Fluticasone in eosinophilic corrugated ringed esophagus

TO THE EDITOR: Bruntet al. (1) have provided valuable information regarding the interpretation of iron deposition in liver biopsy specimens. Specifically, a “reticuloendothelial pattern” was found to provide strong evidence against the presence of C282Y homozygosity, or compound heterozygosity with respect to the HFE gene. In contrast, the “hepatocellular pattern” was supportive of, but not specific to, theseHFE genotypes. However, we were surprised by the absence of information on transferrin saturation levels, an important initial test in the investigation of HFE-associated hereditary hemochromatosis (HH) (2). At our institution, we reviewed the genotypes of individuals referred forHFE testing on the basis of liver biopsy histology suggestive of HH. In particular, we reviewed those patients who also had nonphlebotimized transferrin saturation values within the normal or mildly elevated range (,56%) to determine if they were part of the HFE-associated spectrum of disease. From our database of 1295 patients, nine were identified who met both of the aforementioned characteristics. Three individuals (two women, one man) had double HFE mutations (one C282Y/C282Y and two C282Y/H63D). The corresponding saturation values ranged from 40% to 55%. Two individuals were heterozygous for the C282Y mutation and were found to also have hepatitis C and alcoholic steatohepatitis, respectively. The four remaining patients had no C282Y mutations. One of these patients had alcoholic steatohepatitis and a transferrin saturation of 42%. The other three had transferrin saturation values of 22%, 22%, and 27%, respectively. These findings indicate that the specificity of a hepatocellular pattern of iron deposition as an indicator of HFEassociated HH can be increased if interpreted in combination with the patient’s transferrin saturation level. Specifically, patients with a low normal transferrin saturation level (,30%) are unlikely to have C282Y mutations. We would be interested to know what the transferrin saturation values were for the patients from the study by Brunt et al. (1) who lacked the C282Y mutation. Also, how many of the patients withHFE C282Y homozygote or compound heterozygote mutations had transferrin saturation levels ,40%?