Lamivudine treatment for acute severe hepatitis B: a pilot study.

BACKGROUND: Experience with lamivudine treatment of immunocompetent patients with acute hepatitis B is limited. AIM OF STUDY: To evaluate the safety and efficacy of lamivudine for the treatment of acute severe hepatitis B virus (HBV) infection in immunocompetent adults. PATIENTS AND METHODS: Fifteen patients (10 men, 5 women, mean age 34.3+/-7.3 years) with severe acute HBV infection were treated with lamivudine 100 mg daily for 3-6 months, starting 3-12 weeks after onset of infection. Prior to treatment, 5 patients had grade 1-4 encephalopathy; all patients had severe coagulopathy (mean INR was 4.5+/-6.4), and all patients had evidence of severe hepatocyte lysis (mean alanine aminotransferase 3738+/-1659 U/L, and mean total serum bilirubin 18+/-6.8 mg/dl). All patients had evidence of highly replicative HBV (mean HBV DNA 13.5 x 10(6)+/-11 x 10(6) copies/ml). RESULTS: Thirteen patients (86.6%) responded to treatment. Encephalopathy disappeared within 3 days of treatment and coagulopathy improved within 1 week. Serum HBV DNA was undetectable (by polymerase chain reaction) within 4 weeks, and serum liver enzyme levels normalized within 8 weeks. Two patients in whom lamivudine therapy was delayed developed fulminant hepatitis and underwent urgent liver transplantation. (One died of vascular complications 1 month later). The 11 patients who were serum HBeAg-positive before treatment seroconverted, and HBeAb developed within 12 weeks in 9 of them; HBsAg was undetectable in all 11 tested patients, and protective titer of HBsAb developed within 12-16 weeks in 9 of them. Therapy was well tolerated in all cases. CONCLUSIONS: These data indicate that lamivudine induces a prompt clinical, biochemical, serological and virological response in immunocompetent patients with de novo HBV infection. Lamivudine may prevent the progression of severe acute disease to fulminant or chronic hepatitis and should be considered for use in selected patients. A large randomized controlled, double-blind prospective study is needed.

Hepatitis C virus infection in renal failure patients in the absence of anti-hepatitis C virus antibodies.

The magnitude and clinical significance of Hepatitis C virus (HCV) infection in dialysis patients is controversial and underestimated. This study was conducted in order to evaluate the correlation between HCV replication and antibody response to HCV in dialysis patients. HCV infection in dialysis patients was evaluated over a period of 3 years and compared to HCV infection in Liver Clinic patients. Sera were collected from 310 dialysis patients and tested for anti-HCV and HCV-RNA. In addition, HCV genotype and HCV viral load were determined in HCV-RNA-positive sera. Anti-HCV was detected in 43 (14%) of the dialysis patients. Of these, 37 (86%) were HCV-RNA-positive. Among the 267 HCV-seronegative dialysis patients, 25 (9%) were found to be HCV-RNA-positive in more than one sample during the study. These patients were characterized by low viral load; at least two orders of magnitude lower than in the group of HCV-seropositives. In contrast, in the Liver Clinic patients, HCV-RNA was found exclusively in HCV-seropositive patients. Comparison of the genotype pattern in the two groups did not reveal a difference. Our results suggest that HCV infection in dialysis units may be underestimated due to cases of low viral load, depending on the method of RNA extraction and sensitivity of the test used. Low viral load might contribute to the lack of humoral immune response seen in some dialysis patients.

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.

Salivary HCV-antibodies; a follow-up cohort study of liver disease patients.

We have recently shown in Liver Clinic patients that saliva instead of serum may be used for anti-HCV detection. As compared to blood withdrawing, saliva is easier to obtain, non invasive, especially for infants. In the present study, sequential determination of serum and salivary anti-HCV was performed in the same cohort for 36 months. Anti-HCV seropositive and seronegative patients were studied. Blood and saliva samples were obtained simultaneously. From the anti-HCV seronegative patients (n=33), 161 sequential serum and 161 matched saliva samples were obtained. All were anti-HCV negative. From the anti-HCV seropositive patients (n=35), 131 sequential serum and 131 matched saliva samples were obtained. All sequential serum samples were anti-HCV positive. Of the saliva samples 126 (96%) were anti-HCV positive and five (4%) were anti-HCV negative. These five samples were obtained from two patients with autoimmune hepatitis and HCV-RNA seronegative by PCR. The results suggest that saliva may serve as a substitute for serum for the detection of anti-HCV antibodies.

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.

[Rational use of albumin].

The use of albumin has been a matter of debate since its introduction in the 1940's. Albumin is not only expensive but may also be harmful when administered inappropriately. Until recently our use of albumin was controlled by a number of authorized physicians who signed all albumin prescriptions. In August 1998, a multidisciplinary team reviewed the indications for albumin use and introduced simple guidelines for its supply and administration. As a result, the use of albumin has decreased by almost 70%. This indicates that rational use of albumin can be achieved by appropriate guidelines, without requiring administrative limitations. We believe that this conclusion holds true for other diagnostic and therapeutic procedures as well.

The effects of hypothyroidism on liver status of cirrhotic patients.

We have shown, in animal models as well as in retrospective human study, that some degree of decreased thyroid function is beneficial for subjects with liver damage of various etiologies. Therefore, we herein present the results of a cohort population study. Between 1991 and 1994, 18 patients (12 women and 6 men; mean age, 59 +/- 24 years) with both biopsy-proven active cirrhosis (5 hepatitis C virus, 4 hepatitis B virus, 1 immunocompromised host, 2 primary biliary cirrhosis, 1 alcoholic, and 5 cryptogenic; Child's-Pugh criteria: A-8, B-8, C-2) and primary or induced (by either drug or surgery) thyroxine-treated hypothyroidism were prospectively followed. Each patient was examined at least twice yearly and served as their own control. The thyroid of the profiled patients ranged between euthyroidism and subclinical hypothyroidism. Liver function tests were evaluated and compared in states of normal versus increased thyroid-stimulating hormone (TSH) blood levels. A significant improvement in alanine aminotransferase (p < 0.001), alkaline phosphatase (p < 0.0001), albumin (p < 0.001), and bilirubin (p < 0.01) was found in the increased TSH group. Prothrombin time was also found to be significantly better (p < 0.001). We conclude that euthyroid patients with liver cirrhosis might benefit from a controlled hypothyroidism.

Fulminant non--A-G viral hepatitis leading to liver transplantation.

BACKGROUND: All hepatotropic viruses are known to cause fulminant hepatic failure (FHF). However, in 30% to 40% of patients with FHF, the precise cause remains unknown. We aimed to better define this subgroup. METHODS: We evaluated the clinical course and outcome of 7 patients admitted during a 22-month period with fulminant viral hepatitis leading to liver transplantation; none had serologic or molecular evidence of hepatitis A, B, C, D, E, or G viral infection, thus the term non-A-G viral hepatitis. All known etiologies of FHF were excluded. RESULTS: All patients had prodromal symptoms suggestive of viral causes. Mean age was 30 years. The interval between onset of jaundice and appearance of encephalopathy was 23 days (range, 4-50 days). Five patients had grade III/IV encephalopathy. Serum alanine aminotransferase levels showed a single peak of activity. The duration between first symptoms and liver transplantation was 28 days (range, 12-71 days). Results of histological study of the explanted liver showed submassive (4 patients) or massive (3 patients) hepatocyte necrosis. In all patients, results of polymerase chain reaction analysis did not detect hepatitis B virus DNA, hepatitis C virus RNA, or hepatitis G virus RNA in the explanted liver. After transplantation, 2 patients showed (6 months later) increased liver enzyme levels of undetermined cause, and results of a liver biopsy showed mild lobular hepatitis; 1 patient had lymphoproliferative disorder (Epstein-Barr virus-originated); and 1 patient, aplastic anemia, which is known to be associated with seronegative viral hepatitis. The latter patient died, whereas the other 6 patients are alive (survival rate, 86%). CONCLUSIONS: Our patients with non-A-G viral hepatitis had a severe acute onset with progressive FHF requiring liver transplantation. There is some suggestion of recurrent viral disease after transplantation implicating other unknown viruses in the etiology.

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.

Altered thyroid status modulates portal pressure in normal rats.

BACKGROUND & AIMS: Disturbances in thyroid function in humans and experimental animal models have been associated with alterations in liver function and portal circulation. We have previously shown that hypothyroidism can significantly reduce portal pressure in portal vein ligated rats as well as inhibit the development of cirrhosis and fulminant hepatic failure following toxic liver injury. The aim of this study was to determine the effects of increased and decreased thyroid function on portal pressure in rats with normal liver histology and portal circulation. METHODS: Three groups of 12 Wistar rats each were studied over a 30 day period: euthyroid (Group 1), hyperthyroid (Group 2) and hypothyroid (Group 3). Hyperthyroidism was induced by subcutaneous injection of triiodothyronine (400 microg/100g body weight) every ten days during the study period. Hypothyroidism was induced by methimazole (0.04% in drinking water) from 2 weeks prior to and throughout the 30 day study. Serum triiodothyronine (T3) and thyroid stimulating hormone (TSH) levels were determined to confirm the induction of hyper- and hypothyroidism. Portal pressure was assessed by direct catheterization of the portal vein prior to sacrifice. Indirect confirmation of changes in portal circulation was obtained by determining splenic weight at the time of sacrificing the animals. Animals were sacrificed at 10 day intervals throughout the 30 day study. RESULTS: Triiodothyronine treated rats were hyperthyroid compared to controls, with an elevation in serum T3 levels (3.8+/-0.9 mmol/L vs 1.3+/-0.4 mmol/L, p<0.05). In rats treated with methimazole, hypothyroidism was confirmed by a 7-fold increase in serum TSH compared to controls (1.8+/-0.4 vs 0.24+/-0.04 mmol/L, p<0.01). Portal pressure was significantly higher in the triiodothyronine treated rats compared to controls (12.8+/-1.7 and 9.6+/-0.75 cm H2O, p<0.001). Splenic weights in hyperthyroid rats were significantly higher than in controls (579+/-44 vs 478+/-46 mg, p<0.01). Portal pressure was significantly lower in the methimazole treated group compared to the control group (8.13+/-0.68 vs 9.6+/-0.75 cm H2O, p<0.01) as were splenic weights (400+/-33 vs 478+/-46 mg, p<0.01). CONCLUSION: These studies demonstrate that disturbed thyroid function exerts significant hemodynamic effects on the portal circulation in normal rats and complements results from previous similar studies in cirrhotic animals.

Fatal Clostridium sordellii ischio-rectal abscess with septicaemia complicating ultrasound-guided transrectal prostate biopsy.

Clostridium sordellii is a Gram-positive spore-forming anaerobic bacillus rarely encountered in human infection. A case of C. sordellii ischio-rectal abscess with rapidly fatal septicaemia is described which complicated ultrasound-guided transrectal biopsy of the prostate, despite ciprofloxacin prophylaxis. Neither C. sordellii ischio-rectal abscess nor ischio-rectal abscess complicating transrectal biopsy have been reported previously. Judging from our experience and the reviewed literature, the addition of prophylactic anti-anaerobe drugs should be strongly considered until an optimal prophylactic regimen will be defined by randomized controlled trials.

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.

Hepatitis C virus infection and genotypes in Southern Israel and the Gaza Strip.

The Gaza Strip borders the southern part of Israel and Egypt. There is a remarkable difference in the prevalence of antibodies to hepatitis C virus (HCV) between Israel (0.5%) and Egypt (10%). A few thousand inhabitants cross the borders daily from the Gaza Strip to both countries. The objectives of this study were to investigate the prevalence of HCV infection in the Gaza Strip, an area that was not studied before, and to study HCV transmission in the Gaza Strip by characterizing the genotypes of HCV in Southern Israel and the Gaza Strip and comparing them with those found in Egypt. HCV prevalence in the Gaza Strip was found to be 2.2%, relatively higher than in Israel but lower than in Egypt. The most common genotypes found were type 1 b in Southern Israel and type 4 in the Gaza Strip, corresponding to the most prevalent genotype in Egypt. Similarity between type 4 isolates from the Gaza Strip and Egypt was illustrated further by sequence analysis of the HCV 5' noncoding region (NCR).

HCV antibodies in saliva and urine.

Infection with hepatitis C virus (HCV) is usually established by detection of serum antibodies (anti-HCV). This study was conducted in order to evaluate whether saliva and urine may substitute serum for anti-HCV detection. Serum, saliva, and urine were obtained simultaneously from 141 patients with a variety of liver diseases and from 52 patients with autoimmune diseases (systemic lupus erythematosus n = 27 and rheumatoid arthritis n = 25). The cell free fraction of saliva and urine samples was tested for anti-HCV using a modification of a serum anti-HCV kit. Western blot analysis was used as a confirmation method. Of the patients with liver diseases, 73 were anti-HCV-seropositive. Salivary and urinary anti-HCV could be detected in 66 (90%) and 36 (49%) of the anti-HCV-seropositive patients, respectively. The presence of anti-HCV in saliva or urine was not related to the severity of liver disease. All the anti-HCV-seronegative liver patients were negative for salivary anti-HCV and 22 (32%) had urinary anti-HCV. The patients with autoimmune diseases were all anti-HCV-seronegative. None had detectable salivary anti-HCV while 33 (63%) were positive for urinary anti-HCV. Western Blot analysis confirmed the presence of anti-HCV in all serum and saliva samples tested but only in 2/12 urine samples. The results suggest that saliva, but not urine, may serve as a substitute for serum for the determination of anti-HCV positivity.

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.

[Embolic splenic infarction: a rare complication of atrial fibrillation].

Splenic infarction is a rare disorder. The typical clinical presentation is sudden pain in the left upper quadrant of the abdomen, and awareness to this possibility is the major clue for diagnosis. We describe a 49-year-old man with chronic atrial fibrillation and splenomegaly who was treated with anticoagulants. Because of hematuria, the regular dose of anticoagulant therapy was reduced. The hematuria stopped but he complained of sudden onset of pain in the left upper quadrant. Computerized tomography and isotope scan of the spleen confirmed the clinical suspicion of splenic infarction. Treatment with anticoagulants and analgesics was followed by clinical improvement.