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Updated: Aug 7, 2026

Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
Published on: November 5, 2019
[Hematological and clinical profile in sickle cell or thalassemic patients]
Daniella Vilachá1, Raquel Salazar
1Laboratorio de Proteínas e Inmunotoxicidad, Departamento de Bioanálisis, Escuela de Ciencias, Núcleo de Sucre, Universidad de Oriente, Cumaná, Estado Sucre, Venezuela.
Clinical and hematological characteristics of 14 patients with sickle cell anemia; one heterozygous AS, and 7, with diagnostic of microcytic hypochromic anemia were analyzed. Hemoglobin phenotypes were identified by electrophoresis, fetal hemoglobin was quantificated for alkaline denaturation and the HbA2 for ionic exchange chromatography; -alpha3,7 -thalassemia was detected by mutation identification using polymerase chain reaction (PCR). SS phenotype was confirmed in 10 patients, two were SSF increased, one was SSFincreasedA2increased, and one was ASFincreased (HbF = 2%). The patient diagnosed as AS was SSFincreased (HbF = 21%). AD-patients presented a moderate clinical course of the illness. Five microcytic hypochromic anemia patients were HbAA, one was HbAAA2increased and another HbAAFincreased; those patients present a high hematological and clinical variation. beta-thalassemia was 19%. -alpha3,7-thalassemia was not detected. Infection was most frequent clinical manifestation (respiratory tract infection and intestinal parasitism). These results shows that -alpha3,7-thalassemia are not modulator genetic factors of clinical and hematological manifestations of patients with microcytic hypochromic anemia and sickle cell anemia. We suggest that environmental factors such as respiratory tract infection and intestinal parasitism may be affect the course of illness.
Clinical and hematological characteristics of 14 patients with sickle cell anemia; one heterozygous AS, and 7, with diagnostic of microcytic hypochromic anemia were analyzed. Hemoglobin phenotypes were identified by electrophoresis, fetal hemoglobin was quantificated for alkaline denaturation and the HbA2 for ionic exchange chromatography; -alpha3,7 -thalassemia was detected by mutation identification using polymerase chain reaction (PCR). SS phenotype was confirmed in 10 patients, two were SSF increased, one was SSFincreasedA2increased, and one was ASFincreased (HbF = 2%). The patient diagnosed as AS was SSFincreased (HbF = 21%). AD-patients presented a moderate clinical course of the illness. Five microcytic hypochromic anemia patients were HbAA, one was HbAAA2increased and another HbAAFincreased; those patients present a high hematological and clinical variation. beta-thalassemia was 19%. -alpha3,7-thalassemia was not detected. Infection was most frequent clinical manifestation (respiratory tract infection and intestinal parasitism). These results shows that -alpha3,7-thalassemia are not modulator genetic factors of clinical and hematological manifestations of patients with microcytic hypochromic anemia and sickle cell anemia. We suggest that environmental factors such as respiratory tract infection and intestinal parasitism may be affect the course of illness.
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