(Dihydrotachysterol Tablets USP):
Each tablet contains:
Dihydrotachysterol 0.125 mg, 0.2 mg, or 0.4 mg.
Each mL of Intensol TM Oral Solution (Concentrate) contains:
Dihydrotachysterol.............................. 0.2 mg
Dihydrotachysterol is a synthetic reduction product of tachysterol, a close isomer of vitamin D. Chemically dihydrotachysterol is 9, 10-Secoer-gosta-5, 7,22-tri-en-3b-ol, which can be represented by the following molecular formula C28H46O with a molecular weight of 398.65. Its chemical structure is:
DOSAGE AND ADMINISTRATION
The following dosage schedule will serve as a guide:
Initial dose: 0.8 mg to 2.4 mg daily for several days.
Maintenance dose: 0.2 mg to 1.0 mg daily as required for normal serum calcium levels. The average maintenance dose is 0.6 mg daily. This dose may be supplemented with 10 to 15 grams of calcium lactate or gluconate by mouth daily.
DHTTM Dihydrotachysterol Tablets USP
0.125 mg white tablets
(Tablets identified 54 280).
NDC 0054-8172-25: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-4190-19: Bottles of 50 Tablets
0.2 mg pink tablets (Identified 54 903).
NDC 0054-8182-25: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC: 0054-4189-25: Bottles of 100 Tablets
0.4 mg white tablets (Tablets Identified 54 772).
NDC 0054-4191-19: Bottles of 50 Tablets
DHTTM Dihydrotachysterol IntensolTM
0.2 mg per mL
NDC 0054-3170-44: Bottles of 30 mL with calibrated dropper (graduated 0.25 mL to 1.0 mL).
Caution: Federal law prohibits dispensing without prescription.
No information provided.
The difference between therapeutic dose and intoxicating dose may be small in any patient and therefore dosage must be individualized and periodically reevaluated.
In patients with renal osteodystrophy accompanied by hyperphosphatemia, maintenance of a normal serum phosphorus level by dietary phosphate restriction and/or administration of aluminum gels as intestinal phosphate binders is essential to prevent metastatic calcification.
Because of its effect on serum calcium, dihydrotachysterol should be administered to pregnant patients or to patients with renal stones only when, in the judgment of the physician, the potential banefits outweigh the possible hazards.
Administration of thiazide diuretics to hypoparathyroid patients who are concurrently being treated with dihydrotachysterol may cause hypercalcemia.
Teratogenic Effects -Pregnancy Category C: Animal reproduction studies have shown fetal abnormalities in several species associated with hypervitaminosis D. These are similar to the supravalvular aortic stenosis syndrome described in infants by Black in England (1963). This syndrome was characterized by supravalvular aortic stenosis, elfin facies, and mental retardation.
There are no adequate and well-controlled studies in pregnant women. Dihydrotachysterol should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when dihydrotachysterol is a administered to a nursing woman.
The effects of dihydrotachysterol can persist for up to one month after cessation of treatment.
Manifestations: Toxicity associated with dihydrotachysterol is similar to that seen with large doses of vitamin D. Overdosage is manifested by symptoms of hypercalcemia, i.e., weakness, headache, anorexia, nausea, vomiting, abdominal cramps, diarrhea, constipation, vertigo, tinnitus, ataxia, hypotonia, lethargy, depression, amnesia, disorientation, hallucinations, syncope, and coma. Impairment of renal function may result in polyuria, polydipsia, and albuminuria. Widespread calcification of soft tissues, including heart, blood vessels, kidneys, and lungs, can occur. Death can result from cardiovascular or renal failure.
Treatment: Treatment of overdosage consists of withdrawal of dihydrotachysterol, bed rest, liberal intake of fluids, a low-calcium diet, and administration of a laxative. Hypercalcemic crisis with dehydration, stupor, coma, and azotemia requires more vigorous treatment. The first step should be hydration of the patient. Intravenous saline may quickly and significantly increase urinary calcium excretion. A loop diurectic (furosemide or ethacrynic acid) may be given with the saline infusion to further increase renal calcium excretion. Other reported therapeutic measures include dialysis or the administration of citrates, sulfates, phosphates, corticosteroids, EDTA (ethylenediaminetetraacetic acids), and mithramycin via appropriate regimens.
Dihydrotachysterol is hydroxylated in the liver to 25-hydroxydihydrotachysterol, which is the major circulating active form of the drug. It does not undergo further hydroxylation by the kidney and therefore is the analogue of 1, 25-dihydroxyvitamin D. Dihydrotachysterol is effective in the elevation of serum calcium by stimulating intestinal calcium absorption and mobilizing bone calcium in the absence of parathyroid hormone and of functioning renal tissue. Dihydrotachysterol also increases renal phosphate excretion. In contrast to parathyroid extract, dihydrotachysterol is active when taken orally, exerts a slow but persistent effect, and may be used for long periods without increasing the dosage or causing tolerance. Dihydrotachysterol is faster-acting than pharmacologic doses of vitamin D and is less persistent after cessation of treatment, thus decreasing the risk of accumulation and of hypercalcemia.
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.