Sickle cell disease is a family of hemoglobin combinations, including Hemoglobin SS known as Sickle-cell anemia, SC S halassemia, SD Punjas, SO Arab, SE, SS (hereditary persistence of fetal hemoglobin). These are all Sickle-cell complications, but some are more severe than others. There are genetic differences in each that we still do not understand, but it causes some to have a mild course and some severe course. (Platt, Sacerdote).
Hemoglobin S known as HbSS or Sickle-cell Anemia the most common form is caused when one inherits two Sickle-cell genes, from each parent. The Anemia can lead to premature gallstones in many cases. The Anemia can become life threatening during aplastic crisis or spleen removed is done for splenic sequestration in older children if it continues to happen over and over. Children and same adults may experience increase bacterial infection. Tissue damages cause pain and scarring. Strokes can occur in children because of blocked blood flow to the brain. Blocked blood flow to the bone may cause pain episodes, and lead to aseptic necrosis of the hip and shoulder bone. Blocking of the eyes blood vessel can lead to bleeding into the eye and even loss of vision. The older a patient gets damage to the lungs and kidneys can cause breathing problems and inability to filter toxins from ones blood. Pain episodes are unpredictable and disruptive to normal life.
Hemoglobin SC HbSC disease is the second most common type of Sickle-cell disease, where one inherits an HbC gene from one parent and HbS from the other. HbSC is sickle syndrome, which is very similar to Sickle-cell Anemia; the hemolysis is usually less severe so the Anemia is milder. The life expectancy for those with HbSC is reported to be in the mid 60’s compared to those with HbSC have less incidence of stroke compared to those with HbSS. Having an enlarged spleen is more common in older children and adults. An enlarged spleen doesn’t work well against fighting infections....