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    Sickle cell disease

    In Africa, only Ghana and the Republic of Benin have established selective and pilot Newborn screening programme, respectively [37, 41, 45, 46]. The clinical severity of SCD is variable and usually defies genetic or phenotypic explanation. Acute VOC and chronic pain syndrome could be disabling to the patient, and studies have demonstrated an association of acute pain syndromes with other complications of SCD, including death [ 19 , 47 ].

    Pain management guidelines and the need to rule out life-threatening comorbidities suggest the need for rapid physician evaluation of patients who present to the emergency department ED with complaints related to SCD [ 47 ]. From the difficulty in identifying sickle-shaped erythrocytes in neonates, Janet Watson postulated, in , that high fetal hemoglobin leads to a decrease in cells that could sickle and therefore a decrease in sickle hemoglobin in those red blood cells [ 49 ]. Several years later it was suggested that by increasing or prolonging the concentration of foetal hemoglobin in erythrocytes, it would be possible to decrease the frequency and severity of the clinical manifestations of SCD [ 50 — 52 ].

    HU, an anti-leukaemia agent with the capacity to increase foetal Hb, was introduced to treat sickle cell disease with significant clinical and symptomatic improvement. In a randomised double-blind study, the Multicentre Study of HU in Sickle Cell Anaemia MSH , showed that this new drug could decrease episodes of painful crises, acute chest syndrome and the need for transfusion [ 53 , 54 ]. The study recruited adults with more than three painful crises in the year prior to the start of HU, and the clinical effect was great enough for the trial to terminate 3 months early [ 54 , 55 ].

    The paediatric studies on the use of hydroxyurea reflected the results of the adult trials, with reduced acute complications and with no toxicity or decreased growth, and suggested reduced end organ damage if administered early [ 56 — 58 ]. Although the treatment of strokes in SCD had been improving, it was a ground breaking trial in the final decade of the twentieth century that changed the way SCD was monitored [ 60 , 61 ] to prevent stoke in this group of patients. These would appear on ultrasonography as increased flow in that region and patients with abnormal flow are at increased risk of stroke [ 60 , 62 ].

    Pulmonary hypertension PAH is recognised to be a common complication of SCD and other haemolytic disorders and is associated with increased mortality and morbidity. Chronic hemolysis represents a prominent mechanistic pathway in the pathogenesis of SCD-associated PAH via a nitric oxide NO scavenging and abrogation of NO salutatory effects on vascular function. These processes lead to acute and chronic pulmonary vasoconstriction [ 65 ]. Many known infectious risk factors for PAH, i.

    Self-reported history of cardiovascular and renal complications, systolic hypertension, high lactate dehydrogenase levels index of haemolysis , high level of alkaline phosphatase, low transferrin concentration indicating iron overload and priapism in men were found to be independent correlates of PAH [ 20 , 67 ].

    Treatment with HU at maximum tolerated dose and judicious use of blood transfusion support and iron-chelating agents where indicated is recommended [ 66 ]. Sildenafil was well tolerated by both male and female patients and it reduced the estimated pulmonary artery systolic pressure and increased the 6-min walk distance [ 68 , 69 ]. Gene therapy has the potential to correct the underlying defect leading to the clinical manifestations of sickle cell disease.

    It would reduce the need for many of the preventative treatments and invasive therapies. A few years ago, this may not have seemed possible; however, gene therapy has been proven to be effective in mouse models [ 1 , 2 ], and there are currently several teams working on phase II trials using viral vectors [ 70 — 72 ].

    Although there have been improvements in the management of SCD in developed countries, much less progress has been made in the developing world in which the disease is common, where it is still an important cause of childhood mortality. In low-income countries, basic facilities for management are lacking, systemic screening is not a common practice, and diagnosis is made late. Research collaborations between sickle cell research groups in rich and poor countries would be of considerable benefit to the health and well-being of patients with SCD in the developing countries. In particular, interactions of this kind offer an opportunity to improve clinical and diagnostic facilities and hence the management of patients in the developing world.

    We cannot yet cure SCD, but we have learnt that simple interventions significantly improve morbidity and mortality. Conversely, there are severe risks and complications including rejection, marrow aplasia, neurological disorders, graft-versus-host disease and death, and standard BMT is limited by a requirement for human leukocyte antigen HLA -matched sibling donors [ 70 ]. Currently transplantation is only considered for those children with HLA-identical siblings and in whom the clinical manifestation of the disease does not respond to standard care.

    The past years have shown great accomplishments for SCD including newborn screening, penicillin prophylaxis, primary stroke prevention using blood transfusion, stroke prevention trial in sickle cell anaemia STOP and controlled trial of transfusions for silent cerebral infarct in sickle cell anaemia. The role of hydroxyurea therapy in adults and children to reduce pain, hospitalisations and most recently as an alternative for controlling cerebral blood velocity—transcranial Doppler TCD with Transfusion Changing to Hydroxyurea TWiTCH therapy.

    Although a risk-free cure has not been found in this last and current century, the following years look to be extremely promising for sickle cell anaemia; stem cell transplantation is now more commonly used in SCD. MC and NW reviewed the literature and wrote the draft of the manuscript, BI designed, reviewed and made the substantial changes the manuscript. All authors discussed, read and approved the manuscript. Dr Serajul Islam contributed to the design, literature review and was initially a co-author but did not review the manuscript following substantial revisions.

    We appreciated his contribution. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers. Login to your personal dashboard for more detailed statistics on your publications. Edited by Baba P. Edited by Andrea Tranquilli. We are IntechOpen, the world's leading publisher of Open Access books.

    Built by scientists, for scientists. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. Downloaded: Introduction Sickle cell disease SCD is due to a single point mutation Glub6Val that causes polymerisation of the mutant hemoglobin Hb S, resulting in sickling of erythrocytes [ 1 ]. Early description James Herrick is widely acknowledged as the first physician to describe a case of sickle cell.

    Discovery of molecular and genetic basis It was not until 40 years after the first description of sickle cell anaemia that a homozygous pattern of inheritance was confirmed simultaneously by two separate studies, one a pedigree study in Africa [ 11 , 12 ]. Prophylactic penicillin and pneumococcal vaccination Studies have shown that infant mortality is particularly high in sickle cell disease. Prenatal and Neonatal SCD Screening SCD is associated with high infant mortality rate; therefore, early preventive intervention is essential in reducing these deaths [ 14 , 36 ].

    The importance of neonatal identification of SCD is emphasised [36, 41, 42]. Pain management The clinical severity of SCD is variable and usually defies genetic or phenotypic explanation. Hydroxyurea HU From the difficulty in identifying sickle-shaped erythrocytes in neonates, Janet Watson postulated, in , that high fetal hemoglobin leads to a decrease in cells that could sickle and therefore a decrease in sickle hemoglobin in those red blood cells [ 49 ].

    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families
    Managing Sickle Cell Disease in Low-Income Families Managing Sickle Cell Disease in Low-Income Families

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