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Secondary polycythemia is the most common cause of polycythemia. It occurs in reaction to chronically low oxygen levels , medications, other genetic mutations that impact the body's ability to transport or detect oxygen, or, rarely because of certain cancers.
Methemoglobinemia can be due to certain medications, chemicals, or food or it can be inherited. [2] Substances involved may include benzocaine , nitrites , or dapsone . [ 3 ] The underlying mechanism involves some of the iron in hemoglobin being converted from the ferrous [Fe 2+ ] to the ferric [Fe 3+ ] form. [ 3 ]
In oncology, polycythemia vera (PV) is an uncommon myeloproliferative neoplasm in which the bone marrow makes too many red blood cells. [1] The majority of cases [2] are caused by mutations in the JAK2 gene, most commonly resulting in a single amino acid change in its protein product from valine to phenylalanine at position 617.
The excessive fluid is usually blood, and can be a sign of a number of conditions with different causes. An excess of blood may be either an excessive blood flow to an area of the body, or an increase in the volume of blood (polycythemia). Extra perfusion to the face is termed facial plethora, a hallmark sign of Cushing's syndrome. [1]
Hydroxycarbamide, also known as hydroxyurea, is an antimetabolite medication used in sickle-cell disease, essential thrombocythemia, chronic myelogenous leukemia, polycythemia vera, and cervical cancer. [4] [5] In sickle-cell disease it increases fetal hemoglobin and decreases the number of attacks. [4] It is taken by mouth. [4]
In some cases, a drug can cause the immune system to mistakenly think the body's own red blood cells are dangerous, foreign substances. Antibodies then develop against the red blood cells. The antibodies attach to red blood cells and cause them to break down too early. It is known that more than 150 drugs can cause this type of hemolytic anemia ...
[122] [126] High doses or levels of AAS, including testosterone, can cause polycythemia—high red blood cell and/or hemoglobin levels that increase the risk of stroke—as an adverse effect. [121] [122] Conversely, whether via castration, NSAA monotherapy, or CAB, decreased erythropoiesis resulting in mild anemia is a common side effect of ADT ...
Antimalarial drugs that can cause acute hemolysis in people with G6PD deficiency include primaquine, pamaquine, chloroquine, and hydroxychloroquine. [11] There is evidence that other antimalarials may also exacerbate G6PD deficiency, but only at higher doses.
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