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ID-NAT and serology are complementary in detecting HBV infection in first-time donors, but HBV-DNA is superior to HBsAg detection in repeat donors.

T he implementation of nucleic acid testing (NAT) in blood donations from areas with high or low prevalence of hepatitis B virus (HBV) infection has resulted in the identification of a small number of infections in the preseroconversion window period (WP) 1 and a considerably larger number of blood units containing no detectable hepatitis B surface antigen (HBsAg) but low levels of HBV DNA associated, in most cases, with anti-HBc, suggesting an established infection. These cases were called occult HBV infection (OBI). 2 In Europe, where HBV genotypes A2 and D are prevalent, OBIs are detected in 1:2,000 to 1:20,000 donations 3,4 and are characterized by occurring in older donors (median age 51), mostly males (90%), and with normal levels of alanine aminotransferase (ALT). Viral load is consistently below 1,000 IU/mL (median, 25 IU/mL) and, compared to the dominance of genotype A2 in HBsAg-positive infections, a significantly higher proportion of OBI genotype D is observed. The remarkably high frequency of multiple amino acid substitutions in the pre-S/S proteins (100% in the major hydrophilic region [MHR] of genotype D OBIs) affecting both humoral and cellular epitopes strongly suggested that OBIs in Europe appears, to a large extent, determined by host immune pressure.

SummaryReasons for performing study: Gastric impaction in the horse is poorly described in the veterinary literature. Objectives: To review the clinical and pathological features of gastric impaction. Methods: The clinical details of horses presenting with colic over a 7-year period and cases in which gastric impaction was considered to determine the outcome were reviewed. Clinical and clinicopathological data were recorded. Results: Twelve cases of gastric impaction were recorded (1.4% of 857 horses hospitalised for colic). Diagnosis was achieved by ultrasonographic examination, gastroscopy, exploratory celiotomy and/or post mortem examination. Five out of 12 horses were successfully treated, 5/12 were subjected to euthanasia (3 at celiotomy and 2 due to recurrence of impaction) and 2/12 died. Three out of 12 horses had spontaneous gastric rupture despite attempted treatment (one was subjected to euthanasia at celiotomy and 2 died). Post mortem examination (7 horses) revealed gross muscular thickening of the stomach wall in 6/7 horses. Histological examination revealed focal fibrosis of the stomach wall in 4/6 and focal myositis in 1/6 horses. Conclusions and practical significance: Gastric impaction is a rare cause of colic and affected horses can present with acute, chronic or recurrent colic in the presence or absence of other gastrointestinal disease. Spontaneous gastric rupture may occur. A proportion of affected horses have gross thickening of the muscular layers of the stomach wall.

BackgroundAbsolute iron deficiency, irrespective of aetiology, remains a major and worldwide cause of morbidity. After correction of the causative lesion, reconstitution of haemoglobin level and body iron stores is traditionally achieved with oral administration of ferrous salts. The latter have significant gastrointestinal tract side-effects that, in the short-term, may impair compliance. With protracted administration these products can cause lipid peroxidation which, in turn, may accelerate atherogenesis. An alternative formulation is an iron polymaltose complex where animal data supported a promoting effect of glycerophosphate. Setting and Trial Design This was a single-centre, open, randomised, multidose four treatment parallel group study. A standard dose of ferric polymaltose complex with two differing levels of glycerophosphate was compared with an equivalent amount of iron supplied as ferrous sulphate in anaemic volunteer blood donors. The endpoints were rate of haemoglobin rise and re-expansion of body iron stores reflected in blood ferritin concentration, as well as percentage saturation of transferrin. Secondary observations were changes in the proportion of hypochromic red cells during the course of treatment, erythropoietin levels and tolerability of the two formulations. Results Outcome in the rat model suggested that the utilisation of iron from polymaltose might be enhanced by glycerophosphate. However, in donors this difference was not evident and, accordingly, the data from the three polymaltose groups combined and compared to those receiving ferrous sulphate. The rate at which haemoglobin level improved, red cell indices returned to normal, and the number of hypochromic and microcytic red cells fell was not significantly different between the groups. Similarly the serum iron, percentage saturation of transferrin and red cell ferritin were comparable. In contrast the serum ferritin levels were higher for those receiving ferrous sulphate. Additionally, side-effects were significantly more frequently encountered with the latter preparation. Conclusion These data demonstrate that the addition of glycerophosphate, observed to be beneficial in rats, did not occur in humans. Secondly, in the blood donors, equivalent amounts of iron provided as the polymaltose, with or without glycerophosphate or ferrous sulphate, corrected haemoglobin concentration and morphologically abnormal erythropoiesis at comparable rates. Similarly iron stores are replenished to an equivalent extent as seen in the matching percentage saturation of transferrin and red cell ferritin levels. Interestingly, there is a discrepancy in the serum ferritin which is higher with the salt and this may reflect oxidative stress. Thirdly, corresponding efficacy can be achieved with better patient tolerance for the complex. Finally it is postulated that the iron polymaltose complex formulation more closely approximates the way in which enterocytes handle dietary iron and thus physiologic regulatory mechanisms would be expected to reciprocally...

ID-NAT in the Western Cape Province of South Africa has contributed significantly to enhancing blood safety, particularly for HBV transmission risk and to a lesser extent for HIV. Anti-HBc testing of NAT nonrepeat reactive donations seems useful in identifying a subgroup of donors with OBI who may be at risk of transmitting HBV.

Red blood cells undergo a series of biochemical fluctuations during 35–42-day storage period at 1°C to 6°C. The sodium/potassium pump is immobilised causing a decrease in intracellular potassium with an increase in cytoplasmic sodium levels, glucose levels decline, and acidosis occurs as a result of low pH levels. The frailty of stored erythrocytes triggers the formation of haemoglobin-containing microparticles and the release of cell-free haemoglobin which may add to transfusion difficulties. Lipid peroxidation, oxidative stress to band 3 structures, and other morphological and structural molecular changes also occur leading to spheroechinocytes and osmotic fragility. These changes that transpire in the red cells during the storage period are referred to as “storage lesions.” It is well documented that gamma irradiation exacerbates storage lesions and the reports of increased potassium levels leading to adverse reactions observed in neonates and infants have been of particular concern. There are, however, remarkably few systematic studies comparing the in vitro storage lesions of irradiated and nonirradiated red cell concentrates and it has been suggested that the impact of storage lesions on leucocyte reduced red blood cell concentrate (RBCC) is incomplete. The review examines storage lesions in red blood cells and their adverse effects in reference to blood transfusion.

To assess the contribution of naturally occurring portal-systemic shunts to the coagulopathy of patients with liver disease, we studied laboratory parameters of hemostasis in 20 adult patients with extrahepatic portal hypertension, secondary to portal vein thrombosis, that had resulted in variceal bleeding. All extrahepatic portal hypertension patients had normal liver function and histological appearance. None had any evidence of preexisting coagulation disorders, and none had bled or undergone sclerotherapy in the 6 mo before study. Age- and gender-matched groups of 20 healthy individuals and 20 stable patients with cirrhosis and portal hypertension who had a history of variceal bleeding served as controls. Both patient groups had thrombocytopenia consistent with hypersplenism and portal hypertension. Prothrombin international normalized ratio (extrahepatic portal hypertension, 1.3 +/- 0.12; cirrhosis, 1.7 +/- 0.2; control, 1.02 +/- 0.06; p < 0.05) and partial thromboplastin time ratios (extrahepatic portal hypertension, 1.12 +/- 0.1; cirrhosis, 1.26 +/- 0.2; controls, 1.01 +/- 0.03; p < 0.05) were significantly prolonged in both patient groups. Extrahepatic portal hypertension and cirrhotic patient groups had significantly increased levels of serum total fibrin(ogen)-related antigen (extrahepatic portal hypertension, 818 +/- 150 ng/ml; cirrhosis, 454 +/- 52 ng/ml; controls, 124 +/- 7.3 ng/ml; p < 0.05), fibrin monomer (extrahepatic portal hypertension, 168.8 +/- 16.9 ng/ml; cirrhosis, 115.6 +/- 11.1 ng/ml; controls, 19.7 +/- 0.4 ng/ml; p < 0.05) and D-dimer (extrahepatic portal hypertension, 118 +/- 9.6 ng/ml; cirrhosis, 129 +/- 10 ng/ml; controls, 53.2 +/- 1.6 ng/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)