Iron is mostly found in hemoglobin in the body (67%) +2 val (iron form)
Iron also has two forms as buffers, ferritin and hemosiderin
In plasma, the iron transporter protein is transferrin
Hepcidin, one of the important regulators of iron metabolism, is a negative regulator. Limits the passage of iron absorbed from the intestine into the plasma
The same inhibition occurs in phagocytes
Hepcidin synthesis increases markedly with infection and inflammation, and interleukin-6 is responsible for this increase. (it is a hepcidin-positive acute phase reactant)
Low levels of hepcidin (mutations of hepcidin or the master regulator of hemojuvelin) play a role in the etiology of hemochromatosis.
80% of the daily requirement for iron is met by the iron released due to the destruction of aging erythrocytes. The rest is taken from outside. The daily requirement of iron is 10-20 mg
Normally, only 10% of dietary iron is absorbed from the duodenum and proximal jejunum
Vitamin C, succinate, citrate and HCL increase iron absorption. Iron in soluble form (ferrous, Fe++) is maintained in an acidic environment and facilitates absorption from the upper GI tract.
Absorption is reduced with phytates, tannins, antacids and tetracyclines
It is the most common anemia in the world
Iron deficiency anemia causes
Iron malabsorption / insufficient intake
Poor nutrition, vegetarian diet
Gastrectomy (first seen in iron deficiency anemia), chlorhydria
pylori infection, use of PPI and H2 . receptor blockers
Acute and chronic inflammation and chronic renal failure (hepcidin excess)
Crohn's disease, celiac disease, etc
Increased need for iron
periods of rapid growth
Lactation and pregnancy
treatment with erythropoietin
Increased iron loss
Acute or chronic blood loss (the most common cause in adults)
It appears in all cases of gastrointestinal bleeding. If there is iron deficiency in adult men and postmenopausal women, GI bleeding should be considered first
Especially in the elderly, malignant neoplasms of the gastrointestinal tract should be excluded
Menstrual bleeding (the most common cause in premenopausal women)
Parasites: Ancylostoma duodenale, Necator americanus
Chronic bleeding diseases: ulcerative colitis, Goodbuster syndrome, etc.
Symptoms
Significant results include weakness, pallor, hair loss, licked nails and pica, angular stomatitis, and blue sclera.
Pica: It swallows things like mud, dirt, ice (pagophagia) and chalk
Pagophagia (eating ice) is a very specific symptom of iron deficiency
There is severe stress due to a defect in iron-containing enzymes
Restless legs syndrome may occur
An enlarged spleen may rarely be seen
Plumer Vinson syndromes (Peterson-Brown-Kelly syndrome)
The triad of dysphagia + atrophic glossitis + iron deficiency
Dysphagia is caused by the development of a membrane in the proximal esophagus
Diagnosis is made by barium radiography or endoscopy
There is an increased incidence of esophageal squamous cell carcinoma
laboratory
Hemoglobin, hematocrit, MCV, MCH, MCHC are low. However, the RDW is high.
ferritin
Low ferritin level (<15-20 mcg/L)
He is the first to decrease and the last to improve with treatment
Ferritin is the test that best demonstrates iron storage
It is a positive acute phase reactor. Although iron deficiency is present in chronic diseases, the level of ferritin is high
Low serum iron
High serum iron binding capacity (binding capacity)
Transferrin saturation is low (usually less than 20%)
It is calculated as serum iron x 100 / serum iron binding capacity
Increased level of soluble transferrin receptors in the blood
The level of the soluble transferrin receptor in the blood is directly proportional to the active serial mass of erythrocytes requiring transferrin (increases in iron deficiency and hemolytic anemia. Decreases in anemia of chronic disease and aplastic anemia)
In iron deficiency (sequence)
Iron stores in the bone marrow decrease, ferritin decreases
serum iron decreases, transferrin saturation decreases; Protoporphyrin increases free red blood cells
Hypovolemic hypochromic anemia develops
There may be reactive thrombocytosis
Reticulocyte level is low
Peripheral smear
There is a lack of pigment and size, different sizes (Anicytosis) and shapes (Poikilocytosis)
Typical stylus cells
Prussian blue (Perls stain) bone marrow biopsy: iron stores negative
Differential diagnosis
In order to distinguish it from other hypochromic and hypochromic anemias, iron parameters are examined
In anemia of chronic disease, both serum iron and iron-binding capacity are low
Iron parameters in thalassemia and sideroblastic anemia are the opposite of iron deficiency
Treatment
The first thing to do is to determine the cause of the disease
Oral iron therapy: This is the primary treatment for asymptomatic patients. Ferrous sulfate, ferrous sulfate and ferrous gluconate may be administered
The duration of oral treatment should be from 6 to 12 months
Side effects; Abdominal pain, nausea, vomiting, constipation, sucking more on an empty stomach
Parenteral iron therapy: Preferred in cases where oral iron cannot be tolerated, persistent or excessive bleeding, or chronic kidney disease. Ferric sodium, iron sucrose, ferric carboxymaltose and iron dextran can be given
The most important and serious side effect is anaphylaxis (mostly iron dextran)
Response to treatment
First of all, the patient's symptoms improve (weakness, fatigue)
The first laboratory indicator is Reticulocytosis, seen on the 4-7th day
Another test that is getting better is ferritin. Usually an average of 6 months
The last clinical outcome to improve is skin and nail changes