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Susana Rocha - One of the best experts on this subject based on the ideXlab platform.
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erythrocyte membrane Protein destabilization versus clinical outcome in 160 portuguese hereditary spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, José Barbot, Esmeralda Cleto, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Petronila Rochapereira, Luís BeloAbstract:Summary Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4·2 – that lead to membrane destabilization. This study aimed to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or membrane-linked Proteins in membrane disturbance and in HS clinical outcome. A total of 215 Portuguese individuals were studied – 203 from 71 families plus 12 individual unrelated subjects; 160 of them were diagnosed with HS. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. Standardized electrophoretic erythrocyte membrane Protein analysis was used to identify and quantify Protein Deficiencies. Band 3 and ankyrin were found to account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing imbalance between combined Protein Deficiencies seemed to underlie HS severity, by increasing membrane destabilization. There was an increased membrane linkage of the cytosolic Proteins, glyceraldehyde-3-phosphate dehydrogenase and peroxiredoxin 2, and of denatured haemoglobin, suggesting that this linkage could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Erythrocyte membrane Protein destabilization versus clinical outcome in 160 Portuguese Hereditary Spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Luís Belo, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Alice Santos-silvaAbstract:Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4.2 – that lead to membrane destabilization. Ours aims were to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or of membrane linked Proteins in membrane disturbance and in HS clinical outcome. We studied 215 Portuguese individuals – 203 from 71 families plus 12 individual unrelated subjects, and found that 160 of them were HS patients. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. We performed the standardized electrophoretic erythrocyte membrane Protein analysis to identify and quantify Protein Deficiencies. We found that band 3 and ankyrin account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing unbalance between combined Protein Deficiencies seem to underlie HS severity, by increasing membrane destabilization. We found an increased membrane linkage of the cytosolic Proteins, G3PD and peroxiredoxin 2, and of methaemoglobin, suggesting that this could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Presence of cytosolic peroxiredoxin 2 in the erythrocyte membrane of patients with hereditary spherocytosis.
Blood Cells Molecules and Diseases, 2008Co-Authors: Susana Rocha, Elisabeth Castro, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Francisco Lemos-amado, Alexandre Quintanilha, Rui Vitorino, Fatima Ferreira, Luís BeloAbstract:Abstract We studied 82 Portuguese individuals, 57 with hereditary spherocytosis (HS) and 25 unaffected controls. We performed standardized diagnosis tests, including electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies underlying HS. Membrane bound hemoglobin (MBH) and band 3 profiles were determined as oxidative stress and aging markers. A Protein of about 22 kDa, present in 21 of 57 HS patients, but not in controls, was identified as peroxiredoxin 2 (Prx2), by mass-spectroscopy and by immunoblotting. Human erythrocyte Prx2 is a peroxiredoxin with thiol-specific antioxidant activity. The presence of Prx2 in erythrocyte membranes was linked to higher levels of oxidative stress, as reflected by significantly increased MBH in those HS patients. No relation with HS clinical severity was observed and Prx2 was detected in all types of membrane Protein abnormalities. Prx2 membrane linkage is associated with a higher oxidative stress susceptibility of HS erythrocytes.
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Protein deficiency balance as a predictor of clinical outcome in hereditary spherocytosis.
European journal of haematology, 2005Co-Authors: Susana Rocha, Elisabeth Castro, José Barbot, Luís Belo, Alexandre Quintanilha, Elísio Costa, Irene Rebelo, Cristina Catarino, José Manuel Cabeda, Alice Santos-silvaAbstract:Vertical and horizontal interactions between membrane constituents account for integrity, strength and deformability of the erythrocyte. Disruption of vertical interactions caused by membrane Protein Deficiencies in hereditary spherocytosis (HS), favor membrane vesiculation with development of spherocytic cells. Our aim was to evaluate the hematological and clinical presentation of HS according to the type and amount of Protein deficiency. We studied 81 Portuguese individuals, 71 belonging to 21 families plus 10 unrelated subjects, and found that 51 of them were HS patients. Patients were classified as presenting mild, typical or severe HS, according to laboratory results and clinical follow-up. We performed screening tests and the standardized electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies. We found band 3 and ankyrin Deficiencies as the major causes for HS. The ratios between the value of the primary and/or secondary Protein Deficiencies showed significantly different values according to the severity of HS, and a significant inverse correlation with the severity of HS was observed. In mild HS, the ratios between Protein Deficiencies reflected equivalent Protein Deficiencies, while an unbalance was observed in typical HS, which was enhanced in severe HS. Our data suggest that the relative quantification of each major membrane Protein and of the ratios between the values of Protein Deficiencies may be helpful in providing additional data about the clinical outcome of HS.
Karine Clément - One of the best experts on this subject based on the ideXlab platform.
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Micronutrient and Protein Deficiencies After Gastric Bypass and Sleeve Gastrectomy: a one-year Follow-up
Obesity Surgery, 2016Co-Authors: Eric O. Verger, Judith Aron-wisnewsky, Maria Carlota Dao, Brandon D. Kayser, Jean-michel Oppert, Jean-luc Bouillot, Adriana Torcivia, Karine ClémentAbstract:Background Roux-en-Y gastric bypass (GBP) and sleeve gastrectomy (SG) have increased dramatically, potentially increasing the prevalence of nutritional Deficiencies. The aim of this study was to analyze the effects of food restriction during the first year after bariatric surgery (BS) on nutritional parameters. Methods Twenty-two and 30 obese patients undergoing GBP and SG were prospectively followed at baseline and 3, 6, and 12 months after BS (N = 14 and N = 19 at T12). We evaluated food intake and nutrient adequacy (T0, T3, T12), as well as serum vitamin and mineral concentration (T0, T3, T6, T12). Results At baseline, GBP and SG patients had similar clinical characteristics, food intake, nutrient adequacy, and serum concentration. The drastic energy and food reduction led to very low probabilities of adequacy for nutrients similar in both models (T3, T12). Serum analysis demonstrated a continuous decrease in prealbumin during the follow-up, indicating mild Protein depletion in 37 and 38 % of GBP patients and 57 and 52 % of SG patients, respectively, at T3 and T12. Conversely, despite the low probabilities of adequacy observed at T3 and T12, systematic multivitamin and mineral supplementation after GBP and SG prevented most nutritional Deficiencies. Conclusions GBP and SG have comparable effects in terms of energy and food restriction and subsequent risk of micronutrient and Protein Deficiencies in the first year post BS. Such results advocate for a cautious monitoring of Protein intake after GPB and SG and a systematic multivitamin and mineral supplementation in the first year after SG.
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micronutrient and Protein Deficiencies after gastric bypass and sleeve gastrectomy a 1 year follow up
Obesity Surgery, 2016Co-Authors: Eric O. Verger, Maria Carlota Dao, Brandon D. Kayser, Jean-michel Oppert, Jean-luc Bouillot, Adriana Torcivia, Karine Clément, Judith AronwisnewskyAbstract:Roux-en-Y gastric bypass (GBP) and sleeve gastrectomy (SG) have increased dramatically, potentially increasing the prevalence of nutritional Deficiencies. The aim of this study was to analyze the effects of food restriction during the first year after bariatric surgery (BS) on nutritional parameters. Twenty-two and 30 obese patients undergoing GBP and SG were prospectively followed at baseline and 3, 6, and 12 months after BS (N = 14 and N = 19 at T12). We evaluated food intake and nutrient adequacy (T0, T3, T12), as well as serum vitamin and mineral concentration (T0, T3, T6, T12). At baseline, GBP and SG patients had similar clinical characteristics, food intake, nutrient adequacy, and serum concentration. The drastic energy and food reduction led to very low probabilities of adequacy for nutrients similar in both models (T3, T12). Serum analysis demonstrated a continuous decrease in prealbumin during the follow-up, indicating mild Protein depletion in 37 and 38 % of GBP patients and 57 and 52 % of SG patients, respectively, at T3 and T12. Conversely, despite the low probabilities of adequacy observed at T3 and T12, systematic multivitamin and mineral supplementation after GBP and SG prevented most nutritional Deficiencies. GBP and SG have comparable effects in terms of energy and food restriction and subsequent risk of micronutrient and Protein Deficiencies in the first year post BS. Such results advocate for a cautious monitoring of Protein intake after GPB and SG and a systematic multivitamin and mineral supplementation in the first year after SG.
Luís Belo - One of the best experts on this subject based on the ideXlab platform.
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erythrocyte membrane Protein destabilization versus clinical outcome in 160 portuguese hereditary spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, José Barbot, Esmeralda Cleto, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Petronila Rochapereira, Luís BeloAbstract:Summary Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4·2 – that lead to membrane destabilization. This study aimed to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or membrane-linked Proteins in membrane disturbance and in HS clinical outcome. A total of 215 Portuguese individuals were studied – 203 from 71 families plus 12 individual unrelated subjects; 160 of them were diagnosed with HS. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. Standardized electrophoretic erythrocyte membrane Protein analysis was used to identify and quantify Protein Deficiencies. Band 3 and ankyrin were found to account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing imbalance between combined Protein Deficiencies seemed to underlie HS severity, by increasing membrane destabilization. There was an increased membrane linkage of the cytosolic Proteins, glyceraldehyde-3-phosphate dehydrogenase and peroxiredoxin 2, and of denatured haemoglobin, suggesting that this linkage could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Erythrocyte membrane Protein destabilization versus clinical outcome in 160 Portuguese Hereditary Spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Luís Belo, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Alice Santos-silvaAbstract:Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4.2 – that lead to membrane destabilization. Ours aims were to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or of membrane linked Proteins in membrane disturbance and in HS clinical outcome. We studied 215 Portuguese individuals – 203 from 71 families plus 12 individual unrelated subjects, and found that 160 of them were HS patients. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. We performed the standardized electrophoretic erythrocyte membrane Protein analysis to identify and quantify Protein Deficiencies. We found that band 3 and ankyrin account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing unbalance between combined Protein Deficiencies seem to underlie HS severity, by increasing membrane destabilization. We found an increased membrane linkage of the cytosolic Proteins, G3PD and peroxiredoxin 2, and of methaemoglobin, suggesting that this could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Presence of cytosolic peroxiredoxin 2 in the erythrocyte membrane of patients with hereditary spherocytosis.
Blood Cells Molecules and Diseases, 2008Co-Authors: Susana Rocha, Elisabeth Castro, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Francisco Lemos-amado, Alexandre Quintanilha, Rui Vitorino, Fatima Ferreira, Luís BeloAbstract:Abstract We studied 82 Portuguese individuals, 57 with hereditary spherocytosis (HS) and 25 unaffected controls. We performed standardized diagnosis tests, including electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies underlying HS. Membrane bound hemoglobin (MBH) and band 3 profiles were determined as oxidative stress and aging markers. A Protein of about 22 kDa, present in 21 of 57 HS patients, but not in controls, was identified as peroxiredoxin 2 (Prx2), by mass-spectroscopy and by immunoblotting. Human erythrocyte Prx2 is a peroxiredoxin with thiol-specific antioxidant activity. The presence of Prx2 in erythrocyte membranes was linked to higher levels of oxidative stress, as reflected by significantly increased MBH in those HS patients. No relation with HS clinical severity was observed and Prx2 was detected in all types of membrane Protein abnormalities. Prx2 membrane linkage is associated with a higher oxidative stress susceptibility of HS erythrocytes.
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Protein deficiency balance as a predictor of clinical outcome in hereditary spherocytosis.
European journal of haematology, 2005Co-Authors: Susana Rocha, Elisabeth Castro, José Barbot, Luís Belo, Alexandre Quintanilha, Elísio Costa, Irene Rebelo, Cristina Catarino, José Manuel Cabeda, Alice Santos-silvaAbstract:Vertical and horizontal interactions between membrane constituents account for integrity, strength and deformability of the erythrocyte. Disruption of vertical interactions caused by membrane Protein Deficiencies in hereditary spherocytosis (HS), favor membrane vesiculation with development of spherocytic cells. Our aim was to evaluate the hematological and clinical presentation of HS according to the type and amount of Protein deficiency. We studied 81 Portuguese individuals, 71 belonging to 21 families plus 10 unrelated subjects, and found that 51 of them were HS patients. Patients were classified as presenting mild, typical or severe HS, according to laboratory results and clinical follow-up. We performed screening tests and the standardized electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies. We found band 3 and ankyrin Deficiencies as the major causes for HS. The ratios between the value of the primary and/or secondary Protein Deficiencies showed significantly different values according to the severity of HS, and a significant inverse correlation with the severity of HS was observed. In mild HS, the ratios between Protein Deficiencies reflected equivalent Protein Deficiencies, while an unbalance was observed in typical HS, which was enhanced in severe HS. Our data suggest that the relative quantification of each major membrane Protein and of the ratios between the values of Protein Deficiencies may be helpful in providing additional data about the clinical outcome of HS.
Alexandre Quintanilha - One of the best experts on this subject based on the ideXlab platform.
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erythrocyte membrane Protein destabilization versus clinical outcome in 160 portuguese hereditary spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, José Barbot, Esmeralda Cleto, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Petronila Rochapereira, Luís BeloAbstract:Summary Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4·2 – that lead to membrane destabilization. This study aimed to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or membrane-linked Proteins in membrane disturbance and in HS clinical outcome. A total of 215 Portuguese individuals were studied – 203 from 71 families plus 12 individual unrelated subjects; 160 of them were diagnosed with HS. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. Standardized electrophoretic erythrocyte membrane Protein analysis was used to identify and quantify Protein Deficiencies. Band 3 and ankyrin were found to account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing imbalance between combined Protein Deficiencies seemed to underlie HS severity, by increasing membrane destabilization. There was an increased membrane linkage of the cytosolic Proteins, glyceraldehyde-3-phosphate dehydrogenase and peroxiredoxin 2, and of denatured haemoglobin, suggesting that this linkage could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Erythrocyte membrane Protein destabilization versus clinical outcome in 160 Portuguese Hereditary Spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Luís Belo, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Alice Santos-silvaAbstract:Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4.2 – that lead to membrane destabilization. Ours aims were to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or of membrane linked Proteins in membrane disturbance and in HS clinical outcome. We studied 215 Portuguese individuals – 203 from 71 families plus 12 individual unrelated subjects, and found that 160 of them were HS patients. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. We performed the standardized electrophoretic erythrocyte membrane Protein analysis to identify and quantify Protein Deficiencies. We found that band 3 and ankyrin account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing unbalance between combined Protein Deficiencies seem to underlie HS severity, by increasing membrane destabilization. We found an increased membrane linkage of the cytosolic Proteins, G3PD and peroxiredoxin 2, and of methaemoglobin, suggesting that this could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Presence of cytosolic peroxiredoxin 2 in the erythrocyte membrane of patients with hereditary spherocytosis.
Blood Cells Molecules and Diseases, 2008Co-Authors: Susana Rocha, Elisabeth Castro, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Francisco Lemos-amado, Alexandre Quintanilha, Rui Vitorino, Fatima Ferreira, Luís BeloAbstract:Abstract We studied 82 Portuguese individuals, 57 with hereditary spherocytosis (HS) and 25 unaffected controls. We performed standardized diagnosis tests, including electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies underlying HS. Membrane bound hemoglobin (MBH) and band 3 profiles were determined as oxidative stress and aging markers. A Protein of about 22 kDa, present in 21 of 57 HS patients, but not in controls, was identified as peroxiredoxin 2 (Prx2), by mass-spectroscopy and by immunoblotting. Human erythrocyte Prx2 is a peroxiredoxin with thiol-specific antioxidant activity. The presence of Prx2 in erythrocyte membranes was linked to higher levels of oxidative stress, as reflected by significantly increased MBH in those HS patients. No relation with HS clinical severity was observed and Prx2 was detected in all types of membrane Protein abnormalities. Prx2 membrane linkage is associated with a higher oxidative stress susceptibility of HS erythrocytes.
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Protein deficiency balance as a predictor of clinical outcome in hereditary spherocytosis.
European journal of haematology, 2005Co-Authors: Susana Rocha, Elisabeth Castro, José Barbot, Luís Belo, Alexandre Quintanilha, Elísio Costa, Irene Rebelo, Cristina Catarino, José Manuel Cabeda, Alice Santos-silvaAbstract:Vertical and horizontal interactions between membrane constituents account for integrity, strength and deformability of the erythrocyte. Disruption of vertical interactions caused by membrane Protein Deficiencies in hereditary spherocytosis (HS), favor membrane vesiculation with development of spherocytic cells. Our aim was to evaluate the hematological and clinical presentation of HS according to the type and amount of Protein deficiency. We studied 81 Portuguese individuals, 71 belonging to 21 families plus 10 unrelated subjects, and found that 51 of them were HS patients. Patients were classified as presenting mild, typical or severe HS, according to laboratory results and clinical follow-up. We performed screening tests and the standardized electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies. We found band 3 and ankyrin Deficiencies as the major causes for HS. The ratios between the value of the primary and/or secondary Protein Deficiencies showed significantly different values according to the severity of HS, and a significant inverse correlation with the severity of HS was observed. In mild HS, the ratios between Protein Deficiencies reflected equivalent Protein Deficiencies, while an unbalance was observed in typical HS, which was enhanced in severe HS. Our data suggest that the relative quantification of each major membrane Protein and of the ratios between the values of Protein Deficiencies may be helpful in providing additional data about the clinical outcome of HS.
Alice Santos-silva - One of the best experts on this subject based on the ideXlab platform.
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Erythrocyte membrane Protein destabilization versus clinical outcome in 160 Portuguese Hereditary Spherocytosis patients
British Journal of Haematology, 2010Co-Authors: Susana Rocha, Petronila Rocha-pereira, José Barbot, Esmeralda Cleto, Luís Belo, Alexandre Quintanilha, Fatima Ferreira, Elísio Costa, Alice Santos-silvaAbstract:Hereditary Spherocytosis (HS) is a haemolytic anaemia caused by erythrocyte Protein membrane defects – spectrin, ankyrin, band 3 or Protein 4.2 – that lead to membrane destabilization. Ours aims were to evaluate the prevalence of Protein Deficiencies and the role of membrane Proteins or of membrane linked Proteins in membrane disturbance and in HS clinical outcome. We studied 215 Portuguese individuals – 203 from 71 families plus 12 individual unrelated subjects, and found that 160 of them were HS patients. They were classified as presenting mild, moderate or severe forms of HS according to the degree of haemolytic anaemia. We performed the standardized electrophoretic erythrocyte membrane Protein analysis to identify and quantify Protein Deficiencies. We found that band 3 and ankyrin account for the majority of the erythrocyte Protein defects underlying HS. Increasing isolated Protein deficiency or increasing unbalance between combined Protein Deficiencies seem to underlie HS severity, by increasing membrane destabilization. We found an increased membrane linkage of the cytosolic Proteins, G3PD and peroxiredoxin 2, and of methaemoglobin, suggesting that this could interfere with membrane structure. Our data suggest that the quantification and the analysis of RBC membrane Proteins may be helpful in predicting the clinical outcome of HS.
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Protein deficiency balance as a predictor of clinical outcome in hereditary spherocytosis.
European journal of haematology, 2005Co-Authors: Susana Rocha, Elisabeth Castro, José Barbot, Luís Belo, Alexandre Quintanilha, Elísio Costa, Irene Rebelo, Cristina Catarino, José Manuel Cabeda, Alice Santos-silvaAbstract:Vertical and horizontal interactions between membrane constituents account for integrity, strength and deformability of the erythrocyte. Disruption of vertical interactions caused by membrane Protein Deficiencies in hereditary spherocytosis (HS), favor membrane vesiculation with development of spherocytic cells. Our aim was to evaluate the hematological and clinical presentation of HS according to the type and amount of Protein deficiency. We studied 81 Portuguese individuals, 71 belonging to 21 families plus 10 unrelated subjects, and found that 51 of them were HS patients. Patients were classified as presenting mild, typical or severe HS, according to laboratory results and clinical follow-up. We performed screening tests and the standardized electrophoretic membrane Protein analysis to identify and quantify Protein Deficiencies. We found band 3 and ankyrin Deficiencies as the major causes for HS. The ratios between the value of the primary and/or secondary Protein Deficiencies showed significantly different values according to the severity of HS, and a significant inverse correlation with the severity of HS was observed. In mild HS, the ratios between Protein Deficiencies reflected equivalent Protein Deficiencies, while an unbalance was observed in typical HS, which was enhanced in severe HS. Our data suggest that the relative quantification of each major membrane Protein and of the ratios between the values of Protein Deficiencies may be helpful in providing additional data about the clinical outcome of HS.