Ferrous gluconate

446.14

464.046448

206-076-3

DTXSID4040478

The color of /ferrous gluconate/ solution depends on pH; they are light yellow at pH 2, brown at pH 4.5, and green at pH 7. The iron rapidly oxidizes at higher pH.

2918160000

264.13000

DryPowder; PelletsLargeCrystals

The melting point for D-gluconic acid, ferrous salt dihydrate (98%) is 188 °C, decomposes. The specific optical rotation is +6.7 deg at 25 °C (c=1, H2O). /Dihydrate/

Soluble in glycerin

Ascorbic acid and aminoacetic acid cause dark coloration; with pyridoxine, green color produced.|Yellowish-gray or pale greenish-yellow powder. Slight odor of caramel. Soluble in water; practically insoluble in alcohol. Aqueous solutions are stabilized by addition of glucose. /Dihydrate/|Ferrous gluconate is affected by light and the ferrous iron slowly oxidizes to ferric on exposure to air.|Approximately neutral solutions undergo rapid oxidation; oxidation is retarded and stability improved by buffering to a pH of 3.5 to 4.5 with citrate buffer. Glycerin also retards oxidation.|Sugar, glycerin, & many organic hydroxy acids hinder precipitation. In neutral solution, soluble carbonates, phosphates, & oxalates produce precipitation. /Ferrous salts/

2

22-24/25

LZ5150000

May be light-sensitive - store in the dark.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Certification of this color additive when used for the coloring of ripe olives is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act.|Substance added directly to human food affirmed as generally recognized as safe (GRAS).|Ferrous gluconate used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.|Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. All substances listed may be in anhydrous or hydrated form. Iron gluconate is included on this list.

Joint FAO/WHO Expert Committee on Food Additives; WHO Food Additives Ser 8: Ferrous gluconate (1975). Available from: http://www.inchem.org/documents/jecfa/jecmono/v08je03.htm as of September 14, 2004.

|Danger|H302 (66.67%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P305+P351+P338, P310, P330, P337+P313, and P501|Aggregated GHS information provided by 23 companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|All ... /iron/ preparations should be kept in child-proof bottles. /Iron preparations/

If inhaled, iron is a local irritant to the lung and gastrointestinal tract. /Iron compounds/

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m. /Iron salts (soluble, as Fe)/

Typical replacement doses of oral iron have not been linked convincingly to serum enzyme elevations during therapy or to idiosyncratic, acute clinically apparent liver injury. In contrast, overdoses of oral iron, whether intentional or accidental, can cause liver injury, largely as a component of iron poisoning. Iron poisoning occurs most common in toddlers (1 to 3 years old) who ingest iron tablets prescribed for adults. Toxicity occurs after ingestion of 3 grams or more of ferrous sulfate (approximately 10 tablets, or ~650 mg of elemental iron), with toxic levels being more than 60 mg/kg of elemental iron and fatal levels more than 180 mg/kg. The typical sequence of events is appearance of nausea, vomiting and abdominal pain within 1 to 3 hours of the ingestion, followed by diarrhea, weakness, irritability, lethargy and stupor. Vomitus may be blood streaked or frank hematemesis. The diarrhea is generally fluid and dark (as a result of iron rather than blood). With higher doses, this initial phase is rapidly followed by pallor, hypotension and shock. Both upper and lower gastrointestinal bleeding can occur and early changes include metabolic acidosis and coagulopathy. In some instances, there is an improvement after a few hours of symptoms which can then be followed by sudden hemodynamic collapse, cardiogenic shock and severe acidosis that may be fatal. Early intervention (with gastric lavage, fluid replacement and iron chelation) appears to ameliorate the course of injury. Liver toxicity generally arises after 24 hours and may be more common in adults than children. Severe liver toxicity, with jaundice and marked aminotransferase elevations (ALT and AST greater than 25 times ULN), generally occurs only with larger overdoses and high initial serum iron levels (>1000 μg/dL). Jaundice is initially mild, while prolongation of the prothrombin time (or INR) and acidosis arise early (Case 1). The usual cause of death from iron poisoning is cardiac arrest, but deaths from hepatic failure as well as emergency liver transplantation for iron poisoning have been reported. Interestingly, the hepatic histological findings of acute iron hepatotoxicity are those of hemorrhagic, submassive necrosis which is predominantly peri-portal (zone 1), a finding typical of direct hepatotoxins that do not require hepatic metabolism for their toxicity. With more severe toxicity, the injury is massive and pan-lobular.

The effects of parenteral metal supplements of salicylate teratogenicity were studied in rats. Ferrous gluconate (16 mg/kg), manganous sulfate (10 mg/kg), cuprous sulfate (6 mg/kg), or deionized water were given ip on days 8, 9, and 10 of gestation. Sodium salicylate (250 or 300 mg/kg) or deionized water was administered /orally/ on day 9, 1 hr after the metal-salt treatment. Mn significantly enhanced the teratogenic effect of salicylate, Fe potentiated the salicylate effect but to a lesser extent than Mn, and Cu has little or no effect on salicylate teratogenicity. Mn and Fe significantly increased total salicylate concentration in both embryos and maternal plasma at 6 hr after salicylate treatment. No interference with plasma protein binding of salicylate could be detected. Postnatal effects of possible salicylate-mental interactions were studied in 40 day old offspring of animals treated with 125 mg/kg aspirin /orally/ and 16 mg/kg ferrous gluconate ip on days 8, 9, and 10. Increased exploratory activity and mean body weight were observed in both the aspirin-Fe and aspirin groups relative to vehicle controls, but maze learning was impaired only in animals exposed to both aspirin and Fe. The potentiation of the pre- and postnatal effects of salicylate by parenteral mental-salt treatment implies a salicylate-mental interaction in the maternal circulation and suggests chelation as a mechanism of the teratogenic action of salicylate.|...The interaction between different amounts of administered iron and the absorption of zinc and copper in humans /was investigated/. Eleven subjects with an ileostomy (mean (+/- SD) age: 55 +/- 9 yr) ingested a stable isotope labeled zinc and copper solution containing 12 mg Zn ((66)Zn and (67)Zn) and 3 mg Cu ((65)Cu) in the presence of 0, 100, or 400 mg Fe as ferrous gluconate on 3 respective test days. Subsequently, 1 mg (70)Zn was injected iv. Subjects collected ileostomy effluent and urine for 24 hr and 7 days, respectively. Zinc status and true zinc absorption were calculated from the urinary excretion of the zinc isotopes. Apparent copper absorption was calculated from ileostomy effluent excretion of the orally administered copper isotopes. Zinc status did not differ significantly between the 3 iron doses. Mean (+/- SEM) zinc absorption was significantly higher in the absence of iron than with the concomitant ingestion of 100 or 400 mg Fe (44 +/- 22% compared with 26 +/- 14% and 23 +/- 6%, respectively; P<0.05), whereas zinc absorption did not differ significantly between the 100- and 400-mg Fe doses. Apparent copper absorption was 48 +/- 14%, 54 +/- 26%, and 53 +/- 7% in the presence of 0, 100, and 400 mg Fe, respectively, and did not differ significantly between the 3 iron doses.|Since in vitro experiments had excluded interactions between Fe-gluconate (Fe-gluc) and magnesium-L-aspartate hydrochloride (MAH) in aqueous solutions the present in vivo studies seemed to be justified. Animal studies: Rats were kept on magnesium-(Mg)- and iron-(Fe)- sufficient and deficient diets. The intragastral administration of Fe-gluc significantly increased plasma Fe after 3 h, either given alone, or in combination with MAH (inducing hypermagnesemia). Same results were obtained when fortified diets were offered to Fe/Mg-deficient animals. Human studies: The combination of Fe-gluc (2 x 50 mg Fe per day, per os) plus MAH (2 x 7.5 mmol Mg per day, p.o.) was well tolerated by healthy volunteers. Single dose experiments revealed that Fe-gluc alone and in combination with MAH increased plasma Fe levels during 3 h to the same extent. Two groups of pregnant women with moderately reduced hemoglobin levels either received Fe-gluc (out-patients) or its combination with MAH (at least temporarily hospitalised because of preterm labor). Treatments were well tolerated. Hemoglobin levels did not further decrease, as expected without Fe supplements, during the course of pregnancy, thus indicating the therapeutic availability of the electrolytes in both study groups. Progesterone-induced constipation is frequently observed during pregnancy; hence stool softening reported by 50% of the women receiving Fe-gluc plus MAH (versus 33% in the Fe-gluc group) can be regarded as desirable effect. It is concluded that MAH does not interfere with the enteral absorption of Fe-gluc when both electrolytes are orally administered together. Taking both electrolytes together instead of 2 to 3 h apart from each other, as actually recommended, means a less complicated dosage regimen and probably improves compliance.|The effect of ferrous sulfate (Fesofor; I) 325 mg or ferrous gluconate (II) 600 mg on methyldopa (Aldomet; III) 500 mg tablet absorption, metabolism and blood pressure control was evaluated in 12 normal volunteers (mean age, 27.6 yr) or 5 hypertensive patients (mean age, 64.8 yr) who had been receiving III for at least one year. When I was taken with III there was a mean decrease in the proportion of III excreted as free III, 49.5% versus 21.1%, a significant mean increase in the proportion excreted as III sulfate, 37.8% versus 65.8%, and a decrease in the percentage of III absorbed, 29.1% versus 7.88%. These factors resulted in an 88% reduction in the quantity of free III excreted. To determine the effect of an iron preparation without sulfate, the study was repeated with II with the same results. In the hypertensive patients, there was an increase in both systolic and diastolic blood pressure in 4 patients and a decrease in blood pressure in all patients after I was discontinued. The increases in blood pressure were substantial in 3 of the patients.

LD50 Rat oral 2237 mg/kg|LD50 Mouse iv 114 mg/kg|LD50 Mouse oral 3700 mg/kg|LD50 Mouse ip 160 mg/kg|For more Non-Human Toxicity Values (Complete) data for FERROUS GLUCONATE (9 total), please visit the HSDB record page.

...There is concern that the individual with metabolic defects that impair the ability to regulate iron absorption will be at risk from excessive exposure to iron, primarily as a result of acceleration of accumulation of iron in the body and an earlier onset of clinical symptoms of the disease. /Iron salts/

Iron is an essential heavy metal that is included in many over-the-counter multivitamin and mineral supplements and is used therapeutically in higher doses to treat or prevent iron deficiency anemia. When taken at the usual recommended daily allowance or in replacement doses, iron has little or no adverse effect on the liver. In high doses and in intentional or accidental overdoses, iron causes serious toxicities, one component of which is acute liver damage.

Trace Elements and Metals

HEMATINIC|...Iron absorption tests were performed on 55 patients 3.2+/-2.0 years after isolated gastric bypass to identify those at higher risk for the late development of anemia. Twenty-nine of this group agreed to a therapeutic trial of iron /gluconate/ alone or with vitamin C over a 2-month period. All 55 patients were followed up for 27.1+/-1.0 months following the study. The iron absorption test identified patients with low iron stores, as indicated by low serum ferritin, and those with sufficient absorption surface to benefit from oral iron. The addition of vitamin C appears to enhance the therapeutic effect of iron by correcting ferritin deficits (P < 0.01) and anemia (P < 0.05). Differences in intestine length bypassed by the operation (10 vs. 100 cm) did not affect late ferritin and hemoglobin values.|...A study was... conducted on 40 women aged 20-35, with iron-deficiency anemia during or immediately after pregnancy all of whom presented Hb <10 gr/dL, Ht <33% and serum iron <60 ug/dL. All women with pregnancy-related pathological conditions, pre-existing on concomitant disease (Type I diabetes, heart diseases etc.) were excluded from the study. The women whose blood chemical parameters were largely homogeneous at the start of the study were divided into four treatment groups of 10 patients each and were treated as follows: Group A with oral liquid ferrous gluconate (75 mg per diem in 2 vials a day); Group B with solid ferrous gluconate (80 mg per diem in a single effervescent tablet); Group C with solid ferrous sulfate (105 mg per diem in a single tablet); and Group D with ferric protein succinylate (80 mg per diem in 2 vials a day). All were given iron treatment for 30 days. Treatment efficacy was analysed by comparing basal and final parameters using the T-test for paired dependent samples. The tolerance of the 4 treatment protocols was assessed by the analysis of any side effects such as nausea, vomiting, epigastric pain, diarrhea, constipation or other disorders reported by patients during treatment. Analysis of the therapeutic efficacy parameters (red blood cells, hemoglobin, hematocrit and serum iron) showed significant improvements but no statistically significant differences between the groups. However, the Group A patients treated with oral doses of liquid ferrous gluconate received a significantly lower cumulative dose of iron elements than the other groups: in detail 150 mg (p<0.05) less than Groups B and D; 900 mg (<0.001) less than Group C. By the end of treatment the Group A patients revealed significant increases versus basal values in red blood cells (p<0.001) 1,051,000 per cu mm or 33%, in Hb (p<0.001) 2.83 gr/dL or 32%, in Ht (p<0.001) 8.32% or 32%, in serum iron (p<0.05) 19.5 ug/dL or 61%. The same group also showed an increase in ferritin amounting to 7.8 ug/dL or 24% of the basal value. As to safety, only Group A patients reported no side effects and produced no drop-outs. Gastrointestinal and other aspecific side effects caused 1 drop-out each in Groups B and C and 2 drop-outs in Group D.

...A study was therefore conducted on 40 women aged 20-35, with iron-deficiency anemia during or immediately after pregnancy all of whom presented Hb <10 gr/dL, Ht <33% and serum iron <60 ug/dL. ...As to safety, only Group A patients reported no side effects and produced no drop-outs. Gastrointestinal and other aspecific side effects caused 1 drop-out each in Groups B and C and 2 drop-outs in Group D.|The effect of long-term oral iron supplementation on morbidity due to diarrhea, dysentery and respiratory infections in 349 children, aged 2-48 months, living in a poor community of Bangladesh, was evaluated in this double-blind study. The treatment group received 125 mg of ferrous gluconate (15 mg elemental iron) plus multivitamins and the controls received only multivitamins, daily for 15 months. House-to-house visits were made on alternate days by trained community health workers for recording symptoms and duration of illnesses and for monitoring medicine intake. Seventy-six percent of the children continued the syrup for over 1 yr. No untoward effects were noticed in either treatment group. The attack rates for diarrhea, dysentery and acute respiratory tract infections (ARI) were 3, 3 and 5 episodes per child per year, respectively. Each episode of diarrhea lasted a mean of 3 days, and those of dysentery and ARI, 5 days. The two treatment groups did not differ in the number of episodes, mean duration of each episode, or total days of illnesses due to diarrhea, dysentery and ARI. However, a 49% greater number of episodes of dysentery was observed with iron supplementation in a subset of the study children who were less than 12 months old (P=0.03).

Agents which improve the quality of the blood, increasing the hemoglobin level and the number of erythrocytes. They are used in the treatment of anemias. (See all compounds classified as Hematinics.)

The iron bioavailability and acute oral toxicity in rats of a ferrous gluconate compound stabilized with glycine (SFG), designed for food fortification, was studied in this work by means of the prophylactic method and the Wilcoxon method, respectively. For the former studies, SFG was homogeneously added to a basal diet of low iron content, reaching a final iron concentration of 20.1 +/- 2.4 mg Fe/kg diet. A reference standard diet using ferrous sulfate as an iron-fortifying source (19.0 +/- 2.1 mg Fe/kg diet) and a control diet without iron additions (9.3 +/- 1.4 mg Fe/kg diet) were prepared in the laboratory in a similar way. These diets were administered to three different groups of weaning rats during 23 d as the only type of solid nourishment. The iron bioavailability of SFG was calculated as the relationship between the mass of iron incorporated into hemoglobin during the treatment and the total iron intake per animal. This parameter resulted in 36.6 +/- 6.2% for SFG, whereas a value of 35.4 +/- 8.0% was obtained for ferrous sulfate.|Gastrointestinal absorption of iron is adequate and essentially equal from...ferrous...sulfate, fumarate, gluconate, succinate, glutamate, and lactate.

Ensure adequate airway, ventilation and circulation. Perform a gastric lavage in patients after intentional ingestion, a positive /kidney-ureter-bladder/ (KUB) radiography, and when the ingestion of elemental iron content exceeds 20 mg/kg . Do not use sodium bicarbonate or phosphosoda. Observation alone is usually sufficient when children have ingested multivitamins, the amount of elemental iron is less than 20 mg/kg and the KUB radiograph is negative. In symptomatic patients give a bolus of 20 mL/kg of isotonic normal saline. Order serum iron levels, creatinine, electrolytes, blood hemoglobin concentration, blood prothrombin time, baseline liver function tests, and arterial blood gases in seriously poisoned patients. Activated charcoal is ineffective. Oral magnesium may reduce serum iron absorption.|Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. /Iron and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with lactated Ringer's /SRP: "To keep open", minimal flow rate/. Watch for signs of fluid overload. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Iron and related compounds/|Maintain an open airway and assist ventilation if necessary. Treat shock caused by hemorrhagic gastrointestinitis aggressively with intravenous crystalloid fluids, and replace blood if needed. Patients are often markedly hypovolemic owing to gastrointestinal losses and third spacing of fluids into the intestinal wall and interstitial space. Treat coma, seizures, and metabolic acidosis if they occur. For seriously intoxicated victims (eg, shock, severe acidosis, and/or serum iron > 500-600 mcg/dL) administer deferoxamine. Monitor the urine for the urine for the characteristic orange or pink deferoxamine-iron complex. Therapy may be stopped when the urine returns to normal or when the serum iron level decreases to the normal range. Prolonged deferoxamine has been associated with adult respiratory distress syndrome and Yersinia sepsis.|For more Antidote and Emergency Treatment (Complete) data for FERROUS GLUCONATE (6 total), please visit the HSDB record page.

/CASE REPORTS/ The treatment of severe iron (I) overdose in 2 children (aged 11 months and 2.5 yr) who ingested approximately 50 tablets of ferrous sulfate and 55 tablets of ferrous gluconate, respectively, is described, and the pathophysiology of I toxicity and management of acute I poisonings are reviewed. Chelation therapy with deferoxamine, gastric decontamination procedures, including use of lavage solutions and whole bowel irrigation, and adjunctive measures are described. Both children recovered with serum I concentrations returning to normal 3-5 days after I ingestion. This article qualifies for one hour U.S. CE credit by the ACPE.

Apo-Ferrous Gluconate

Capsules 435 mg (equivalent to 50 mg of elemental iron); Elixir 300 mg (equivalent to 37.5 mg of elemental iron)/5 mL; Tablets 320 mg (equivalent to 40 mg of elemental iron).|Grades: Pharmaceutical, NF

All other chemical product and preparation manufacturing|Iron, bis(D-gluconato-.kappa.O1,.kappa.O2)-: ACTIVE|Members of /Vitamin/ B-Complex are compatible /except pyridoxine/.|Ferrous gluconate ... contains 12% iron ...

Method: AOAC 977.30; Procedure: spectrophotometric method; Analyte: ferrous gluconate; Matrix: drugs; Detection Limit: not provided.

Food additives

Food Additives -> COLOUR_RETENTION_AGENT; NUTRIENT_SUPPLEMENT;