In clinical practice, we often encounter the disease of giant cell anemia, which is mainly caused by a deficiency of folic acid and/or vitamin B12. For this type of anemia, clarity is key. This article will delve into the relationship between folic acid and vitamin B12 and how to determine the diagnosis and protocol in the face of giant cell anemia.
First of all, let's be clear that folic acid and vitamin B12 play a very important role in the human body. Folic acid is a water-soluble vitamin that is an essential coenzyme in the process of DNA synthesis, and a lack of folic acid can lead to impaired DNA synthesis, which can lead to megaloblastic anemia. Vitamin B12 is involved in the methylation process of red blood cell maturation, and the lack of vitamin B12 can lead to red blood cell maturation disorders and cause megaloblastic anemia.
However, in clinical practice, we have found that the symptoms of folic acid and vitamin B12 deficiency may mask each other. For example, in the case of vitamin B12 deficiency, intracellular folate utilization can be affected, and intracellular folate may be deficient even when serum folate levels are normal. At this time, vitamin B12 supplementation alone may not improve anemia and folic acid supplementation is required to be effective.
On the other hand, if there is a folate deficiency and vitamin B12 is normal, then the utilization of vitamin B12 will also be affected after folic acid supplementation. In this case, serum vitamin B12 levels may drop, making the diagnosis difficult. At this point, we need to help confirm the diagnosis with other markers such as serum homocysteine and methylmalic acid.
In addition to this, there are some special circumstances to be aware of. For example, when confronted with a true vitamin B12 deficiency, vitamin B12 levels may be falsely elevated. This may be due to the release of vitamin B12 from the liver during acute hepatic necrosis or, in some cases such as autoimmune diseases, lymphoma, etc., the release of vitamin B12-binding protein by activated macrophages.
In addition, serum folate levels are also very erratic, and patients with a true decrease in serum folate at the time of admission may erroneously elevate after a nutritious hospital meal. Therefore, we need to take these factors into account when making a diagnosis so as not to mislead the diagnosis.
For the use of anticonvulsants, these drugs inhibit the absorption of folic acid in the small intestine, so serum folate concentrations may be normal in patients taking these drugs, even if they are folate deficient. For such patients, we need to assume that they are deficient in folic acid and undergo empirical treatment**.
Overall, folate and vitamin B12 deficiencies are a complex issue in clinical practice. We need to consider the patient's medical history, laboratory findings, and other relevant factors to determine the best option. For giant cell anemia, folic acid and vitamin B12 supplementation are common, but how to accurately determine the type and extent of deficiency is key. At the same time, we also need to pay attention to the impact of some special circumstances on the diagnosis and ** to ensure that the patient receives timely and effective **.