VITAMIN D2
  • VITAMIN D2

  • (Generic for DRISDOL)
  • QTY 12 • 1250 MCG • Capsule • Near 77381

ERGOCALCIFEROL (er goe kal SIF e role) is a man made form of vitamin D. It helps your body keep the right amount of calcium and phosphorus for healthy bones and teeth.

VITAMIN D2 Pediatric Monographs
  • General Administration Information
    For storage information, see the specific product information within the How Supplied section.

    Route-Specific Administration

    Oral Administration
    -While vitamin D may be taken without regard to food, it is better absorbed when taken with foods containing fat.

    -Selection of pediatric dose forms: When high doses of ergocalciferol (vitamin D2 ) need to be administered, caution is necessary if oral vitamin D preparations containing propylene glycol such as ergocalciferol oral solution (e.g., Drisdol) are used, due to the potential propylene glycol toxicity. Possible alternative approaches for small children, to avoid such toxicity, include:-1) soaking a 50,000-IU capsule in a small amount of water to soften it and administering the intact capsule in blended food such as applesauce, OR
    -2) crushing a 25,000-IU or 50,000-IU vitamin D tablet before administration.

    Oral Liquid Formulations
    -Administer using a calibrated measuring device to ensure dosage accuracy. Due to the risk of inadvertently administering an incorrect dose, for infants the FDA recommends using a product with a dropper that will measure no more than 400 International Units per dose.
    -Administer directly into the mouth or mix with breast milk, formula, fruit juice, cereal, or other foods. If mixed, make sure the infant or child drinks or eats the entire portion to ensure they receive the total amount of the medication.
    -Storage: After opening, store away from direct light.

    In general, the use of supplemental vitamin D according to recommended dietary intakes is not associated with serious adverse reactions. Vitamin D may cause side effects in overdose, but such symptoms associated with hypervitaminosis D (and resultant hypercalcemia) are rarely reported. An excess of vitamin D causes abnormally high levels of calcium in the blood and is almost always caused by vitamin D analogs (e.g., calcitriol, doxercalciferol, paricalcitol), rather than vitamin D found in dietary supplements (e.g., cholecalciferol, ergocalciferol). However, patients taking higher doses of vitamin D supplements should report any of the following potential signs of high vitamin D/calcium concentrations: nausea/vomiting, constipation, loss of appetite, increased thirst (polydipsia), increased urinary frequency, mental/mood changes or irritability, headache, unusual fatigue or tiredness. These symptoms may require clinical evaluation. Anorexia, weight loss, polyuria, and arrhythmias may also be observed. In addition, hypercalcemia due to bone resorption leading to hypercalciuria may be observed in prolonged hypervitaminosis D. In early stages of vitamin D toxicity, hypercalcemia is mild and renal function remains normal. As vitamin D toxicity continues, continued bone resorption and increased calcium levels lead to suppression of parathyroid production. Calcification of the vasculature and other tissues has been associated with prolonged vitamin D toxicity. Data do not support that vitamin D toxicity is associated with kidney stones. Death due to vitamin D intoxication is likely due to renal and cardiovascular failure. Long-term doses of vitamin D of 10,000 to 40,000 International Units/day and long-term serum 25(OH)D concentrations of 500 to 600 nmol/L (200 to 400 ng/mL) are associated with vitamin D toxicity. Symptoms of vitamin D toxicity can become apparent within 4 weeks of continual excessive ingestion. Due to the long half-life of vitamin D, symptoms of toxicity may be prolonged. Excessive sun exposure does not result in vitamin D toxicity.

    Risk of growth inhibition in infants due to vitamin D supplements is based on a 1938 report of 35 infants up to 45 weeks of age where high-dose vitamin D supplementation (1,800 to 4,500 International Units/day for 6 months) was associated with growth inhibition in comparison with lower dose vitamin D supplements (less than 340 International Units/day for 6 months). In a subsequent but smaller study (n = 11) performed in 1966, no association between vitamin D supplements and growth inhibition was found. However, due to a possible association, no RDI for vitamin D has been set for infants. A large observational study from Finland in 2011 reported no association between growth inhibition later in life (as evaluated at 14 and 31 years of age) and the administration of vitamin D supplements (2,000 International Units/day) during infancy.

    Ergocalciferol is contraindicated in patients with hypercalcemia, hypervitaminosis D, and vitamin D hypersensitivity or hypersensitivity to any of the excipients in the formulation. Certain vitamin D formulations contain FD&C yellow dye No. 5 (tartrazine); these formulations should not be used in patients with tartrazine dye hypersensitivity. Hypersensitivity to vitamin D is one etiologic factor in infants with idiopathic hypercalcemia; in these patients, vitamin D intake must be seriously restricted. Some formulations of ergocalciferol oral solution (i.e., higher adult concentrations) contain propylene glycol. The clinician should be aware of the toxic potential for young children (e.g., neonates and premature neonates, infants, and children younger than 4 years) and ensure the correct formulation of vitamin D is chosen. Excessive propylene glycol can cause lactic acidosis, hyperosmolality, tachypnea, tachycardia, diaphoresis, and central nervous system toxicity (e.g., seizures, intraventricular hemorrhage).

    Patients with renal disease, especially renal failure, may be at increased risk for vitamin D-induced hypercalcemia even with usual dosages. Close clinical monitoring is needed to ensure adequate supplementation and, in pediatric patients, proper growth. In patients with stage 3 or higher kidney disease, use of a vitamin D analog appears preferred, following recommendations of the National Kidney Foundation.

    Ergocalciferol is contraindicated in patients with malabsorption syndrome. Pediatric patients with fat malabsorption due to cystic fibrosis, Crohn's disease, some forms of hepatic disease, gallbladder disease or biliary tract disease may require higher doses of vitamin D due to decreases in intestinal absorption. Some patients taking concurrent medications (e.g., certain anticonvulsants) may require higher doses as well. The prescription of active vitamin D analogs may be preferred in some cases.

    Description: Vitamin D is a fat-soluble vitamin and has two primary forms: cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2). The chemical structure differences between the two forms of vitamin D do not affect the metabolism or clinical responses once activated within the body. Although animal experiments have indicated a difference in toxicity between vitamin D3 and vitamin D2, human studies have been inconclusive. Ergocalciferol is available as a dietary supplement and is also found in fortified milk and cereal products; liver, fish liver oils, fatty fish, and egg yolks from hens have also been supplemented with vitamin D. Vitamin D must undergo hydroxylation in the liver and kidney to its active form. Vitamin D is responsible for appropriate calcium and phosphate balance and is required for normal bone growth and mineralization. Vitamin D deficiency is primarily associated with rickets in children. Vitamin D status is determined by monitoring 25-hydroxyvitamin D [25(OH)D] serum concentrations, which reflects both sources of vitamin D, dietary and sunlight. Consensus has not been reached as to what serum concentration determines vitamin D insufficiency in pediatric patients. In pediatrics, ergocalciferol is primarily used for vitamin D supplementation and the prophylaxis and treatment of vitamin D deficiency and rickets. Children with fat malabsorption syndromes or are taking chronic anti-seizure medication may be at increased risk of vitamin D deficiency and require higher doses of vitamin D supplements. Prevention of vitamin D deficiency during childhood may reduce the incidence of various conditions in adulthood including cancer, osteoporosis, and type 1 diabetes. Vitamin D has been administered clinically to children as young as neonates for the prevention and treatment of deficiency and the treatment of rickets.

    NOTE: In the US, nutraceuticals are marketed under the Dietary Supplement and Health Education Act of 1994 (DSHEA). Consequently, nutraceuticals are not regulated under the same restrictions as pharmaceuticals; scientific data supporting claimed benefit(s) are not always available for nutraceuticals. Consumers should also note that rigid quality control standards are not required for nutraceuticals, and substantial variability can occur in both the potency and the purity of these products.

    NOTE: For dosing conversion, 1 mcg vitamin D = 40 International Units.

    For nutritional supplementation of vitamin D based on recommended dietary reference intakes:
    NOTE: Patients with increased risk for deficiency of vitamin D (e.g., cystic fibrosis and other conditions causing chronic fat malabsorption, patients taking certain enzyme-inducing medications, etc.) may require higher supplemental doses than those recommended for healthy individuals to maintain normal vitamin D status. In such persons, 25(OH)D concentrations can be used to guide adequate dietary supplementation.
    Oral dosage:
    Premature Neonates weighing < 1500 g: 200-400 International Units/day PO is recommended by AAP. If the infant is receiving < 400 International Units/day, increase the dosage to 400 International Units/day when a weight of > 1500 g is reached and full enteral nutrition is tolerated. The Adequate Intake (AI) recommendation for neonates and infants 0-6 months is 400 International Units/day PO; a recommended AI for premature neonates is not specified. Premature infants < 32 weeks gestational age and < 1250 g who received a high-mineral containing cow milk based formula and daily vitamin D supplements of about 400 International Units maintained normal serum 25-hydroxyvitamin D concentrations. There does not appear to be any benefit to intake of vitamin D doses > 400 International Units/day in preterm infants.
    Premature Neonates weighing >= 1500 g: 400 International Units/day PO is recommended by AAP. The Adequate Intake (AI) recommendation is 400 International Units/day PO. There does not appear to be any benefit to intake of vitamin D doses > 400 International Units/day in preterm infants.
    Neonates and Infants: 400 International Units/day PO beginning within the first few days of life is considered Adequate Intake (AI). RDAs have not been established for infants. Infants that are exclusively breast-fed without vitamin D supplements are at increased risk for deficiency. Because most exclusively formula-fed infants ingest nearly 1 L/day of formula after the first month of life, they will achieve a vitamin D intake of 400 International Units/day. Infants who receive a mixture of human milk and formula should get a vitamin D supplement of 400 International Units/day to ensure the AI value. As infants are weaned from human milk and/or formula, intake of vitamin D-fortified milk should be encouraged to provide at least 400 International Units/day of vitamin D. Vitamin D supplementation should continue until the infant consumes at least 1000 mL per day (1 quart per day) of vitamin D-fortified milk (NOTE: Whole milk (cow's milk) is not recommended until after 12 months of age).
    Children: 600 International Units/day (15 mcg/day) PO is the RDA for vitamin D in children. The AAP recommends 400 International Units/day PO supplementation if the child is consuming < 1000 mL/day of vitamin D-fortified milk.
    Adolescents: 600 International Units/day (15 mcg/day) PO is the RDA for vitamin D in adolescents. The AAP recommends 400 International Units/day PO supplement if the adolescent is not obtaining at least 400 International Units PO through dietary sources. All dietary sources of vitamin D (e.g., fortified milk, eggs, other food) may be included in determining the daily intake.

    For the treatment of vitamin D deficiency:
    NOTE: In adults, vitamin D deficiency is defined as 25(OH)D concentrations < 50 nmol/L (< 20 ng/mL) and vitamin D insufficiency as 25(OH)D concentrations of 50-80 nmol/L (20-32 ng/mL). However, consensus has not been reached as to what serum concentration determines vitamin D insufficiency in pediatric patients ; a concentration of <= 37.5 nmol/L (<= 15 ng/mL) has been considered indicative of deficiency in most children, although, some studies suggest deficiency may occur at concentrations similar to those defined for adults.
    NOTE: Patients with vitamin D deficiency due to GI or liver diseases (e.g., cystic fibrosis, cholestatic liver disease, celiac disease, gastric or small bowel resection, etc.) or concomitant medications (e.g., anti-convulsants, corticosteroids, rifampin, etc.) may require higher doses and/or different treatment strategies.
    Oral dosage:
    Neonates: 25 mcg (1000 International Units) PO once daily has been recommended to treat deficiency. Treatment may continue for 2-3 months to replete deficient stores, followed by maintenance dosing in accordance with RDAs. Individualize dose based upon 25(OH)D concentrations.
    Infants: 25-125 mcg (1000-5000 International Units) PO once daily has been recommended to treat deficiency. One study demonstrated that 2000 International Units/day PO OR 50,000 International Units PO once weekly resulted in equivalent outcomes in the short-term treatment of hypovitaminosis D among otherwise healthy infants of >= 8 months of age, and appeared to be safe. Treatment may continue for 2-3 months to replete deficient stores, followed by maintenance dosing in accordance with RDAs. Individualize dose based upon 25(OH)D concentrations.
    Children and Adolescents: At least 125 mcg (5000 International Units) PO once daily has been recommended to treat deficiency. High doses have been used: 225-250 mcg/day (9000-10,000 International Units/day) or 5-7 mcg/kg/day (200-280 International Units/kg/day) PO. Also, weekly regimens (with higher doses once weekly or as a single course over 1 to 5 days) are occasionally used if compliance is an issue that prevents adequate repletion. One study demonstrated that 2000 International Units/day PO OR 50,000 International Units PO once weekly resulted in equivalent outcomes in the short-term treatment of hypovitaminosis D among otherwise healthy toddlers 12-24 months of age, and appeared to be safe. Treatment may continue for 2-3 months to replete deficient stores, followed by maintenance dosing in accordance with RDAs. Individualize dose based upon 25(OH)D concentrations.

    For the treatment of nutritional rickets:
    Oral dosage:
    Neonates: 25 mcg (1,000 International Units) PO once daily has been recommended. Radiologic evidence of healing is usually observed in 2 to 4 weeks, and the active treatment duration is usually 2 to 3 months, after which the supplementation may be reduced to maintenance dosing in accordance with RDAs to prevent further deficiency. Supplementation with calcium is necessary due to the risk of hypocalcemia during bone remineralization. It is important to ensure adequate dietary intake of calcium and phosphorus. Individualize dose based upon 25(OH)D concentrations.
    Infants: 25 to 125 mcg (1,000 to 5,000 International Units) PO once daily has been recommended. Radiologic evidence of healing is usually observed in 2 to 4 weeks, and the active treatment duration is usually 2 to 3 months, after which the supplementation may be reduced to maintenance dosing in accordance with RDAs to prevent further deficiency. Supplementation with calcium is necessary due to the risk of hypocalcemia during bone remineralization. It is important to ensure adequate dietary intake of calcium and phosphorus. Weekly regimens (e.g., high doses, such as 50,000 International Units PO once weekly) have been considered in older infants if compliance is an issue that prevents adequate repletion. Individualize dose based upon 25(OH)D concentrations.
    Children and Adolescents: Typical dose ranges are 2,000 to 20,000 International Units PO daily for 4 to 8 weeks, with the duration of treatment determined by evidence of radiologic healing. Thereafter, supplement with the RDA to prevent further deficiency. Alternatively, at least 125 mcg (5,000 International Units) PO once daily has also been recommended for initial treatment; weekly regimens (e.g., high doses, such as 50,000 International Units PO once weekly) or a single higher-dose course over 1 to 5 days may be considered if compliance is an issue that prevents adequate repletion. Large single dose regimens (200,000 to 600,000 International Units PO divided into 2 to 4 doses administered over 1 day) have been used when compliance is a concern, but are sometimes controversial due to a purported risk for hypercalcemia. It is important to ensure adequate dietary intake of calcium and phosphorus. Active treatment may continue for 2 to 3 months to replete deficient stores, followed by maintenance dosing with the RDA. Individualize dose based upon 25(OH)D concentrations.

    For the treatment of Hereditary 1,25-Dihydroxyvitamin D Resistant Rickets (HVDRR), also known as hereditary vitamin D resistant rickets type 2:
    Oral dosage:
    Children and Adolescents: Treatment for HVDRR is not standardized. Despite significant improvements in vitamin D concentrations following high-dose ergocalciferol (or use of a vitamin D analog like calcitriol) alone, patients may remain hypocalcemic and hypophosphatemic. High doses of ergocalciferol (vitamin D2) have been used in these patients. The following regimens have been used with variable results: 225 to 250 mcg/day PO; 5 to 7 mcg/kg/day PO; 4,000 to 40,000 International Units/day PO. However, doses as high as 200,000 International Units/day PO have not been effective in improving the disease in other patients. Patients should receive a 3 to 6 month trial of high dose vitamin D along with high-dose calcium therapy. Patients without alopecia appear more likely to respond. The manufacturer lists a recommended dose of 12,000 to 500,000 International Units PO daily. Calcium intake should be adequate. Blood calcium and phosphorus determinations are recommended every 2 weeks or more frequently if clinically indicated. X-rays of the bones are recommended every month until condition is corrected and stabilized. Individualize dose based upon 25(OH)D concentrations.

    For the treatment of hypoparathyroidism with calcium supplementation:
    Oral Dosage:
    Children and Adolescents: 1,250 to 5,000 mcg (50,000 to 200,000 International Units) PO once daily; ensure calcium supplementation is adequate. Dosage must be individualized.

    For the treatment of familial hypocholesterolemia (eg., abetalipoproteinemia, hypobetalipoproteinemia, and chylomicron retention disease, CRD):
    Oral dosage:
    Infants, Children, and Adolescents: 800 to 1,200 International Units PO daily has been recommended. If Vitamin D supplementation is started early, it prevents development of osteopenia in these patients. Alternative regimens for children 1 to 5 years of age are 100,000 International Units PO once every 2 months; if older than 5 years of age, then 600,000 International Units PO once every 2 months may be used.

    Therapeutic Drug Monitoring:
    Serum 25(OH)D concentrations are recommended for monitoring vitamin D status because it is reflective of both sources of vitamin D, sunlight and dietary. It is not, however, reflective of vitamin D body stores. Circulating 1,25(OH)2D is not a good indicator of vitamin D status due to its shorter half-life and its tight regulation by parathyroid hormone, calcium, and phosphorus. Levels of 1,25(OH)2D do not usually decrease until severe vitamin D deficiency.

    The Institute of Medicine recommends the following regarding the interpretation of 25(OH)D concentrations and vitamin D status for normal healthy persons:
    -< 30 nmol/L (< 12 ng/mL): Vitamin D deficiency, leading to rickets in infants and children.
    -30-50 nmol/L (12-20 ng/mL): Vitamin D insufficiency; concentrations are generally considered inadequate for bone and overall health.
    ->= 50 nmol/L (>= 20 ng/mL): Generally considered adequate for bone and overall health.
    ->= 75 nmol/L (>= 30 ng/mL): No consistent evidence of increased benefit.
    -> 125 nmol/L (> 50 ng/mL): Evidence supports a risk of adverse effects, especially at those concentrations > 150 nmol/L (> 60 ng/mL). Vitamin D toxicity has been associated with 25(OH)D concentrations of 500-600 nmol/L (200-240 ng/mL).

    Maximum Dosage Limits:
    NOTE: The Tolerable Upper Intake Level (UL) is defined as the highest daily intake of a nutrient that is likely to pose no risk in otherwise healthy individuals. The ULs are not intended to apply to individuals with specific disease states. Maximum doses for other uses is indication specific.
    -Neonates
    The Tolerable Upper Intake Level (UL) is 1000 International Units/day (25 mcg/day) PO.
    -Infants
    Infants 1-6 months: The Tolerable Upper Intake Level (UL) is 1000 International Units/day (25 mcg/day) PO.
    Infants 7-12 months: The Tolerable Upper Intake Level (UL) is 1500 International Units/day (38 mcg/day) PO.
    -Children
    Children 1-3 years: The Tolerable Upper Intake Level (UL) is 2500 International Units/day (63 mcg/day) PO.
    Children 4-8 years: The Tolerable Upper Intake Level (UL) is 3000 International Units/day (75 mcg/day) PO.
    Children >= 9 years: The Tolerable Upper Intake Level (UL) is 4000 International Units/day (100 mcg/day) PO.
    -Adolescents
    The Tolerable Upper Intake Level (UL) is 4000 International Units/day (100 mcg/day) PO.

    Patients with Hepatic Impairment Dosing
    Specific guidelines for dosage adjustments in hepatic impairment are not available; higher doses may be needed to compensate for reductions in intestinal absorption.

    Patients with Renal Impairment Dosing
    Specific guidelines for dosage adjustments in renal impairment are not available. However, ergocalciferol is activated in the kidney; close monitoring is required to ensure the appropriate dose.

    *non-FDA-approved indication

    Monograph content under development

    Mechanism of Action: Ergocalciferol is metabolized to its active form, calcitriol (1,25-dihydroxyvitamin D); all vitamin D activity is due to this metabolite. Calcitriol promotes intestinal absorption of calcium, maintains normal calcium and phosphorous levels to enable normal bone mineralization and prevent hypocalcemia. Calcitriol is also required for normal bone growth and remodeling by osteoblasts and osteoclasts. Calcitriol promotes intestinal absorption of calcium through binding to a specific receptor in the mucosal cytoplasm of the intestine. Subsequently, calcium is absorbed through formation of a calcium-binding protein. The synthesis of calcitriol is enhanced by elevated parathyroid hormone levels and low plasma phosphorus levels. Hypocalcemia causes release of parathyroid hormone, which stimulates the production of calcitriol.

    The vitamin D receptor (VDR) is present in numerous tissues throughout the body and some cells, other than renal cells, can convert vitamin D to calcitriol; the exact action of calcitriol within these tissues is not completely understood. There is evidence that calcitriol plays a role in cell growth, neuromuscular function, inflammation processes, and the immune system. Many genes that regulate cell proliferation, differentiation, and apoptosis are modulated in some part by vitamin D.

    Pharmacokinetics: Ergocalciferol is administered orally. Maximal clinical effects of a given dosage are usually observed in 4 weeks. Dietary vitamin D is absorbed from the GI tract in the presence of bile salts and is initially bound to chylomicrons, then is slowly transferred to vitamin D binding protein (DBP) in the serum. The uptake by chylomicrons results in vitamin D update by adipose tissue and muscle; remaining vitamin D in circulation is then metabolized by the liver. The uptake by the liver and other tissues accounts results in a plasma half-life of 4-6 hours for supplemental vitamin D. However, studies have shown that the whole-body half-life is about 2 months due to the stores in these tissues.

    Ergocalciferol is considered a prohormone and is converted in the liver by a group of activating cytochrome P450 (CYP) enzymes, CYP2R1, CYO27A1, and CYP27B1, to 25-hydroxyvitamin D (25(OH)D, calcidiol), the predominant form of vitamin D in the blood. This metabolite has a half-life of about 15 days. Serum 25(OH)D concentrations increase in a non-linear fashion in response to increased vitamin D intake based on baseline concentrations and duration of supplementation. Increasing serum 25(OH)D levels to > 50 nmol/L requires a greater amount of vitamin D than increasing baseline levels that are < 50 nmol/L. The impact on serum 25(OH)D concentrations is less when doses are > 1000 International Units/day compared to doses < 1000 International Unites/day. For example, for vitamin D doses >= 1000 International Units/day, the increase in serum 25(OH)D concentrations is about 1 nmol/L for each 40 International Units of vitamin D. Conversely, for vitamin D doses <= 600 International Units, the increase in 25(OH)D concentrations is about 2.3 nmol/L for each 40 International Units of vitamin D. In the kidneys, 25-hydroxyvitamin D is further converted to its active, hormonal form, 1,25-dihydroxyvitaminD (1,25(OH)2D, calcitriol), which has a half-life of about 15 hours and accounts for only a small portion of the total body amount of vitamin D. Synthesis to this active form by renal CYP27B1 is tightly regulated by parathyroid hormone and serum phosphate levels. All metabolites of vitamin D are excreted through the bile into the feces; very little is excreted in the urine.


    -Route-Specific Pharmacokinetics
    Oral Route
    Ergocalciferol is well absorbed orally in most individuals without conditions associated with fat malabsorption. There is a time lag of 10 to 24 hours between the oral administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active metabolites in the liver and kidneys.


    -Special Populations
    Hepatic Impairment
    Ergocalciferol absorption can be decreased in patients with any hepatic disease associated with fat malabsorption.

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