Schilling test and megaloblastic anemia

The Schilling test is a medical test performed on patients with vitamin B12 deficiency. The purpose of the test is to determine if the patient has pernicious anemia. The Schilling test has two parts

Part 1: Vitamin B12 is given orally (through the mouth) and intramuscularly

Part 2: Vitamin B12 is orally administered with intrinsic factor.

Part 1: In this part of the test, a known amount of radiolabeled B12 is given by mouth.

An excess of unlabeled vitamin B12 is administered intramuscularly to the patient. An excess of vitamin B12 introduced into the muscles saturates the stores of the vitamin in tissues and prevents the absorption of labeled B12. If B12 is absorbed in the intestine, then it is excreted in the urine (daily urine).

In the presence of intrinsic factor, radioactively labeled vitamin B12 is absorbed in the intestine. Since the liver has receptors for B12, the reserves in the liver are saturated with the unlabeled vitamin, and the labeled one will be excreted in the urine.

Normally, >8-10% of the labeled vitamin B12 is excreted in the urine during the first 24 hours.

In patients with pernicious anemia or vitamin B12 deficiency, absorption is impaired and less than 8% of the labeled vitamin is excreted in daily urine .

Part 2 of the Schilling test: vitamin B12 and intrinsic factor.

If the first part of the Schilling test revealed a violation in the excretion of B12 in the urine, then the test is repeated, but this time labeled B12 with intrinsic factor is injected into the patient through the mouth.

This part of the test is performed in order to differentiate between pernicious anemia and malabsorption. If this time, more than 8-10% of labeled B12 was excreted in the urine per day, then this is an indicator of the absence of the factor’s own production and the basis for the diagnosis of pernicious (malignant) anemia. If the test is abnormal this time, then it is a reflection of a malabsorption due to any cause.

For the differential diagnosis of anemia associated with vitamin B12 deficiency or folic acid, the content of vitamin B12 is determined. The content of vitamin B12 in the blood less than 150 ng / ml allows you to diagnose vitamin B12-mediated megalo-jaw anemia. The content of folic acid in erythrocytes below 150 ng / ml) is the best evidence of folate deficiency megaloblastic anemia. Plasma folic acid concentration (less than 3 ng/mL) is not informative.

Absorption and metabolism of vitamin B12 and folic acid
The reserves of folic acid in the body are very small (for several weeks), so the availability of syntheses with the participation of folic acid depends on an adequate diet. Folic acid is found in green leafy vegetables and liver. Folic acid is absorbed in the small intestine and circulates in free form or associated with albumin.
Vitamin B 12 (cyanocobalamin) – unlike folic acid – is stored by the body in large quantities, which is normally enough for 2-6 years. Since vitamin B12 absorption is complex and can be impaired by a variety of mechanisms, a larger supply is biologically feasible. Vitamin B12 is synthesized by intestinal microbes and comes from animal food proteins. When animal protein enters the stomach, vitamin B12 is released from the protein and bound to specific “R” proteins that protect vitamin B12 from being destroyed in the stomach. The B12-R protein complex travels to the duodenum, where pancreatic enzymes break down the R proteins. The released vitamin B12 binds to intrinsic factor (IF). The B12-intrinsic factor complex is absorbed in the ileum. The absorbed vitamin B12 is bound by the transport protein transcobalamin II and enters the tissues.
Both vitamin B12 and folic acid are key components in DNA synthesis.

The daily norm of folic acid is 200-500 mcg. Reducing the average intake of folic acid in the diet to 2-300 mcg/day leads to folic acid deficiency.

Increased folic acid requirements in pregnancy, hemolytic anemia, and psoriasis can lead to a rapidly developing folate deficiency if the needs are not met by dietary sources or absorption is impaired.
Patients with moderate folic acid deficiency are more susceptible to toxicity from drugs such as trimethoprim, pyrimethamine, and methotrexate.

Oral contraceptives and anticonvulsants require an increase in folic acid intake.

Alcoholics do not absorb folic acid well. In addition, folic acid metabolism leads to functional folic acid deficiency. Alcoholics are not unable to store folic acid or deplete stores at normal levels of serum folic acid.

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