The SCH772984 Pitfall

However, we found no correlation between cardiac R2* and either liver R2* or ferritin level. It has been suggested that cardiac iron loading only occurs once a critical threshold level of liver iron loading (350?��g/m) or ferritin (1800?��g/l) is reached, beyond which it rises exponentially (Jensen et?al, 2003a). All of our patients with cardiac R2*?>?50?Hz had liver R2*?>?370?Hz http://www.selleckchem.com/products/sch772984.html (Fig?1B). However, although liver iron loading seemed to be a prerequisite for cardiac iron loading, this was not the sole determinant, as 16 patients had liver iron loading above this threshold but no evidence of cardiac iron loading. In particular, four patients had severe liver iron with R2*?>?900?Hz but no cardiac iron, suggesting that other factors are contributory. http://www.selleck.cn/products/gdc-0068.html We therefore investigated the usefulness of a new parameter, ferritin AUC, as a predictor of cardiac iron loading. To illustrate, two patients with similar lengths of follow-up and similar snapshot ferritin levels were plotted with ferritin against time (Fig?1C). MDS4 had received a total of 142 red cell units and MDS12 had received 32?units. The ferritin AUC for patient MDS4 was more than three times greater than that for MDS12 despite similar snapshot ferritin values (2174 vs. 2284), reflecting exposure to higher ferritin levels over time. Ferritin AUC correlated with units of blood transfused (r?=?0��8, P? http://www.selleckchem.com/products/Bortezomib.html However, the retrospective collection of data in our cohort limits the study of AUC, as we had enough data for AUC calculation in only 25 of the 43 cases. One possible contributor to cardiac iron loading is genetic susceptibility. In particular, one of our patients (MDS33) had only received 65?units and yet developed cardiac iron loading (R2* 58?Hz). A similar previously reported patient (cardiac R2* 178?Hz after only 48?units) was found to be homozygous for a SLC40A1 polymorphism (V221V) (Di Tucci et?al, 2008). For this study, we investigated the HFE, HFE2 and HAMP status of 22 of the above patients (17 normal, five abnormal for cardiac iron) and showed no predilection for any genotype in patients developing cardiac iron loading (data not shown). No SLC40A1 mutations were found in our cardiac iron overload patients, but four were heterozygous for the SLC40A1 V221V polymorphism. However, we commonly find this in our Caucasian population. It is unlikely that a single variable could identify which patients are at risk of cardiac iron loading. The concept of ferritin AUC is promising and we suggest prospective data collection in larger numbers to investigate whether ferritin AUC predicts which patients are at risk of cardiac iron overload and if there is a threshold level.