Expression of cell-surface transferrin receptor following in vitro stimulation of peripheral blood lymphocytes in patients with beta-thalassaemia and iron-deficiency anaemia.
In a semilogarithmic plot, the slope of the regression line obtained in patients with beta-thalassemia major was significantly lower than that of IDA (p < 0.01), suggesting a blunted EPO response to anemia in patients polytransfused for beta-thalassemia major.
In contrast, DMT-1 mRNA levels were at least twofold greater in patients with hereditary hemochromatosis and iron deficiency anemia when compared to controls (P = 0.02, P = 0.01, respectively).
In contrast, DMT-1 mRNA levels were at least twofold greater in patients with hereditary hemochromatosis and iron deficiency anemia when compared to controls (P = 0.02, P = 0.01, respectively).
In contrast, DMT-1 mRNA levels were at least twofold greater in patients with hereditary hemochromatosis and iron deficiency anemia when compared to controls (P = 0.02, P = 0.01, respectively).
HFE mutations increase iron absorption in patients with haemochromatosis, and the mean transferrin saturations and ferritin levels are mildly increased in heterozygotes, suggesting that HFE mutations may protect against iron depletion and iron deficiency anaemia.
There was no significant difference in high-fluorescence reticulocyte and soluble transferrin receptor values between the two groups, but a correlation was observed between high-fluorescence reticulocytes and soluble transferrin receptors in iron-deficiency anemia, probably due to increased receptor synthesis as a response to decreased iron content in erythrocytes.
There was no significant difference in high-fluorescence reticulocyte and soluble transferrin receptor values between the two groups, but a correlation was observed between high-fluorescence reticulocytes and soluble transferrin receptors in iron-deficiency anemia, probably due to increased receptor synthesis as a response to decreased iron content in erythrocytes.
The TNFRSF1A GG genotype was significantly associated with IDA in established RA (OR 4.3, p = 0.01), and this was confirmed in a group of patients with early RA (OR 4.8, p = 0.04).
Soluble transferrin receptor is an additional parameter to ferritin for the diagnosis of IDA and differential diagnosis of ID+ACD, but calculation of the sTfR/F index did not improve the diagnostic value of determining sTfR alone.
The significant negative correlation between erythropoietin and hemoglobin levels observed in IDA patients was also found in a group of anemic but not hypoferremic hereditary spherocytosis subjects, but not in ACD patients.
The activity of both IRP1 and IRP2 and the levels of IRP2 were: (i) higher in monocytes and macrophages of HH patients than in those of control subjects; (ii) increased in the duodenal samples of the patients with HH and iron-deficiency anemia.
The activity of both IRP1 and IRP2 and the levels of IRP2 were: (i) higher in monocytes and macrophages of HH patients than in those of control subjects; (ii) increased in the duodenal samples of the patients with HH and iron-deficiency anemia.
The activity of both IRP1 and IRP2 and the levels of IRP2 were: (i) higher in monocytes and macrophages of HH patients than in those of control subjects; (ii) increased in the duodenal samples of the patients with HH and iron-deficiency anemia.
[Iron status with particular consideration of soluble transferrin receptors in children and youth with gastritis, with or without Helicobacter pylori infection].
We determined whether the rise in post-prandial serum iron is increased in fully treated patients with hereditary haemochromatosis (HFEC282Y+/+; HH) compared to iron deficiency anaemia (IDA), iron-replete heterozygous subjects (HFEC282Y+/-) and iron-replete controls (HFEC282Y-/-).
Here, we show that iron deficiency anemia refractory to oral iron therapy can be caused by germline mutations in TMPRSS6, which encodes a type II transmembrane serine protease produced by the liver that regulates the expression of the systemic iron regulatory hormone hepcidin.