Megaloblastic Macrocytic Anemiaswww.merck.com/mmpe/sec11/ch130/ch130h.htmlNonmegaloblastic MacrocytosisMacrocytosis in Liver Disease
Most macrocytic (ie, MCV >100 fL/cell) anemias are megaloblastic. Nonmegaloblastic macrocytosis occurs in various clinical states, not all of which are understood. Anemia is commonly associated but usually develops because of mechanisms independent of macrocytosis.
Macrocytosis from excess RBC membrane occurs in patients with chronic liver disease in whom cholesterol esterification is defective. Macrocytosis with an MCV of about 100 to 105 fL/cell can occur with chronic alcohol use in the absence of folate deficiency. Mild macrocytosis can occur in aplastic anemia, especially as recovery occurs. Macrocytosis is common in myelodysplasia also. Because RBC membrane molding occurs in the spleen after cell release from the marrow, RBCs may be slightly macrocytic after splenectomy, although these changes are not associated with anemia.
Nonmegaloblastic macrocytosis is suspected in patients with macrocytic anemias in whom testing excludes vitamin B12 and folate deficiencies. The macro-ovalocytes on peripheral smear and the increased RBC distribution width that are typical of classic megaloblastic anemia may be absent. If nonmegaloblastic macrocytosis is unexplained clinically (eg, by the presence of aplastic anemia, chronic liver disease, or alcohol use) or if myelodysplasia is suspected, then bone marrow examination and cytogenetic analysis are done to exclude myelodysplasia. In nonmegaloblastic macrocytosis, the marrow is not megaloblastic, but in myelodysplasia and advanced liver disease there are megaloblastoid RBC precursors with dense nuclear chromatin that differ from the usual fine fibrillar pattern in megaloblastic anemias.
Megaloblastic anemiaen.wikipedia.org/wiki/Megaloblastic_anemiaMegaloblastic anemia is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis in red blood cell production. This is often due to
deficiency of vitamin B12 and/or folic acid. Megaloblastic anemia not due to hypovitaminosis may be caused by
antimetabolites that poison DNA production, such as alcohol and some chemotherapeutic or antimicrobial agents (for example azathioprine or trimethoprim).
It is characterized by
many large immature and dysfunctional red blood cells (megaloblasts)causes:
Vitamin B12 deficiency:
achlorhydria-induced malabsorption
Deficient intake
Deficient intrinsic factor (pernicious anemia or gastrectomy)
Biological competition for B12 by diverticulosis, fistula, intestinal anastomosis, and
infection by the marine parasite Diphyllobothrium latumSelective B12 malabsorption (congenital and drug-induced)
Chronic pancreatitisIleal resection and bypass
Nitrous oxyde anaesthesis
Folate deficiency:
alcoholism
Deficient intake.
Increased needs: pregnancy, infant, rapid cellular proliferation, and cirrhosis
Malabsorption (congenital and drug-induced)
Intestinal and jujenal resection
Combined Deficiency (Tropical sprue): Vitamin B12 & Folate.
Inherited Pyrimidine Synthesis Disorders: Orotic Aciduria
Inherited DNA Synthesis Disorders: Deficient thiamine and factors (e.g., enzymes) responsible for folate metabolism.
Toxins and Drugs:
Folic acid antagonists (methotrexate)
Purine synthesis antagonists (6-mercaptopurine)
Pyrimidine antagonists (cytosine arabinoside)
Phenytoin
Erythroleukemia
Marine parasite Diphyllobothrium latumen.wikipedia.org/wiki/DiphyllobothriumDiphyllobothrium is a genus of tapeworm which can cause Diphyllobothriasis in humans through consumption of raw or undercooked fish.
Symptoms of diphyllobothriasis are generally mild, and can include
diarrhea, abdominal pain, vomiting, weight loss, fatigue, constipation and discomfort. www.parasitetesting.com/picturesofparasites/view.nhtml?profile=picturesofparasites&UID=10010Approximately four out of five cases are asymptomatic and may go many years without being detected. In a small number of cases, this leads to
severe vitamin B12 deficiency due to the parasite absorbing 80% or more of the host’s B12 intake, and a
megaloblastic anemia indistinguishable from pernicious anemia.
The anemia can also lead to
subtle demyelinative neurological symptoms (subacute combined degeneration of spinal cord).
Infection for many years is ordinarily required to deplete the human body of vitamin B-12 to the point that neurological symptoms appear.more info:
www.wrongdiagnosis.com/d/diphyllobothrium_latum_infection/symptoms.htm#symptom_listJeany