobin, lowest hemoglobin values and platelets. CONCLUSIONS: The decline rates of ALT from baseline to week 2 and 4 of IFN and RBV combination therapy are good predictors of an SVR. A significant drop in WBC and neutrophil values is a predictor of failure to achieve an SVR. The hemoglobin, platelets and lowest hemoglobin values failed to predict an SVR.

Elderly patients are at greater risk of cytopenia during antiviral therapy for hepatitis C.

UNLABELLED: The results of antiviral therapy for hepatitis C virus (HCV) have improved recently with the use of pegylated interferon (PEG-IFN)/ribavirin (RBV) combination therapy. At this point, most patients with chronic HCV remain untreated. Thus, it is anticipated that therapy will be more appealing and prescribed more broadly than in the past, including in patients considered marginal. AIM: To examine the effects of PEG-IFN-based antiviral therapy in elderly patients with chronic HCV. METHODS: The charts of patients treated with chronic HCV were reviewed. Patients were defined as elderly if they were 60 years of age or older. The control group consisted of patients younger than 60 years of age who were matched to the treated elderly patients based on sex, treating physician, prescribed treatment and intended prescribed treatment duration. The data recorded included end of treatment response, sustained virological response (SVR), adverse events, dose modification and withdrawal of therapy. RESULTS: Thirty of 147 (20.4%) elderly patients attending a hepatitis C clinic were treated. The average age of the elderly patients was 65+/-4 years. Forty-three per cent were men and 57% were women. Ten per cent received IFN monotherapy, 70% received a combination of IFN/RBV therapy and 20% received a combination of PEG-IFN/RBV therapy. The overall response rates in the elderly patients compared with the younger patients was 46.7% versus 65.8% (P=0.11) for end of treatment response and 33.3% versus 51.2% (P=0.13) for SVR. The rate of dose modification was 50% in the elderly patients compared with 29% in the control group (P=0.08). Therapy was discontinued in 53% of the elderly compared with 34% of younger patients (P=0.17). The younger patients reported more side effects than elderly patients; although, there were more laboratory abnormalities (anemia, thrombocytopenia and neutropenia) in the elderly patients during therapy than in the younger group (0.93 per patient versus 0.49 per patient, P=0.01). CONCLUSION: Elderly patients with chronic HCV can be treated successfully. However, they are more at risk to develop cytopenias while on treatment. In such patients, the close monitoring of blood counts is necessary. Larger studies are needed to confirm these findings and to determine whether SVR differs in this population.

Splanchnic and systemic hemodynamic effects of sustained euglycemic hyperinsulinemia in rats.

Insulin, in addition to its metabolic function, was found to induce skeletal muscle vasodilatation after acute administration. The vasoactive effects of sustained euglycemic hyperinsulinemia, especially in the splanchnic circulation, are less well known. The aim of this study was to evaluate the systemic and splanchnic hemodynamic effects of sustained euglycemic hyperinsulinemia. Hyperinsulinemia was induced by a sustained-release insulin implant in the scurf area of male rats (release rate -1 U/day). Beginning on the 3rd day, the study group was fed a glucose-rich diet. Hemodynamic studies were performed on the 5th day using the radioactive microsphere technique. Serum insulin was measured by radioimmunoassay. At the time of the hemodynamic measurements, plasma insulin level was higher in the insulin-treated (n=8) compared to control rats (n=8) (23.6 +/- 4.7 vs. 13.2+/-3.9 microu/mL, respectively; p<0.001). Plasma glucose level of the two groups was similar (5.43 +/- 1.07 vs. 5.83 +/- 1.44 mmol/L, respectively). Abdominal skeletal muscle blood flow was higher in the insulin-treated group (0.11 +/- 0.05 vs. 0.05 +/- 0.04 mL x min(-1) x g(-1), respectively; p<0.02). No significant changes were observed in cardiac output and renal blood flow. In the splanchnic circulation: stomach, pancreatic, intestinal, splenic, hepatic arterial and total hepatic blood flow were also not significantly different. In summary, short-term, sustained euglycemic hyperinsulinemia in rats increased blood flow to skeletal muscle but had no hemodynamic effects on cardiac output or splanchnic circulation.

Systemic and splanchnic hemodynamics following hemorrhage and volume restitution with Haemaccel in portal hypertensive rats: the effect of propranolol.

BACKGROUND AND AIMS: Recently, we found in a portal hypertensive rat model that hemorrhage and volume restitution with Haemaccel, a low viscosity plasma expander, induced an increase in cardiac output and portal venous inflow. The present study was conducted to evaluate whether pretreatment with propranolol will attenuate these hyperdynamic changes. METHODS: Portal hypertension was induced by portal vein constriction. Treatment was initiated 14--21 days later. Propranolol (30 mg/kg per day) or water were administered for 7 days via a gastric gavage. Under ketamine anesthesia, 18 h after the last given dose, blood was withdrawn at a constant rate of 0.3 mL/min for 15 min followed by a 15-min stabilization. Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after volume restitution in both groups by using radioactive microspheres. RESULTS: Eight rats were studied in each group. In the propranolol-treated animals, portal venous inflow was decreased (2.4 +/- 0.8 vs 3.8 +/- 0.7 mL/min per 100 g bodyweight; P < 0.01), while splanchnic arteriolar and porto-collateral resistance were increased (52.8 +/- 21.0 vs 32.8 +/- 13.0 and 6.0 +/- 1.4 vs 4.1 +/- 0.7 mmHg x min x 100 g bodyweight/mL; P < 0.05, respectively). Cardiac output, mean arterial pressure, heart rate, total peripheral resistance and portal pressure were not significantly different between the two groups. CONCLUSION: In this model, pretreatment with propranolol prevented the increase in portal venous inflow, which occurs following hemorrhage and volume restitution with Haemaccel. Although caution should be taken in extrapolating data from animal models to humans, our results suggest that volume replacement during a portal hypertensive-related bleeding episode may be safer in a patient treated with non-selective beta-adrenoreceptor antagonists.

Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.

BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.

Bcl-2 rearrangement in patients with chronic hepatitis C associated with essential mixed cryoglobulinemia type II.

Hepatitis C virus (HCV) infection is found in 80% to 90% of patients with essential mixed cryoglobulinemia (EMC) type II, which is associated with monoclonal IgMk produced by monoclonal B cells. It was investigated whether bcl-2 rearrangement is associated with the clonal B-cell proliferation of EMC induced by hepatitis C. The study groups were composed of 15 patients with HCV and EMC, 12 patients with HCV without EMC, and 7 patients with chronic liver disease (CLD) unrelated to HCV. Fluorescence in situ hybridization with probes was applied to JH and to bcl-2 to study whether JH/bcl-2 translocation was present in these patients. Thirteen of 15 (86%) of patients with HCV-related EMC had the JH/bcl-2 translocation, a significantly higher rate than in HCV patients without EMC (16%; P < .001). Bcl-2 rearrangement was not detected in the patients with CLD not related to HCV. The JH/bcl-2 translocation may constitute a pathogenetic link for the development of NHL in patients with HCV infection. (Blood. 2000;96:2910-2912)

[Transmission of hepatitis C in hemodialysis patients--does one-time exposure result in chronic hepatitis?].

Acquired infection with hepatitis C virus (HCV) in hemodialysis patients has been described lately. In dialysis units in Italy and France, the prevalence and incidence of HCV are 20-60% and 1-2%, respectively. Most infected patients develop chronic hepatitis. The clinical presentation of acute HCV in hemodialysis patients is very mild and therefore the diagnosis is often made only by laboratory tests. Acute infection is usually followed by mild elevation of liver enzymes and the presence of HCV-RNA and anti-HCV in serum. We report a 48-year-old man on hemodialysis who developed acute hepatitis C. The diagnosis was made by finding mild elevation of liver enzymes and the presence of HCV-RNA in his serum. A few months later, he developed severe hepatitis which was followed by rapid deterioration in liver function. However, the virus was eradicated and liver function tests became normal. Surprisingly, serum anti-HCV antibodies were detected 5 months later.

Severe interstitial nephritis in a patient with renal amyloidosis and exacerbation of Crohn's disease.

A 57-year-old man with long-term untreated Crohn's disease presented with exacerbation of his bowel disease, volume depletion, nephrotic syndrome and rapid decline in renal function. Renal biopsy revealed amyloidosis and extensive interstitial infiltration. Initiation of steroid therapy was associated with improvement in renal function and postponement of dialysis, suggesting that control of interstitial inflammation might have a therapeutic role in renal amyloidosis. We hypothesize that volume depletion could magnify toxicity of proteinuria, thus augmenting interstitial inflammation and accelerating the deterioration in renal function.

Acute hemodynamic changes following hemorrhage and volume restitution, using a low viscosity plasma expander, in anesthetized portal hypertensive rats.

BACKGROUND/AIM: The aim of this study was to examine, in a portal hypertensive rat model, the hemodynamic changes following hemorrhage and volume restitution with blood and Haemaccel (a low viscosity, volume expander). METHODS: Portal hypertension was induced by portal vein constriction. Under ketamine anesthesia, blood was withdrawn at a constant rate of 0.3 ml/min, for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Twelve rats were studied in each group. During blood withdrawal, significant reductions in arterial pressure and portal pressure were observed. Volume replacement with blood was accompanied by increased mean arterial pressure and portal pressure to baseline. Arterial pressure following volume replacement with Haemaccel was lower and portal pressure was higher than baseline (128+/-16 and 17.1+/-3.9 vs 146+/-13 and 15.9+/-3.0 mmHg, respectively; p<0.05). Volume replacement with Haemaccel, compared to blood, was followed by increased cardiac output and portal venous inflow (39.3+/-11.6 and 4.4+/-1.5 vs 28.9+/-3 and 2.9+/-0.8 ml x min(-1) x 100 g bw(-1), respectively; p<0.05), decreased hematocrit and viscosity (29.3+/-3.8% and 2.8+/-1.3 vs 35.7+/-3.4% and 4.0+/-1.3, respectively; p<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.6+/-1.4 and 29.2+/-14.0 vs 5.0+/-1.4 and 43.9+/-12.7 mmHg x ml(-1) x min x 100 g bw, respectively; p<0.05). There were no significant changes in vascular hindrance in any vascular beds between the two groups. CONCLUSION: In this model, volume replacement with Haemaccel induced an increase in cardiac output and portal venous inflow, thus preventing the reduction in portal pressure which might be expected when viscosity is reduced.

Autoimmune hepatitis in a genetically susceptible patient: is it triggered by acute viral hepatitis A?

The pathogenic mechanisms for autoimmune hepatitis (AIH) are not completely known. Susceptibility to AIH is associated with the human leukocyte antigens (HLA) class II: DR3 and DR4. Nevertheless, AIH does not have a strong genetic predisposition, suggesting that other factors are involved. Perhaps the strongest evidence of a viral cause for AIH exists for hepatitis C virus. AIH has been reported to develop rarely after acute infection with hepatitis A virus. We report on a 55-year-old woman in whom AIH developed during the convalescence period of serologically proven acute viral hepatitis type A. HLA class II DRB1*0401, which was reported to be associated with AIH with a moderate coarse and late appearance in life, was found in this patient. Steroid therapy was followed by a complete clinical remission. Our case supports the possibility that acute hepatitis A may trigger the development of AIH in a genetically susceptible subject.

Beneficial effect of phlebotomy on hepatitis C virus-associated musculoskeletal manifestations.

Chronic hepatitis C virus (HCV) infection may lead to many extrahepatic manifestations which pose a serious therapeutic challenge. Recently, increasing evidence suggesting an association between iron overload and chronic HCV infection has emerged. However, the effect of iron reduction therapy on extrahepatic manifestations of HCV infection is unknown. We describe two patients with chronic HCV infection and severe rheumatic manifestations, namely: myalgia and seronegative nonerosive symmetrical polyarthritis. Interestingly, the response to anti-inflammatory and second line drugs was poor but unexpectedly recurrent phlebotomies was followed by marked improvement of the symptoms. This observation suggests that iron overload may have some role in the pathophysiology of HCV associated rheumatic complications. Further studies are needed to confirm our observation and to clarify the underlying mechanism.

Musculoskeletal manifestations and autoantibody profile in 90 hepatitis C virus infected Israeli patients.

OBJECTIVES: Recent interest has been expressed in rheumatic manifestations in hepatitis C virus (HCV)-infected populations. The aim of this study was to determine the prevalence and characteristics of the musculoskeletal manifestations and serological markers of autoimmunity in HCV-infected patients in Israel. METHODS: Ninety anti-HCV-positive patients were consecutively interviewed and examined. The prevalence of autoantibodies and their association with rheumatologic symptoms were also determined. RESULTS: Rheumatic manifestations were found in 28 subjects (31%), and included arthralgias (9%), arthritis (4%), cryoglobulinemia (11%), sicca symptoms (8%), cutaneous vasculitis (2%), polymyositis (1%), and antiphospholipid syndrome (1%). Rheumatic complications were not associated with liver disease severity, or subjects' gender. In addition, myalgia was reported by 22 patients (24%), and fibromyalgia was diagnosed in 14 (16%). Sixty-nine percent of the patients had at least one autoantibody detected in their serum, the most prevalent being rheumatoid factor (RF), 44%; antinuclear antibody (ANA), 38%; and IgM and IgG anticardiolipin antibodies (ac1), 28% and 22%, respectively. The frequency of autoantibodies was not associated with liver disease severity or rheumatic disorders. CONCLUSIONS: Musculoskeletal manifestations and autoimmune markers are common in HCV infection. An investigation of risk factors for HCV infection is pertinent in a patient presenting new rheumatic manifestations and should be included in the history of present illness. Future studies of these disorders may uncover the full spectrum of these associations and provide new insights into their operating mechanisms.

Premedication with Xylocaine spray does not lead to a false positive rapid urease test.

Rapid urease tests are used for quick identification of Helicobacter pylori during upper gastrointestinal endoscopy. Rapid urease test solutions contain urea, which in the presence of H. pylori urease, generates ammonia, which changes the test medium color to indicate a positive result. Theoretically, Xylocaine spray (ASTRA, Södertalje, Sweden), which has a basic pH value, could cause a similar positive reaction in the test medium. To determine whether patients premedicated with Xylocaine spray have a higher rate of false positive urease tests, we compared the results of a rapid urease test and histologic stains in 107 patients, 54 premedicated with Xylocaine spray and 53 premedicated with intravenous midazolam but not Xylocaine spray. There were no significant differences in test sensitivity, specificity, or predictive values between the study groups. We conclude that patients can be premedicated with Xylocaine spray without concern that the false positive rate of rapid urease tests will increase.

[Multiple angiodysplastic lesions of the colon--a therapeutic challenge].

Colonic angiodysplasia is one of the most frequent causes of recurrent lower gastrointestinal tract bleeding, mainly in the elderly. In 50% of patients multiple angiodysplastic lesions were reported when they were the cause of rectal bleeding. Bleeding from angiodysplasia is more severe and less responsive to treatment in those with coagulation disorders. A 74-year-old woman with an artificial mitral valve who was treated with coumadine is reported. A few years after operation she began to develop severe recurrent rectal bleeding because of multiple angiodysplastic lesions along the right colon, proven by colonoscopy. She was frequently hospitalized for blood transfusions; endoscopic treatment was not feasible and the surgical risk of colectomy was very high. Treatment with estrogen and progesterone significantly decreased recurrent episodes of bleeding.

[Spontaneous internal jugular vein thrombosis complicating chronic pulmonary disease].

Spontaneous internal jugular thrombosis is a rare vascular disorder. It usually occurs as a result of external pressure due to a tumor, infection or as a result of damage to the vessel wall after trauma or central venous catheterization. We report a 35-year-old woman who suffered from severe pulmonary hypertension due to chronic cystic lung disease. She was admitted due to sudden, severe, right-sided neck pain. Internal jugular occlusion by a thrombus was demonstrated by ultrasound and CT-scans but no apparent cause was found. We postulated that the important factors in the development of her thrombosis were stasis due to pulmonary hypertension and high blood viscosity.

Fibromyalgia in hepatitis C virus infection. Another infectious disease relationship.

BACKGROUND: Fibromyalgia syndrome (FS) is a common disorder of diffuse pain in the muscles or joints accompanied by tenderness at specific tender points and a constellation of related symptoms. The potential role of infections in the pathogenesis of FS has only recently been investigated. OBJECTIVES: To evaluate the prevalence of FS and to assess tenderness thresholds in patients infected with hepatitis C virus (HCV). METHODS: The study included 90 patients with HCV, 128 healthy, anti-HCV-negative controls, and 32 patients with non-HCV-related cirrhosis. Tenderness was measured by manual palpation (18 tender points) and with a dolorimeter. Fibromyalgia syndrome was diagnosed according to the 1990 American College of Rheumatology criteria. RESULTS: The diagnosis of FS was established in 14 patients (16%) with HCV, in 1 patient (3%) with non-HCV-related cirrhosis, and in none of the healthy controls (P < .001). Thirteen of the HCV-positive patients with FS were women. The patients with HCV had significantly (P < .01) more tender points (mean [+/- SD] 3.6 +/- 5.3) than the healthy controls (0.1 +/- 0.5) and the patients with non-HCV-related cirrhosis (1.2 +/- 2.7). Specifically, the patients with cirrhosis were most tender on both tenderness measures owing to the high proportion of women in this group. Patients with FS were significantly more tender than those without FS: their dolorimetry thresholds were 2.9 kg vs 6.0 kg (P < .001). CONCLUSIONS: A high prevalence of FS was observed in patients infected with HCV, especially women. Recognizing FS in patients with HCV will prevent misinterpretation of FS symptoms as part of the liver disease and will enable the physician to reassure the patient about these symptoms and to alleviate them.

Open access endoscopy for hospitalized patients.

OBJECTIVES: Most requests for gastroenterology consultations for hospitalized patients are for endoscopic procedures. Open access endoscopy has been evaluated in several institutions for outpatients. Our aim was to evaluate an open access policy for hospitalized patients. METHODS: Since April of 1996, patients hospitalized in the Soroka Medical Center have been referred directly for upper endoscopy (esophagogastroduodenoscopy, EGD) and flexible sigmoidoscopy (FS). The numbers of procedures and consultation requests between July 1, 1996, and September 30, 1996, were compared with the corresponding months of 1995. A survey of physician satisfaction with the new open access system was conducted. RESULTS: The mean number of monthly consultations during the study period was 30.7 +/- 2.4, compared with 119.3 +/- 5.4 during the same months in 1995 (p = 0.006). Open access endoscopy was performed on 114 patients during the study period. Upper GI bleeding (n = 41) and abdominal pain (n = 33) were the most common indications for EGD. There were nine duodenal ulcers, five gastric ulcers, and eight gastric carcinomas. Sixteen patients (21%) had normal EGDs. The most common indications for FS were rectal bleeding (n = 24) and diarrhea (n = 13). Seven patients had colorectal cancer; 12 FSs were normal. In all, 286 EGDs and FSs were conducted in the study period compared with 253 in 1995 (not significant). All physicians expressed satisfaction with the new system and favored its continuation. CONCLUSIONS: The open access policy for hospitalized patients led to a considerable reduction in requests for consultations, with no significant increase in the number of endoscopies. The majority of patients referred directly for endoscopy had appropriate indications.