Mg Of Ferrous Sulfate Research Articles

Anemia: A Cause of Intolerance to Thyroxine Sodium

Anemia: A Cause of Intolerance to Thyroxine Sodium

Self-assessment questions

A 16-year-old Indian girl has been in the UK for 3 months and is due to take part in an arranged marriage. A week before, she saw her GP for nausea in the mornings. He prescribed Iron as she was pale, but ordered no investigations. She presents to A&E 6 hours after ingesting 20 x 200 mg of Ferrous Sulphate. Her fiancee acts as interpreter and says she had forgotten to take some tablets and then attempted to catch up in one go. Her past medical history was unremarkable and there was no significant family history. She ate a balanced diet and her weight was stable, normal periods, no melena and no other medication. On examination she was pale and vomiting. Cardiorespiratory systems stable, mildly tender abdomen but no hepatosplenomegaly. No central or peripheral neurological deficit. Hb 10.1 g/dl, MCV 62 fl, MCH 20 pg, PLT 237 10 9/l, WCC 11 10 9/l. B12, folate & ferritin within normal limits.

Effectiveness of Iron-Fortified Infant Cereal in Prevention of Iron Deficiency Anemia

Iron deficiency continues to be a common problem among infants throughout the world. Iron-fortified formula is effective in preventing iron deficiency but the benefit of iron-fortified cereal is controversial. We compared iron-fortified rice cereal to unfortified rice cereal in infants who were exclusively breast-fed for more than 4 months and to iron-fortified formula in infants who were weaned to formula before 4 months of age. The design was double blind in respect to the presence or absence of fortification iron in the cereal or formula and included 515 infants who were followed on the protocol from 4 to 15 months of age. Rice cereal was fortified with 55 mg of electrolytic iron per 100 g of dry cereal and infant formula with 12 mg of ferrous sulfate per 100 g of dry powder, levels approximating those in use in the United States. Measures of iron status were obtained at 8, 12, and 15 months. Infants with hemoglobin levels of < 105 g/L were excluded from the study and treated. Consumption of cereal reached plateaus at means of about 30 g/d after 6 months of age in the formula-fed groups and 26 g/d after 8 months in the breast-fed groups; these amounts are higher than the 19-g/d mean intake by the 73% of infants who consume such cereal in the United States. Among infants weaned to formula before 4 months, the cumulative percentages of infants excluded for anemia by 15 months were 8%, 24%, and 4%, respectively, in the fortified cereal, unfortified cereal and formula, and fortified formula groups (P < .01 unfortified vs either fortified group; the difference between the two fortified groups was not significant). In infants breast-fed for more than 4 months, the corresponding values were 13% and 27%, respectively, in the fortified and unfortified cereal groups (P < .05). Mean hemoglobin level and other iron status measures were in accord with these findings. Iron-fortified infant rice cereal can contribute substantially to preventing iron deficiency anemia.

The effect of oral iron supplementation on erythropoiesis in autologous blood donors.

The effect of oral iron supplementation on erythropoiesis was studied prospectively in 34 autologous blood donors. The subjects, all of whom were to undergo total hip surgery, had normal iron status at the start of the study. During the preoperative period, in which 4 units of blood were collected, 17 patients received oral iron supplementation with 287 mg of ferrous sulfate (105 mg of elemental iron/day), while 17 patients did not use any iron supplementation. Oral iron supplementation during the 4-week preoperative period lessened the decrease in ferritin levels after two phlebotomies. Neither the decrease in hemoglobin nor the increase in erythropoietin levels was influenced by iron supplementation. In both iron-supplemented and control patients, serum erythropoietin levels returned to initial values within a few days after surgery. In autologous blood donors with a normal iron status, the use of supplemental iron does not affect erythropoiesis and is insufficient to maintain iron stores.

Reduced cortisol secretion in patients with iron deficiency.

The iron-containing protein cytochrome P-450 is present in high concentration in the adrenal cortex and is involved in the synthesis of corticosterone. This study was designed to determine the cortisol response to adrenocorticotropin (ACTH) in patients with severe iron deficiency. Eleven patients with iron deficiency and 15 normal controls were studied. Fasting blood samples were taken from all the subjects before and 30, 60 and 120 min after infusion of 25 units of ACTH for plasma cortisol determination. Six patients had blood samples collected at night, too. The same test was performed in 6 patients with iron deficiency, 7 days after therapy with 800 mg of ferrous sulfate. No significant differences were observed between patients and controls for the baseline cortisol values. The cortisol secretion and the increment at 30, 60 and 120 min after ACTH infusion were significantly lower in patients than in controls, either before or after ferrous sulfate therapy. There were no significant differences between baseline and stimulated cortisol values in patients before and after 7 days of ferrous sulfate therapy. There was no change in cortisol secretion rhythm in patients with iron deficiency (cortisol level at night = 5.1 +/- 4.3 micrograms/dl). In conclusion, the results of the present study showed that, in patients with severe iron deficiency, the cortisol secretion after ACTH stimulation was decreased.

Effect of iron on the guaiac reaction

Most studies show that oral ingestion of iron does not cause a positive stool guaiac reaction. However, all in vitro studies show that iron does cause a positive guaiac reaction and some in vivo studies have shown a positive stool guaiac reaction in response to oral iron. This study examines this unresolved question. Twenty-five normal volunteers were given 900 mg of ferrous sulfate a day. Two Hemoccult II and two HemoQuant tests were obtained before and during iron therapy. All Hemoccult II tests were negative before and after oral iron. Four HemoQuant tests were slightly elevated before oral iron and one was slightly elevated after oral iron. Ferrous sulfate, 300 mg, was dissolved in 1 L of water. The solution was acidic (pH = 3.9) and produced a positive Hemoccult II test. When the solution was titrated with sodium hydroxide to a pH of ≥6.0, iron precipitated out and the mixture no longer produced a positive Hemoccult II reaction. Our data show that ferric iron (Fe3+) in solution will give a positive guaiac reaction directly and ferrous iron (Fe2+) will give a positive guaiac reaction after hydrogen peroxide is added because it oxidizes Fe2+ to Fe3+. Iron solutions are acidic and when titrated toward a neutral pH, the iron is precipitated out and the solution is then guaiacnegative. Thus, our in vivo data confirm most previous in vivo studies; furthermore, the discrepancy between in vivo and in vitro studies can be explained as a pH-dependent phenomenon of in vitro iron solutions. Oral iron should not cause a positive guaiac reaction, and the HemoQuant results show no increase in occult blood loss in subjects on oral iron therapy.

The effects of oral iron supplementation on ferritin levels in pregnant Burmese women

The usefulness of serum ferritin levels in assessing iron stores in pregnant women before and after supplementation with iron was studied. One hundred thirty-five healthy pregnant women between 22 to 28 wk were randomly allotted to daily dose regimes of 60, 120, or 240 mg of ferrous sulphate. The tablets were given after meals under strict personal supervision. Before supplementation, iron deficiency (ferritin level less than 10 micrograms/L) was present in 54.8% of the pregnant women, compared to an incidence of 17.8% when assessed by serum iron concentration of less than 50 micrograms/dl. The mean ferritin level of pregnant women was 14.15 micrograms/L and was less than one-half that of healthy single women and one-sixth of that of healthy males. Supplementation with oral iron for 12 wk produced an increase in ferritin levels in all the groups, but significant increases were seen only in women given 120 and 240 mg of ferrous sulphate with or without folic acid. However, there were no differences in final Hb levels among the supplemented groups.

The relationship between hematocrit levels in gravidae and their newborn.

The changes in hematocrit levels during pregnancy in 90 Nigerian women, both anemic and nonanemic, were studied. The maternal levels at term were compared to the hematocrit levels of their newborns. The anemic patients received 200 mg of ferrous sulfate three times daily throughout pregnancy. Generally, the hematocrit level either decreased slightly or remained unchanged during the first half of pregnancy, with or without iron supplements. The decrease was, however, more noticeable in the nonanemic patients. Babies delivered by patients who remained anemic at term had hematocrit levels that were actually in the upper limits of the normally acceptable range.

The effects of iron deficiency on the respiratory function and cytochrome content of rat heart mitochondria.

We have examined the effects of total body iron deficiency on the function of mitochondria isolated from rat hearts. Male Wistar rats were weaned at 21 days and divided into an experimental iron-deficient group and a control group. Both groups received identical diet but an iron supplement (180 mg of ferrous sulfate per kg of diet) was added for the control group. Rats were studied at 7 and 14 weeks. Iron-deficient rats weighed less than controls but showed significantly increased ventricle to body weight ratio at both 7 and 14 weeks, indicating relative cardiac hypertrophy. Isolated mitochondrial fractions from iron-deficient and control rats contained similar proportions of whole homogenate protein and succinic cytochrome c reductase activity, indicating that the fractions isolated from the experimental and control rats were comparable. In iron-deficient rats NADH cytochrome c reductase, succinic cytochrome c reductase, succinic dehydrogenase, and NADH ferricyanide oxidoreductase activities were all significantly reduced at 7 and 14 weeks. Cytochrome c oxidase activity was significantly reduced only at 14 weeks as were the concentrations of cytochromes a3, c1, and b. The rate of oxygen uptake by mitochondria was significantly lower at both 7 and 14 weeks but the P/O ratio was unaltered. We conclude that iron deficiency is associated with impairment of myocardial mitochondrial electron transport.

Iron metabolism in patients undergoing regular dialysis therapy.

Thirteen patients with chronic renal failure maintained on regular renal dialysis were studied. Seven proved to have iron deficiency on the basis of marrow iron studies, reticulocyte iron uptake, and saturation of the serum iron-binding capacity. They absorbed iron when given it by mouth and were able to utilize it for haemoglobin formation. Iron-deficient patients given 600 mg of ferrous sulphate daily for three months showed an increase in haemoglobin, but the failure to replace stores of iron is probably related to their relatively limited ability to absorb iron and the variable but sometimes considerable blood loss occurring with each dialysis.The loss may be occult, and prolonged iron therapy may be required. This is most safely achieved by giving iron by mouth.

Interrelationship of iron and manganese metabolism.

A relationship between iron and manganese metabolism has been suggested by the observation of the incorporation of manganese into the porphyrin molecule of red cells and the increased gastrointestinal absorption of manganese in iron deficiency (1, 2). The present studies were performed to determine variations in the metabolism of each of these elements induced by deficiency or overload of the other.Methods. Male albino rats (Wistar strain) weighing 200-250 g were used. The animals were fed a standard rat diet (General Biochemicals, Chagrin Falls, Ohio) except that the iron and manganese content was modified from test to test as stated. Iron absorption was measured following a test dose of 0.5 μCi of ferrous-59 Fe citrate per 0.25 mg of ferrous sulfate per 0.5 ml of distilled water, administered through a 17-gauge endoesophageal tube to rats fasted for 16 hr. Whole body radioactivity (0.8 MeV —→ ∞) was measured in a small-animal, whole-body liquid scintillation detector (Packard Armac, LaGrange, Illinois),...