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Low-Concentration morphine infusion does not compromise packed red blood cell transfusion
178 RNA positive patients had a better prognosis than the other 2 groups (P .007). During the study period, 1 of the 27 GBV-C positive patients died (3.7%), whereas 17 of 56 anti-E2 positive patients died (30.4%) and 6 of 15 unexposed patients died (40.0%), indicating a higher risk of death in the absence of GBV-C RNA (P = .01). The presence of GBV-C viremia was also shown to correspond with a lower mean HIV load (3.89 _+ 0.9 log copies per milliliter versus 4.27 -+ 0.97 log copies per millimeter for anti-E2 positive patients and 4.59 • 0.7 log copies per millimeter for unexposed patients [P = .03]). A bivariate analysis found a significant inverse correlation between the GBV-C load and the HIV load (r = -0.33 [Pearson correlation[, P < .001). These researchers found no correlation between GBV-C and CD4+ cell counts (r = 0.1, P = .22). Survival in the years after the introduction of highly active antiretroviral therapy was analyzed separately, and GBV-C RNA positive status remained predictive of longer survival (P = .02). The investigators stated that the GBV-C load increased in patients started on highly active antiretroviral therapy as the HIV load decreased. One patient discontinued this therapy and showed an increase in the HIV load, with a decrease in the GBV-C load (data not provided). Because the GBV-C load had an inverse correlation to the HIV load and no relationship to the CD4+ cell count, the investigators postulated that GBV-C may impair HIV replication. A similar effect has been noted with coinfection of human T-cell lymphotrophic virus type II and acute symptomatic scrub-typhus. The mechanism of the beneficial effect of GBV-C viremia is not yet understood. Coinfection with hepatitis B, hepatitis C, or human T-cell lymphotrophic virus type I on the other hand has been shown to have an adverse effect on the survival of HIV-infected patients. GBV-C has been shown to be transmitted by transfusion, is not associated with any known disease, and is no longer considered a cause of viral hepatitis. Further studies defining the mechanism of these observations are anxiously awaited. (C.H.)
Low-Concentration Morphine Infusion Does Not Compromise Packed Red Blood Cell Transfusion. E. Wozniak, A. Finley, K. Dooley, et al. Pain Symptom Management 22:668-671, 2001. The American Association of Blood Banks standards state that with the exception of normal saline, drugs and medications should not be added to blood or blood components unless there is documentation available to show that the addition is safe and does not adversely affect the blood or component. In the case of children undergoing chemotherapy or surgical treatment who require continuous intravenous opioid infusions, transfusion requires interruption of analgesia or starting a new intravenous line. The goal of this study was to determine whether packed red cells are adversely affected by coadministration with a continuous morphine infusion. Sixteen and 19-day-old CP2Dirradiated red cells were run at 45mL/hr through a blood administration set by peristaltic pump. Normal saline alone, undiluted morphine (10 mg/mL of sterile water), or normal saline mixed with morphine in the usual clinical concentrations of 0.1 or 1.0 mg/mL was added to the red cells with a connector and infused through a mock central venous catheter. In the second set of experiments, a more concentrated undiluted morphine was used (25 mg/mL of sterile water) and diluted with normal saline to obtain the same final concentrations. Contact time
JOURNAL CLUB between the morphine and red cells was approximately 4.5 minutes. Aliquots of blood exposed to saline or morphine solutions were analysed for red cell count and evidence of hemolysis, including lactate dehydrogenase, plasma hemoglobin, and potassium levels. There was no evidence of hemolysis in packed cells that had been in contact with morphine 0.1 or 1.0 mg/mL. Hemolysis occurred at the 10 mg/mL concentration of morphine and was more pronounced with the less-concentrated, undiluted morphine solution. The investigators hypothesize that hypotonicity from the sterile water contained in the morphine solution was the probable cause of hemolysis. This study, therefore, supports the safe coadministration of morphine 0.1 to 1.0 mg/mL in normal saline with packed red blood cells. This study did not evaluate the efficacy of pain control during coinfusion. However, the investigators state that in clinical experiences of coadministration in the palliative care setting, good analgesic control was maintained. (M.G.)
The presence of a newly identified infectious agent (SEN Virus) in patients with liver diseases and in blood donors in Japan. M. Shibata, R.Y./-/. Wang, M. Yoshiba, et a/. J Infect Dis 184:400-404, 2001. The goal of this study was to determine whether the newly discovered SEN virus is associated with non-A through E hepatitis. By using polymerase chain reaction methods, the investigators compared the prevalence of SENV-H and SENV-D in groups of Japanese patients with various forms of liver disease and also in a group of blood donors who screened negative for the usual viral markers. These specific SENV variants were selected because of their previous association with posttransfusion hepatitis. The results show a relatively high prevalence of SENV in all groups studied, with a predominance of SENV-D strains. The prevalence of SENV was significantly higher in patients with fulminant hepatic failure (7/ 22, 32%), acute hepatitis (15/86, 17%), chronic hepatitis (38/ 139, 27%) and cirrhosis (29/93, 31%) compared with 10% in blood donors (27/277). However, the prevalence was also higher in patients with autoimmune hepatitis (5/15, 33%) and primary biliary cirrhosis (11/24, 46%), conditions for which a viral origin is unlikely. Furthermore, in patients with a potentially infectious condition (hepatic failure, acute hepatitis, chronic hepatitis or cirrhosis), the prevalence of SENV was not significantly higher among those with none of the usual markers of viral hepatitis (19/63, 30%) compared with those with hepatitis A, B, and C infection (69/277, 25%). In a multivariate analysis conducted among patients with liver disease, other variables including age, sex, disease status, and origin were not associated with SENV positivity. Because of the similar prevalence of SENV in patients with diverse hepatic conditions, regardless of the likelihood of an infectious origin, the investigators conclude that the results do not support the hypothesis of a causal link between SENV and non-ABC hepatitis. We agree with this conclusion; however, these results do not rule out the possibility that SENV may be responsible for some cases of hepatitis. Furthermore, the cross-sectional design of this study is not ideal for determining causality. Finally, no hypothesis is offered nor any data provided by the investigators to explain the higher prevalence of SENV in patients with liver disease compared with healthy blood donors. (M.G.)
Low-Concentration Morphine Infusion Does Not Compromise Packed Red Blood Cell Transfusion. E. Wozniak, A. Finley, K. Dooley, et al. Pain Symptom Management 22:668-671, 2001. The American Association of Blood Banks standards state that with the exception of normal saline, drugs and medications should not be added to blood or blood components unless there is documentation available to show that the addition is safe and does not adversely affect the blood or component. In the case of children undergoing chemotherapy or surgical treatment who require continuous intravenous opioid infusions, transfusion requires interruption of analgesia or starting a new intravenous line. The goal of this study was to determine whether packed red cells are adversely affected by coadministration with a continuous morphine infusion. Sixteen and 19-day-old CP2Dirradiated red cells were run at 45mL/hr through a blood administration set by peristaltic pump. Normal saline alone, undiluted morphine (10 mg/mL of sterile water), or normal saline mixed with morphine in the usual clinical concentrations of 0.1 or 1.0 mg/mL was added to the red cells with a connector and infused through a mock central venous catheter. In the second set of experiments, a more concentrated undiluted morphine was used (25 mg/mL of sterile water) and diluted with normal saline to obtain the same final concentrations. Contact time
JOURNAL CLUB between the morphine and red cells was approximately 4.5 minutes. Aliquots of blood exposed to saline or morphine solutions were analysed for red cell count and evidence of hemolysis, including lactate dehydrogenase, plasma hemoglobin, and potassium levels. There was no evidence of hemolysis in packed cells that had been in contact with morphine 0.1 or 1.0 mg/mL. Hemolysis occurred at the 10 mg/mL concentration of morphine and was more pronounced with the less-concentrated, undiluted morphine solution. The investigators hypothesize that hypotonicity from the sterile water contained in the morphine solution was the probable cause of hemolysis. This study, therefore, supports the safe coadministration of morphine 0.1 to 1.0 mg/mL in normal saline with packed red blood cells. This study did not evaluate the efficacy of pain control during coinfusion. However, the investigators state that in clinical experiences of coadministration in the palliative care setting, good analgesic control was maintained. (M.G.)
The presence of a newly identified infectious agent (SEN Virus) in patients with liver diseases and in blood donors in Japan. M. Shibata, R.Y./-/. Wang, M. Yoshiba, et a/. J Infect Dis 184:400-404, 2001. The goal of this study was to determine whether the newly discovered SEN virus is associated with non-A through E hepatitis. By using polymerase chain reaction methods, the investigators compared the prevalence of SENV-H and SENV-D in groups of Japanese patients with various forms of liver disease and also in a group of blood donors who screened negative for the usual viral markers. These specific SENV variants were selected because of their previous association with posttransfusion hepatitis. The results show a relatively high prevalence of SENV in all groups studied, with a predominance of SENV-D strains. The prevalence of SENV was significantly higher in patients with fulminant hepatic failure (7/ 22, 32%), acute hepatitis (15/86, 17%), chronic hepatitis (38/ 139, 27%) and cirrhosis (29/93, 31%) compared with 10% in blood donors (27/277). However, the prevalence was also higher in patients with autoimmune hepatitis (5/15, 33%) and primary biliary cirrhosis (11/24, 46%), conditions for which a viral origin is unlikely. Furthermore, in patients with a potentially infectious condition (hepatic failure, acute hepatitis, chronic hepatitis or cirrhosis), the prevalence of SENV was not significantly higher among those with none of the usual markers of viral hepatitis (19/63, 30%) compared with those with hepatitis A, B, and C infection (69/277, 25%). In a multivariate analysis conducted among patients with liver disease, other variables including age, sex, disease status, and origin were not associated with SENV positivity. Because of the similar prevalence of SENV in patients with diverse hepatic conditions, regardless of the likelihood of an infectious origin, the investigators conclude that the results do not support the hypothesis of a causal link between SENV and non-ABC hepatitis. We agree with this conclusion; however, these results do not rule out the possibility that SENV may be responsible for some cases of hepatitis. Furthermore, the cross-sectional design of this study is not ideal for determining causality. Finally, no hypothesis is offered nor any data provided by the investigators to explain the higher prevalence of SENV in patients with liver disease compared with healthy blood donors. (M.G.)