A physician or group of physicians considers presentation and evolution of a real clinical case, reacting to clinical information and data (boldface type). This is followed by a discussion/commentary Hereditary xerocytosis revisited

[1]  S. Rivella,et al.  IDENTIFICATION OF ERYTHROFERRONE AS AN ERYTHROID REGULATOR OF IRON METABOLISM , 2014, Nature Genetics.

[2]  M. Bezerra,et al.  Erythropoiesis‐driven regulation of hepcidin in human red cell disorders is better reflected through concentrations of soluble transferrin receptor rather than growth differentiation factor 15 , 2014, American journal of hematology.

[3]  M. Golub,et al.  Developmental plasticity of red blood cell homeostasis , 2014, American journal of hematology.

[4]  G. Lettre,et al.  Lessons and Implications from Genome-Wide Association Studies (GWAS) Findings of Blood Cell Phenotypes , 2014, Genes.

[5]  K. Kissa,et al.  Piezo1 plays a role in erythrocyte volume homeostasis , 2014, Haematologica.

[6]  D. Vandorpe,et al.  Dehydrated stomatocytic anemia due to the heterozygous mutation R2456H in the mechanosensitive cation channel PIEZO1: a case report. , 2014, Blood cells, molecules & diseases.

[7]  F. Costa,et al.  Iron overload in a teenager with xerocytosis: the importance of nuclear magnetic resonance imaging , 2013, Einstein.

[8]  D. Bowden,et al.  Transfusion suppresses erythropoiesis and increases hepcidin in adult patients with β-thalassemia major: a longitudinal study. , 2013, Blood.

[9]  A. Patapoutian,et al.  Dehydrated Hereditary Stomatocytosislinked to gain-of-function mutations in mechanically activated PIEZO1 ion channels , 2013, Nature Communications.

[10]  Ivan Limongelli,et al.  Multiple clinical forms of dehydrated hereditary stomatocytosis arise from mutations in PIEZO1. , 2013, Blood.

[11]  Frederick Sachs,et al.  Xerocytosis is caused by mutations that alter the kinetics of the mechanosensitive channel PIEZO1 , 2013, Proceedings of the National Academy of Sciences.

[12]  A. Iolascon,et al.  Missense mutations in the ABCB6 transporter cause dominant familialpseudohyperkalemia , 2013, American journal of hematology.

[13]  Christian Gieger,et al.  Seventy-five genetic loci influencing the human red blood cell , 2012, Nature.

[14]  Brian E. Smith,et al.  Mutations in the mechanotransduction protein PIEZO1 are associated with hereditary xerocytosis. , 2012, Blood.

[15]  F. Sachs,et al.  The mechanosensitive ion channel Piezo1 is inhibited by the peptide GsMTx4. , 2011, Biochemistry.

[16]  D. Vandorpe,et al.  Hypoxia Activates a Ca2+-Permeable Cation Conductance Sensitive to Carbon Monoxide and to GsMTx-4 in Human and Mouse Sickle Erythrocytes , 2010, PloS one.

[17]  N. Andrews,et al.  Genes determining blood cell traits , 2009, Nature Genetics.

[18]  P. Lacor,et al.  Congenital spherocytosis with hereditary hemochromatosis without pathogenic mutations in the HFE gene. , 2004, European journal of internal medicine.

[19]  T. Rouault,et al.  MCV as a guide to phlebotomy therapyfor hemochromatosis , 2001, Transfusion.

[20]  M. Cappellini,et al.  Association of hereditary spherocytosis and idiopathic hemochromatosis. A synergistic effect in determining iron overload. , 1986, American journal of clinical pathology.

[21]  M. Wheby,et al.  Patients with hereditary spherocytosis may have clinically significant iron overload when they are also heterozygous for hemochromatosis. , 1985, Transactions of the American Clinical and Climatological Association.

[22]  M. Skolnick,et al.  Iron overload in hereditary spherocytosis: Association with hla‐linked hemochromatosis , 1982, American journal of hematology.

[23]  O. Platt,et al.  Exercise-induced hemolysis in xerocytosis. Erythrocyte dehydration and shear sensitivity. , 1981, The Journal of clinical investigation.

[24]  B. Glader,et al.  Congenital hemolytic anemia associated with dehydrated erythrocytes and increased potassium loss. , 1974, The New England journal of medicine.

[25]  J. Bates,et al.  A new variant of hereditary hemolytic anemia with stomatocytosis and erythrocyte cation abnormality. , 1971, Blood.