Megaloblastic Anemia
It reflects DNA disturbance which affects the blood cells (erythrocytes, leukocytes, platelets) and the bone marrow, and it is characterized by large and immature blood cells in the bone marrow (macrocytic anemia), mainly caused by both vitamins B9 (Folic Acid) and B12. Anemia of Protein-Energy Malnutrition
As explained before, hemoglobin is a protein which means that its production requires adequate and enough intake of protein from the diet, but in case of protein-energy malnutrition, hemoglobin will not be produced sufficiently leading to anemia. As a result there is a reduction in cell mass and thus fewer RBCs are required to oxygenate the tissue ( reduced number of RBCs with a low hemoglobin). Copper Deficiency Anemia
Copper and copper proteins are needed for adequate hemoglobin formation, use of iron by the developing erythrocyte (ceruloplasmin), optimal functions of the erythrocyte membrane. Ceruloplasmin (copper containing protein) is required for normal mobilization of iron from its storage sites. Thus, in a copper- deficient state; iron cannot be released à low serum iron and hemoglobin levels (even in the presence of normal iron stores). Sideroblastic Anemia
It is an inherited defect of heme synthesis enzyme which results in derangement in the final pathway of heme synthesis and buildup of immature Fe- containing RBCs. It is classified as microcytic and hypochromic type of anemia and it is nutritional because it is Vitamin B6-responsive. Hemolytic Anemia
A defect in RBC membranes causes oxidative damage and lysis the cells. Vitamin E has shown to be protective as it has an antioxidative function.
Ecallantide (trade name Kalbitor) is a drug used for the treatment of hereditary angioedema (HAE) and in the prevention of blood loss in cardiothoracic surgery. It is an inhibitor of the protein kallikrein and a 60-amino acid polypeptide which was developed from a Kunitz domain through phage display to mimic antibodies inhibiting kallikrein. Medical uses
Angioedema
On November 27, 2009, ecallantide was approved by the FDA for the treatment of acute attacks of hereditary angioedema for persons over 16 years of age. A single dose requires three separate injections, which are given under the skin.Ecallantide does not appear to be efficacious for the treatment of angioedema due to ACE inhibitors. Adverse effects
The most common adverse effects are headache, nausea, fatigue and diarrhea. Less common, but observed in more than 5% of patients in clinical trials, are respiratory tract infections, fever, vomiting, itching and upper abdominal pain. Up to 4% of patients showed anaphylaxis, which led to a black box warning in the US. Interactions
As of 2011, no interaction studies have been conducted. Mechanism of action
HAE is caused by a mutation of the C1-inhibitor gene. Defective or missing C1-inhibitor permits activation of kallikrein, a protease that is responsible for liberating bradykinin from its precursor kininogen. An excess of bradykinin leads to fluid leakage from blood vessels, causing swelling of tissues typical of HAE. Ecallantide suppresses this pathogenetic mechanism by selectively and reversibly inhibiting the activity of plasma kallikrein. Ecallantides inhibitory constant (Ki) for kallikrein is 25 picoMolar, indicating high affinity.