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 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We summarize clinical, laboratory and pathologic details regarding a patient who presented with extrahepatic disease manifestations of hepatitis C virus (HCV) infection, including cryoglobulinemic leg ulcers due to cutaneous vasculitis, peripheral sensorimotor neuropathy, and recurrent pulmonary infiltrates. The patient had evidence for B-cell lymphoproliferation, diagnosed as extranodal lymphoma on initial (though not subsequent) bone marrow examination, retroperitoneal lymphadenopathy, and the presence of a Type II IgM6 monoclonal rheumatoid factor which became cryoprecipitable on complexing to IgG. Chronic hepatitis was mild on liver biopsy, though fibrotic changes developed over a three-year period of follow-up. She had consistently normal liver function tests, except for a brief rebound effect on discontinuing interferon-alpha, and preterminally. Symptoms were only partially responsive to trials of corticosteroids, cytotoxic agents, plasmapheresis and interferon, and the patient ultimately died at The Mount Sinai Hospital of sepsis. We review current information regarding the spectrum of extrahepatic HCV infection, including pathogenic factors relevant to its overlapping autoimmune, rheumatic and lymphoproliferative disease manifestations. The exact prevalence of these HCV-related syndromes among the 1% of the world population estimated to be infected by this virus remains to be delineated. Chronicity of infection, and lack of efficacy of currently available therapy in effecting sustained clearance of the virus from the host, have made this an important public health problem that is likely to increase in significance. Possible relationships to non-Hodgkin's lymphoma may present novel opportunities to delineate the basis for oncogenesis in HCV infection.
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PMID:Hepatitis C virus, autoimmunity and lymphoproliferation. 1074 67

Hepatitis C is the most common cause of end-stage liver disease leading to liver transplant. The disease can recur after transplant, resulting in clinical hepatitis in up to 75% of patients and severe disease in approximately 7%. Treatment of rejection with steroid boluses and treatment of steroid-resistant rejection with OKT3 have both been shown to increase the incidence of recurrent hepatitis C. The use of OKT3 for steroid-resistant rejection is reportedly associated with more severe recurrence. The calcineurin inhibitors tacrolimus and cyclosporine have not been conclusively associated with different rates or severity of recurrence. Viral levels rise 10- to 15-fold after transplant and appear to be associated with the use of immunosuppression. Studies suggest that high viral levels, either pretransplant or early after transplant, may be associated with severe recurrent disease. Although the role of genotype is still unclear, genotype 1b is known to be associated with a poorer prognosis in nontransplanted patients and a lesser response to treatment than other genotypes. Furthermore, some reports suggest that after transplant, recurrent disease may progress more rapidly in patients with genotype 1. Treatment options after recurrence remain poor. Neither interferon nor ribavirin alone provides any true benefit. Combination therapy appears to have a better short-term outcome but may be poorly tolerated, and long-term benefits are unknown. Prophylaxis with combination therapy may be a better option but requires further study. Finally, retransplantation for recurrent hepatitis C is complicated not by rapid recurrence of disease in the new allograft but by high perioperative mortality that may be predicted by the presence of renal failure or sepsis preretransplant.
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PMID:Hepatitis C after liver transplantation. 1094 24

Injecting drug use, mainly of heroin, currently represents a major public health issue in the North East of Scotland. The recent tendency of the committed injecting drug user to inject into the groin has created novel problems for the Infection Unit. Data are presented on 20 consecutive patients admitted between 1994 and 1999 with iliofemoral venous thromboses, often complicated by severe soft tissue infections and bacteraemia as a result of heroin injection into the femoral vein. Nine had coexistent groin abscesses, four had severe streptococcal soft tissue infection of the right thigh, groin and lower abdomen, and two had coincidental soft tissue infections of the upper limb. Nine were bacteraemic on admission. All of the patients were chronic injecting drug users with a median injection duration of 6.5 years. The 18 patients tested for hepatitis C virus were all seropositive. None of the 14 patients tested was positive for HIV. Seventeen patients were treated with subcutaneous low molecular weight heparin (tinzaparin), three having received intravenous unfractionated heparin initially. The tinzaparin was self administered and given for a median duration of seven weeks. One patient declined to have any treatment. Three months after presentation eight patients were asymptomatic, seven had a persistently swollen leg, and five were lost to follow up. None developed clinically apparent pulmonary embolism after institution of anticoagulant therapy. The management of iliofemoral venous thrombosis in injection drug users is problematic because of poor venous access, non-compliance with prescribed treatment, ongoing injecting behaviour, and coexistent sepsis. It is unlikely that a randomised trial of standard treatment with heparin and warfarin versus low molecular weight heparin alone would be practical in this patient group. These retrospective data indicate that the use of tinzaparin in injecting drug users is feasible and appears to result in satisfactory clinical responses. The possibility of concomitant infection in injecting drug users with venous thrombosis should always be addressed, as it appears to be a common phenomenon. Early drainage of abscesses and antimicrobial chemotherapy, often administered intramuscularly or orally because of lack of peripheral venous access, is central to the appropriate care of these patients.
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PMID:High prevalence of iliofemoral venous thrombosis with severe groin infection among injecting drug users in North East Scotland: successful use of low molecular weight heparin with antibiotics. 1096 21

Our objective was to describe clinical features and predisposing factors attributed to lactic acidosis in 4 HIV-infected patients on long-term nucleoside reverse transcriptase inhibitor (NRTI) therapy. All patients had received at least 6-20 months of NRTI-containing antiretroviral therapy: all used stavudine (d4T), in one combined with lamivudine (3TC), in the other 3 with didanosine (ddI); in one hydroxyurea was added. In all, the initial symptoms were gastrointestinal (nausea and vomiting), followed by tachypnoea preceding the lactic acidosis; death followed 6-22 days after admission (liver failure and uncontrollable arrhythmias). Treatment with riboflavin was unsuccessful in one patient. The only definite risk factor in all cases was NRTI-induced mitochondrial toxicity; one patient was concomitantly treated for Kaposi's sarcoma (with bleomycin and vinblastine) and one just recovered from pneumococcal sepsis. None of the patients had a history of chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. In all patients, some sort of toxicity to other previously used NRTIs had occurred earlier. Lactic acidosis occurred after months of NRTI therapy in patients who had already suffered other forms of NRTI toxicity. Concomitant diseases or comedication might have aggravated the mitochondrial toxicity of the NRTIs. Screening methods to detect mitochondrial toxicity are necessary, since lactic acidosis occurs rather unexpectedly, with a rapid, fatal course.
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PMID:Clinical features and risk factors of lactic acidosis following long-term antiretroviral therapy: 4 fatal cases. 1099 8

Liver transplantation is the treatment of choice for end-stage liver disease. During the past 8 years we performed 102 liver transplants in 84 adults and 16 children. In the adults, 9 were combined transplants: 1 a liver-pancreas transplant for type I diabetes, and 8 liver-kidney transplants. In the children, transplants included 5 whole-livers, 5 left-lateral liver segments from living-related donors, 4 reduced-grafts of right or left lobes, and 2 split left-lateral segments. At a mean follow-up of 31 months (range 1-96) 70 were alive, 3 had died during surgery and 15 during the first postoperative months. Mortality was due to primary graft non-function (7), sepsis (10), intracranial hemorrhage (1), tumors (4), recurrent hepatitis B (2), biliary strictures (2) and chronic rejection (1). The 1- and 4-year survival rates were 79.5% and 69.6%, respectively. After transplantation, 10 developed biliary stricture (5 corrected by balloon dilatation) and 8 anastomotic stricture (7 corrected by surgery), and there were 2 multiple intrahepatic strictures. There was hepatic artery thrombosis in 5, including 4 children. In 3, grafts were salvaged by thrombectomy and 2 others underwent re-transplantation. In those who survived transplantation by more than 1-month, recurrent hepatitis B was seen in 6 of 17 (35%) and recurrent hepatitis C in 12 of 19 (63%). Thus, results of our first 100 liver transplants are similar to those reported by larger centers, showing that in an appropriate setting good results can be achieved by small transplant programs.
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PMID:[Experience with 100 liver transplant recipients at the Rabin Medical Center and the Schneider Children's Medical Center]. 1106 44

Transfusion-associated bacterial sepsis is a persistent problem in transfusion medicine, posing a greater threat than the combined risks of receiving a blood product contaminated with HIV-1 or 2, hepatitis C virus (HCV), hepatitis B virus (HBV), and human T-cell lymphtrophic virus (HTVL) -I or -II. This article provides a brief overview of the current incidence, clinical presentation, associated blood products and organisms, and the most feasible and effective methods available to reduce the potential risk of transfusion-associated sepsis. Because bacterial contamination of blood products is the most frequent cause of transfusion-transmitted infectious disease, and as no single existing strategy can completely eliminate its risk, it is important that clinical suspicion be high, and any partial solutions additively be implemented.
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PMID:Transfusion-related bacterial sepsis. 1160 79

Pneumoccocal vaccination of HIV-positive individuals is recommended to prevent pneumococcal infection. We present a case of a 44-year-old HIV-infected male who came to the emergency room with bacterial pneumonia and sepsis. The patient also had a history of HBV and HCV infection. He expired in the emergency room and blood cultures were positive for Streptococcus pneumoniae. The autopsy confirmed the clinical diagnosis and, in addition, hepatitis C-related cirrhosis and splenic abnormalities. The patient had no history of opportunistic infections. His CD4 count 3 months prior to coming to the emergency room was 216 cells/microL with a viral load of 1,270 copies/mL. The patient had received Pneumovax two years before his death. The organism isolated from blood cultures was Streptococcus pneumoniae isotype 3, a strain included in Pneumovax. This is a case of pneumococcal vaccine failure with a fatal outcome in a person with an HIV infection and hepatitis C-related liver cirrhosis.
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PMID:Pneumococcal vaccine failure in an HIV-infected patient with fatal pneumococcal sepsis and HCV-related cirrhosis. 1168 68

Available data suggest that hepatitis C virus positive (HCV+) renal transplant patients may be at an increased risk of morbidity and mortality compared with HCV- patients. Limited data are available regarding the impact of HCV status in pancreas transplant patients. We compared the outcomes of 10 HCV+ patients undergoing pancreas transplantation (seven simultaneous kidney-pancreas, one pancreas after kidney, two pancreas alone) between 1/96 and 10/99 with 20 HCV- recipients that were matched for age, race, gender, timing of transplant, type of pancreas transplant, and surgical technique. Length of follow-up was not significantly different between the HCV+ group compared with the HCV- group (24 +/- 14 vs. 20 +/- 13 months; p=0.45). There was a trend toward a higher incidence of all cause mortality in HCV+ recipients compared with HCV- recipients, 30 vs. 10%, respectively (p=0.17). Additionally, the HCV+ recipients had a trend toward a higher incidence of sepsis-related mortality compared with HCV- recipients, 20 vs. 5%, respectively (p=0.19). Renal allograft survival was 50% in the HCV+ group compared with 94% in the HCV- group (p=0.02). Pancreas allograft survival was not significantly different between the groups, 60 vs. 80%, respectively (p=0.24). At 3, 6, 12 months, and end of follow-up, there were no differences in serum creatinine, amylase, C-peptide, or fasting glucose levels. However, there was a significantly higher incidence of proteinuria at last follow-up in the HCV+ recipients with a renal allograft when compared with HCV- recipients, 50 vs. 12.5%, respectively (p=0.05). In order to maintain comparable glycemic control between the groups, there was a significant increase in oral hypoglycemic requirement in HCV+ recipients compared with HCV- recipients, 33 vs. 0%, respectively (p=0.01). These data suggest that HCV+ pancreas transplant patients may be at an increased risk of graft dysfunction and morbidity. Further studies with more patients and longer follow-up are needed to fully define the impact of HCV status on pancreas graft survival and function.
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PMID:Impact of hepatitis C virus status in pancreas transplantation: a case controlled study. 1209 79

Historically, the leading cause of death among persons with haemophilia and other congenital coagulation disorders was uncontrolled bleeding. Mortality was associated with severe deficiency of coagulation factors VIII or IX and especially with high-titre antifactor neutralizing antibodies (inhibitors). The catastrophic contamination of plasma donor pools with human immunodeficiency virus (HIV) resulted in acquired immunodeficiency syndrome replacing haemorrhage as the leading cause of death among persons with haemophilia. Rather little has been written, however, about mortality among those not infected with HIV. The objective of this study was to identify conditions associated with all-cause mortality among HIV-uninfected patients who were followed for a mean of 8.8 years in the Multicentre Hemophilia Cohort Study. Among the 364 children (mean age 8 years), there were four deaths; two related to cancer, one to trauma, and the fourth to haemorrhage, end-stage liver disease and sepsis. Among the 387 HIV-uninfected adults (mean age 35 years) there were 29 deaths, with haemorrhage the leading cause of death, followed by hepatic, stroke and cancer deaths. Prognostic factors for all-cause mortality among the adults included haemophilia Type A with neutralizing antibodies [age-adjusted relative rate (RR) 3.1, 95% confidence interval (CI) 1.4-6.9] and serologic evidence of both hepatitis B and C virus (RR 4.1, 95% CI 0.97-17.6). Although hepatitis C viral load was slightly lower in patients with hepatitis B virus surface antigenaemia, it was unrelated to vital status. We conclude that causes of death and prognostic factors for current HIV-uninfected haemophilia patients are similar to those noted before the HIV epidemic. Better understanding, prevention and control of neutralizing antibodies and hepatitis infections may substantially improve longevity for people with haemophilia.
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PMID:Factors predictive of death among HIV-uninfected persons with haemophilia and other congenital coagulation disorders. 1219 76

Infections remain among the major causes of disease, hospitalization and death in uremic patients, especially in those treated by dialysis. Several pathophysiologic factors enhance this infectious risk: (1) breakdown of protective barriers; (2) affinity of bacteria for foreign materials; (3) bioincompatibility; (4) uremic toxin retention; (5) deficiency and resistance to vitamin D; (6) carriership of germs, and (7) malnutrition. Twenty to 30% of dialysis patients develop infection, and 20-30% of these die from their infection. Sepsis is significantly more frequent, and mortality secondary to sepsis is 50 times higher than in the normal population. Bacteremia (prevalence 1 episode/100 patient-months) is mainly caused by Gram-positive species, especially in vascular access-related infection and infection of unknown origin. Among these Gram-positive germs, staphylococci play a predominant role. The most frequent and most morbid viral infections are associated with hepatitis. Whereas the incidence of hepatitis B decreases, hepatitis C has become the major variant. The incidence of tuberculosis has increased up to 15 times, and in the Western world it mainly affects patients who immigrated from endemic areas. Fungal infections are also frequent, especially in the setting of peritoneal dialysis. In conclusion, infections remain a frequent and morbid problem in dialysis patients. Preventive measures should be applied more vigorously.
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PMID:Incidence of infectious morbidity and mortality in dialysis patients. 1220 97


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