Iron(II) Sulfate

Uses

Ferrous sulfate is an iron supplement used to prevent or treat iron deficiency anemia.

Ferrous sulfate is used for the prevention and treatment of iron deficiency anemia in adults and children.

Iron(II) Sulfate is also used to associated treatment for these conditions: Anaemia folate deficiency, Anemia, Folate deficiency, Iron Deficiency (ID), Iron Deficiency Anemia (IDA), Hypochromic anemia, Iron replacement therapy

How Iron(II) Sulfate works

Iron is required to maintain optimal health, particularly for helping to form red blood cells (RBC) that carry oxygen around the body. A deficiency in iron indicates that the body cannot produce enough normal red blood cells. Iron deficiency anemia occurs when body stores of iron decrease to very low levels, and the stored iron is insufficient to support normal red blood cell (RBC) production. Insufficient dietary iron, impaired iron absorption, bleeding, pregnancy, or loss of iron through the urine can lead to iron deficiency. Symptoms of iron deficiency anemia include fatigue, breathlessness, palpitations, dizziness, and headache.

Taking iron in supplement form, such as ferrous sulfate, allows for more rapid increases in iron levels when dietary supply and stores are not sufficient. Iron is transported by the divalent metal transporter 1 (DMT1) across the endolysosomal membrane to enter the macrophage. It can then can be incorporated into ferritin and be stored in the macrophage or carried of the macrophage by ferroportin. This exported iron is oxidized by the enzyme to ceruloplasmin to Fe3+, followed by sequestration by transferrin for transport in the serum to various sites, including the bone marrow for hemoglobin synthesis or into the liver. Iron combines with porphyrin and globin chains to form hemoglobin, which is critical for oxygen delivery from the lungs to other tissues.

Toxicity

The toxicity of ferrous sulfate in humans depends on the amount of iron ingested. Up to 20 mg/kg of elemental iron is not toxic, 20-60 mg/kg has mild toxicity, and more than 60 mg/kg can lead to severe symptoms and morbidity.

Overdose information

Iron containing products are the primary cause of drug overdose in children under 6 years of age. Iron is toxic to the gastrointestinal system, cardiovascular system, in addition to central nervous system. The most early reported effects following the excess ingestion of iron include nausea, flatulence, abdominal pain, diarrhea, constipation, and black/tarry stools. Symptoms of overdose in the later stages include bluish lips, fingernails, and palms, drowsiness, tachycardia, seizures, metabolic acidosis, hepatic injury, and cardiovascular dysfunction. Sequelae of iron sulfate overdose include intestinal obstruction, pyloric stenosis, and gastric scarring. If the patient is comatose or seizing, gastric lavage with sodium bicarbonate should be performed. Deferoxamine is the antidote for iron poisoning. Other supportive treatments to support fluid and electrolyte balance and correct metabolic acidosis are also advised. Hospitalization should continue for 24 h after the patient becomes asymptomatic to monitor for delayed onset of shock/gastrointestinal bleeding.

Food Interaction

• Avoid milk and dairy products. Take ferrous sulfate at least 2 hours before or after milk.
• Limit caffeine intake. Food and beverages containing caffeine may reduce iron absorption.
• Take at least 2 hours before or after calcium supplements.
• Take separate from antacids. Take ferrous sulfate at least 2 hours before or after antacids.
• Take with food. This may reduce gastric irritation.
• Take with foods containing vitamin C. Foods rich in vitamin C increase the absorption of iron.

Volume of Distribution

About 60% of iron is distributed the erythrocytes. The remainder of the iron is found in muscle tissues (as a part of myoglobin), and in a variety of different enzymes, as well as in storage form. Most stored iron is in the form of ferritin, which can be found in the liver, bone marrow, spleen and, and muscle. Iron crosses the placenta and is also found in breast milk.

Elimination Route

Approximately 5 – 10% of dietary iron is absorbed, and this absorption rate increases to up to 30% in iron deficiency states. Oral iron supplements are absorbed up to 60% via active and passive transport processes. Gastrointestinal absorption of iron occurs via strict regulation by the enterocyte and duodenal cytochrome and ferric reductase enzymes. The hormone hepcidin heavily regulates iron absorption and distribution throughout the body.

The median time to maximum serum concentration (Tmax) is generally 4 hours after administration. Between 2-8 hours post administration, average serum iron concentrations fluctuate by 20%, according to one study. Bioavailability of iron depends on whether it is administered in a film coated tablet or enteric coated tablet. One pharmacokinetic study in healthy volunteers revealed a 30% bioavailability for enteric coated tablets. The AUC of enteric coated tablets varied between a lower limit of -46.93 to 5.25 µmolxh/l. Cmax is higher for film coated tablets, ranging from 3.4 to 22.1 µmol/h/l.

It is advisable to take ferrous sulfate with ascorbic acid, as this practice may increase absorption. Avoid antacids, tea, coffee,tea, dairy products, eggs, and whole-grain bread for at least an hour after taking ferrous sulfate. Calcium can decrease iron absorption by 33% if taken concomitantly.

Half Life

The half-life of orally administered iron is not readily available in the literature, with total effects lasting 2-4 months (congruent with the red blood cell life span) with an onset of action of 4 days and peak activity at 7-10 days.

Elimination Route

Oral iron is recycled, with some loss in the urine, sweat, and desquamation. Some iron can be lost during menstrual bleeding This loss is balanced by changes in intestinal absorption. The enzyme hepcidin promotes the excretion of iron via the sloughing of enterocytes with ferritin stores into the feces.

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