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The Center for Hematology is a full-service facility for all blood disorders, both non-cancerous and cancerous. Our program also offers follow-up and referral within Massachusetts General Hospital or all hematology conditions.
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These include:. Our program has also become renowned for its world-class expertise in the specialized care of the following hematological conditions:. An accurate diagnosis is crucial to developing a successful treatment plan. The hematopathologists at the Center for Hematology are world renowned for their sub-specialized expertise in the diagnosis of blood diseases. Our specialists have extensive experience identifying even the most rare disorders, and their second opinions are sought by physicians around the country.
State-of-the art technology further enhances the capabilities of the pathology department, including:.
In addition to our expert diagnostic, treatment and evaluation services, our program offers state-of-the-art drug and other therapies, including:. Our program evaluates and manages the full range of blood disorders. Our program is committed to improving therapies for blood diseases. With that goal in mind, our physicians and research scientists are involved in or leading numerous clinical trials for novel therapies for several disorders.
Find Clinical Trials for blood disorders. Find Targeted Therapy Trials for blood disorders. A checklist of items to bring with you for your first visit and helpful information. We offer a variety of education and support resources to help you and your family. A simple way to connect with the various resources available to you at the Cancer Center.
We offer a wide range of integrative therapies, workshops and support groups. Our support programs can help patients and their families cope with the challenges of a cancer diagnosis. This helped lead to new knowledge and breakthrough therapies.
Hematology, ASH Education Program | American Society of Hematology
Contact the Mass General Cancer Center to make an appointment or to learn more about our programs. The Center for Hematology offers comprehensive diagnosis, treatment, and referral for all blood disorders, ranging from simple anemia to clotting disorders to major hematological cancers. Contact Information. Support the Center for Hematology Help the team at the Center for Hematology offer comprehensive diagnosis and treatment for all blood disorders.
American Society of Hematology
In the years since the first edition of Elsevier's Integrated Pharmacology , there has been a significant surge in availability of new drugs and biologics. These new compounds are briefly addressed in this section. Nitisinone is the first drug approved for the treatment of hereditory tyrosinemia type 1. This is a rare disorder arising from a genetic deficiency in fumarylacetoacetase—the enzyme that catalyzes the final step in tyrosine metabolism.
The resulting accumulation of metabolic precursors and toxic by-products leads to significant organ toxicity liver, kidney. Nitisinone inhihibits an earlier step in the pathway and prevents the accumulation of the toxic metabolites. Unfortunately, as a side effect, it produces an accumulation of tyrosine, and so dietary intake of tyrosine and its precursor amino acid, phenylalanine must be restricted.
Eculizumab is the first agent approved for the treatment of paroxysmal nocturnal hemoglobinuria, which is a rare disease that results froma genetic mutation that produces red cells that lack complement inhibitors and are susceptible to complement-mediated destruction. The disease is mis named, because the cell destruction occurs throughout the day, but is manifested at night when the urine is concentrated.
The mutation is in an X-linked gene responsible for providing lipid glycosyl-phosphatidylinositol membrane anchors for a number of blood cell surface proteins see Chapter 2 for an introduction to this concept. Currently, patients with paroxysmal nocturnal hemoglobinuria are treated with transfusions and immunosuppression. Eculizumab is a monoclonal antibody against complement that alleviates the hemolysis and improves symptoms and quality of life without addressing the underlying genetic defect. Because it inhibits aspects of the immune response, however, eculizumab increases the risk of infection especially risk of meningococcal infections.
Therefore this drug bears a black box warning that patients must be prophylactically treated with a meningococcal vaccine before treatment. As a biologic, this drug also causes side effects resembling influenza. Seropterin is the first drug to be approved for the reduction of phenylalanine concentrations in patients with phenylketonuria PKU —as opposed to merely restricting dietary intake of the amino acid.
PKU is the manifestation of genetic defects in phenylalanine hydroxylase the enzyme that converts phenylalanine to tyrosine and is the rate-limiting step in phenylalanine metabolism. There are more than documented mutations in phenylalanine hydroxylase and some result in a reduced activity that is responsive to increasing the levels of the rate-limiting substrate tetrahydrobiopterin BH 4 this disease is also known as BH 4 -responsive PKU. Unfortunately, we are unable to predict BH 4 -responsiveness at this time, so treatment efficacy is based on trial and error.
Seropterin has a very favorable side effect profile, however, headache is a most common complaint. Eltrombopag small molecule receptor antagonist and romiplostim biologic are two new drugs—with fundamentally different approaches to the same problem—for treatment of immune thrombocytopenic purpura. Interestingly, the two drugs were approved within months of each other in Immune thrombocytopenic purpura is an autoimmune disorder in which the body produces antibodies against platelets resulting in serious bleeding disorders heavy menstruation, petechial rash, bruising, nosebleeds.
Romiplostim is a chimeric recombinant biologic thrombopoietin receptor agonist fused to Fc-peptide that increases platelet production. As a biologic, romiplostim bears significant influenza side effects. It has also been shown to also increase reticulin deposition in the bone marrow with subsequent risk of fibrosis of the marrow. Eltrombopag is a new small molecule thrombopoietin receptor antagonist that also stimulates platelet production. It bears the advantage of oral administration as opposed to subcutaneously.
Themajor problem is that it has a black box warning for potential hepatotoxicity so liver enzymes should be carefully monitored. As with romiplostim, eltrombopag also has a risk of increasing reticulin deposition in marrow, as well as producing too robust a stimulation of platelets. Hereditary angioedema is a genetic deficiency of the C1-esterase inhibitor, a naturally occurring plasma regulator of the complement system. This deficiency produces potentially life-threatening inflammatory responses. Human C1 inhibitor is purified from human plasma and is approved to temporarily increase C1 inhibitor activity after intravenous administration.
Current therapies steroids and danazol are relatively ineffective and display significant side effects. The C1 inhibitor, being a natural human protein, has a favorable side effect profile. Because all animal products contain vitamin B 12 , only strict vegetarians are at risk of B 12 dietary deficiencies. Other risk factors for vitamin B 12 deficiencies include decreased gastrointestinal absorption possibly from removal of the bowel and inadequate utilization because of transcobalamin a transport protein deficiency in the gastrointestinal tract.
Folate deficiency is more common than vitamin B 12 deficiency. Humans must obtain folate through their diet, and the most common cause of folate deficiency is lack of dietary green vegetables. In addition to inadequate intake, other risk factors include decreased absorption and hyperutilization.
Folate demand increases during pregnancy.
Evidence now shows that periconceptional folate supplementation in normal women reduces the incidence of fetal neuronal tube defects spina bifida, meningocele, anencephaly. Folate is absolutely necessary for the developing fetal nervous system. Newborns with congenital folate malabsorption syndrome are born with mental retardation, cerebral calcifications, seizures, and peripheral neuropathies. Thrombocytopenia reduced platelet numbers and functional platelet abnormalities result in a bleeding tendency. Thrombocytopenia can arise as a result of reduced platelet production e.
Dental treatment in haemophiliacs should be carried out only in liaison with specialist haematology services. Potential hazards from dental work include delayed bleeding in the retropharyngeal space after inferior dental nerve block and bleeds into the tongue after cuts from dental instruments. All blood donations are now screened for these viruses. Many drugs can also cause thrombocytopenia e.
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Drugs affecting platelet function. Steven E. Bone marrow failure manifests as pancytopenia or, at times, cytopenia of a single cell type.
A variety of associated conditions include the following:. Idiosyncratic: Chloramphenicol, anti-inflammatory drugs, antiepileptics, gold. Categorization has important prognostic and therapeutic implications. The usual approach to the newly diagnosed child with severe acquired aplastic anemia is to perform bone marrow transplantation if there is an HLA-identical sibling to serve as the donor.
These children receive medical therapy, usually the combination of antithymocyte, cyclosporine, and hematopoietic growth factors, such as granulocyte-macrophage colony-stimulating factor or granulocyte colony-stimulating factor G-CSF. Locasciulli A: Acquired aplastic anemia in children: incidence, prognosis and treatment options, Paediatr Drugs —, Fanconi anemia , or constitutional aplastic anemia, is a genetic disorder in which numerous physical abnormalities are often present at birth, and aplastic anemia occurs at about the age of 5 years.
The more common physical abnormalities include hyperpigmentation, anomalies of the thumb and radius, small size, microcephaly, and renal anomalies e. Patients with Fanconi anemia are also susceptible to leukemia and epithelial carcinomas.