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an abnormally large, immature, and dysfunctional red blood cell found in the blood of
persons with pernicious anemia or certain other disorders.
Megaloblastic anemia (or megaloblastic anaemia) is an anemia (of macrocytic
classification) that results from inhibition of DNA synthesis during red blood cell
production.[1] When DNA synthesis is impaired, the cell cycle cannot progress from
the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth
without division, which presents as macrocytosis. Megaloblastic anemia has a rather
slow onset, especially when compared to that of other anemias. The defect in red cell
DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of
vitamin B12 and/or folic acid. Vitamin B12 deficiency alone will not cause the
syndrome in the presence of sufficient folate, as the mechanism is loss of B 12
dependent folate recycling, followed by folate-deficiency loss of nucleic acid
synthesis (specifically thymine), leading to defects in DNA synthesis. Folic acid
supplementation in the absence of vitamin B 12 prevents this type of anemia (although
other vitamin B12-specific pathologies may be present). Loss of micronutrients may
also be a cause. Copper deficiency resulting from an excess of zinc from unusually
high oral consumption of zinc-containing denture-fixation creams has been found to
be a cause.[2]
Megaloblastic anemia not due to hypovitaminosis may be caused by antimetabolites
that poison DNA production directly, such as some chemotherapeutic or antimicrobial
.agents (for example azathioprine or trimethoprim)
The pathological state of megaloblastosis is characterized by many large immature
and dysfunctional red blood cells (megaloblasts) in the bone marrow[3] and also by
hypersegmented neutrophils (those exhibiting five or more nuclear lobes
("segments"), with up to four lobes being normal). These hypersegmented neutrophils
are found in the "peripheral blood" (i.e., a diagnostic smear of a blood-sample taken
from the circulation
DNA gyrase, also known as topoisomerase II or simply as gyrase, is an enzyme that
relieves strain while double-stranded DNA is being unwound by helicase.[1][2] This
causes negative supercoiling of the DNA. The gyrase supercoils (or relaxes positive
supercoils) into DNA by looping the template so as to form a crossing, then cutting
one of the double helices and passing the other through it before releasing the break,
changing the linking number by two in each enzymatic step. This process occurs in
prokaryotes (in particular, in bacteria), whose single circular DNA is cut by DNA
gyrase and the two ends are then twisted around each other to form supercoils. Gyrase
has been found in the apicoplast of the malarial parasite Plasmodium falciparum, a
unicellular eukaryote.[3][4] Bacterial DNA gyrase is the target of many antibiotics,
.including nalidixic acid, novobiocin, and ciprofloxacin
Stevens-Johnson syndrome is a rare, serious disorder of your skin and mucous
membranes. It's usually a reaction to a medication or an infection. Often, StevensJohnson syndrome begins with flu-like symptoms, followed by a painful red or
purplish rash that spreads and blisters. Then the top layer of the affected skin dies and
.sheds
Stevens-Johnson syndrome is a medical emergency that usually requires
hospitalization. Treatment focuses on eliminating the underlying cause, controlling
.symptoms and minimizing complications
Recovery after Stevens-Johnson syndrome can take weeks to months, depending on
the severity of your condition. If it was caused by a medication, you'll need to
permanently avoid that drug and others closely related to it