Myocardial iron deposition can be reproducibly quantified using myocardial T2* and this is the most significant variable for predicting the need for ventricular dysfunction treatment. Myocardial iron content cannot be predicted from serum ferritin or liver iron, and conventional assessments of cardiac function can only detect those with advanced disease. Early intensification of iron chelation therapy, guided by this technique, should reduce mortality from this reversible cardiomyopathy.

SummaryHeart failure from iron overload causes 71% of deaths in thalassaemia major, yet reversal of siderotic cardiomyopathy has been reported. In order to determine the changes in myocardial iron during treatment, we prospectively followed thalassaemia patients commencing intravenous desferrioxamine for iron-induced cardiomyopathy during a 12-month period. Cardiovascular magnetic resonance assessments were performed at baseline, 3, 6 and 12 months of treatment, and included left ventricular (LV) function and myocardial and liver T2*, which is inversely related to iron concentration. One patient died. The six survivors showed progressive improvements in myocardial T2* (5AE1 ± 1AE9 to 8AE1 ± 2AE8 ms, P ¼ 0AE003), liver iron (9AE6 ± 4AE3 to 2AE1 ± 1AE5 mg/g, P ¼ 0AE001), LV ejection fraction (52 ± 7AE1% to 63 ± 6AE4%, P ¼ 0AE03), LV volumes (end diastolic volume index 115 ± 17 to 96 ± 3 ml, P ¼ 0AE03; end systolic volume index 55 ± 16 to 36 ± 6 ml, P ¼ 0AE01) and LV mass index (106 ± 14 to 95 ± 13, P ¼ 0AE01). Iron cleared more slowly from myocardium than liver (5AE0 ± 3AE3% vs. 39 ± 23% per month, P ¼ 0AE02). These prospective data confirm that siderotic heart failure is often reversible with intravenous iron chelation with desferrioxamine. Myocardial T2* improves in concert with LV volumes and function during recovery, but iron clearance from the heart is considerably slower than from the liver.

Objective: To determine the rate of perinatal hepatitis B virus (HBV) transmission in an Australian setting and to identify maternal virological factors associated with highest risk of transmission. Design, participants and setting: A prospective, observational study of perinatal transmission of HBV. Participants were pregnant women attending Sydney South West Area Health Service antenatal clinics who tested positive for hepatitis B surface antigen (HBsAg), and their babies. All babies were routinely offered hepatitis B immunoglobulin (HBIG) and HBV vaccination. Babies positive for HBsAg at 9‐month follow‐up underwent further virological testing, including HBV DNA sequencing. The study was conducted between August 2002 and May 2008. Main outcome measures: HBV DNA levels and demographic characteristics of HBsAg‐positive pregnant women; proportion of their infants with active HBV infection at 9‐month follow‐up; maternal characteristics affecting transmission rate; HBV DNA sequencing of infected infants and their mothers. Results: Of 313 HBsAg‐positive pregnant women, 213 (68%) were HBV DNA‐positive and 92 (29%) were positive for hepatitis B “e” antigen (HBeAg); 138 babies born to HBV DNA‐positive mothers were tested for HBV infection (HBsAg positivity) at about 9 months of age. Four cases of transmission were identified. All four mothers had very high HBV DNA levels (> 108 copies/mL) and were HBeAg‐positive. Three of the four infants were infected with wild‐type HBV strains, with identical maternal/infant isolates. The fourth mother–infant pair had an S gene variant, HBV D144E, which has been previously reported in association with vaccine/HBIG escape. (Unfortunately, HBIG was inadvertently omitted from the immunisation schedule of this infant.) Transmission rates were 4/138 (3%) from HBV DNA‐positive mothers overall, 4/61 (7%) from HBeAg‐positive mothers, and 4/47 (9%) from mothers with very high HBV DNA levels. No transmission was seen in 91 babies of mothers with HBV DNA levels < 108 copies/mL. Conclusion: In this cohort, HBV perinatal transmission was restricted to HBeAg‐positive mothers with very high viral loads.

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Clinical complications of transfusional iron overload are still common in patients with thalassaemia major (TM) and it is not clear how best to monitor body iron stores during long‐term follow‐up to anticipate tissue damage. In this study, we have reviewed a group of 32 patients who underwent liver biopsy between 1984 and 1986. We developed a method of assessing the trend in serum ferritin (TSF) during long‐term monitoring and compared this with mean serum ferritin (MSF) and initial liver iron (LI) concentration to determine whether, individually or in combination, they were accurate in predicting clinical outcome. LI levels were low (< 7 mg/g), medium (7–15 mg/g) and high (> 15 mg/g dry weight) in 15, 7 and 10 patients respectively. MSF was low (< 1500 μg/l), medium (1500–2500 μg/l) and high (> 2500 μg/l) in 10, 14 and 8 patients. TSF was low, medium and high risk in 9, 9 and 11 out of 29 evaluable patients. During a median follow‐up of 13·6 years (range 2·3–14·8 years) after biopsy, nine patients died and an additional three patients developed heart failure. Hypothyroidism developed in five, hypoparathyroidism in four, and diabetes mellitus in seven patients. Cirrhosis developed in four of 10 evaluable patients. The clinical end‐point of death or cardiac failure was significantly associated with increasing iron load using all three means of assessment. Although numbers were insufficient for statistical analysis, MSF or TSF were more closely associated with complications of iron overload than LI. There was no clear additional value in combining LI with MSF or TSF. The data show that quantitation of liver iron from a single liver biopsy has little value in long‐term monitoring of iron stores. Most complications can be avoided if ferritin levels can be brought down to <1500 μg/l.