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Sulfhemoglobinemia is a rare condition in which there is excess sulfhemoglobin (SulfHb) in the blood. The pigment is a greenish derivative of hemoglobin which cannot be converted back to normal, functional hemoglobin.
The significance of the sickle-cell trait is that it does not show any symptoms, nor does it cause any major difference in blood cell count. The trait confers about 30% protection against malaria [clarification needed] and its occurrence appears to have risen tremendously in Africa, India and the Middle East. Some findings also show the ...
Sulfhemoglobinemia [b] Polycythemia; Congenital cyanosis (HbM Boston) arises from a mutation in the α-codon which results in a change of primary sequence, H → Y. Tyrosine stabilizes the Fe(III) form (oxyhaemoglobin) creating a permanent T-state of Hb. Peripheral cyanosis in an individual with peripheral vascular disease. Others:
Symptoms include wheezing, chest pain, fever, pulmonary infiltrate (visible on x-ray), and hypoxemia. After sickling crisis (see above) it is the second-most common cause of hospitalization and it accounts for about 25% of deaths in patients with SCD. Most cases present with vaso-occlusive crises, and then develop acute chest syndrome. [30] [31]
Hemoglobinopathy is the medical term for a group of inherited blood disorders involving the hemoglobin, the protein of red blood cells. [1] They are single-gene disorders and, in most cases, they are inherited as autosomal co-dominant traits.
Exact signs and symptoms of DLHA are anemia-alike [3] (dyspnea, palpitations, fatigue, pallor and hemolysis-alike [3] (jaundice, dark urine and pain). Some signs and symptoms indicate a medical emergency and that the patients with DLHA require to be hospitalized: [11] Rapidly progressive anemia; Worsening anemia; Severe anemia; Respiratory distress
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Hemoglobinopathies (congenital abnormality of the hemoglobin molecule or of the rate of hemoglobin synthesis) . Sickle cell disease; Thalassemia; Methemoglobinemia; Anemias (lack of red blood cells or hemoglobin)