Medical Editor: John P. Cunha, DO, FACOEP Last updated on RxList: 2/15/2022
Drug Description

What is DHT and how is it used?

DHT is a prescription and over the counter medicine used to treat the symptoms of Hypocalcemia (lack of calcium in the blood) and Hypoparathyroidism (lack of parathyroid hormone). DHT may be used alone or with other medications.

DHT belongs to a class of drugs called Vitamins, Fat-Soluble.

What are the possible side effects of DHT?

DHT may cause serious side effects including:

  • hives,
  • difficulty breathing,
  • swelling of your face, lips, tongue, or throat,
  • bone pain,
  • hard lumps under your skin,
  • increased sensitivity to light,
  • eye redness or discharge,
  • weight loss,
  • metallic taste in your mouth,
  • increased urination,
  • nausea,
  • vomiting,
  • severe stomach pain,
  • fever, and
  • irregular heartbeats

Get medical help right away, if you have any of the symptoms listed above.

The most common side effects of DHT include:

  1. dry skin,
  2. changes in your bowel habits,
  3. dry mouth, and
  4. muscle pain

Tell the doctor if you have any side effect that bothers you or that does not go away.

These are not all the possible side effects of DHT. For more information, ask your doctor or pharmacist.

Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.


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

Alcohol 20%

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:

Dihydrotachysterol acts as a blood calcium regulator.

Inactive ingredients:

The tablets contain butylated hydroxyanisole, FD&C Red No. 3 (0.2 mg only), lactose, magnesium stearate, propyl gallate, starch, and sucrose.

Indications & Dosage


Dihydrotachysterol is indicated for the treatment of acute, chronic, and latent forms of postoperative tetany, idiopathic tetany, and hypoparathyroidism.


The dosage depends on the nature and seriousness of the disorder and should be adapted to each individual patient. Serum calcium levels should be maintained between 9 to 10 mg per 100 mL.

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.



According to the USDA, there is no difference between a “portion” and a “serving.” See Answer
Side Effects & Drug Interactions


No information provided.


Administration of thiazide diuretics to hypoparathyroid patients who are concurrently being treated with dihydrotachysterol may cause hypercalcemia.

Warnings & Precautions


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.

Laboratory Tests

To prevent hypercalcemia, treatment should always be controlled by regular determinations of blood calcium level, which should be maintained within the normal range.

Drug Interactions

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.

Nursing Mothers

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.

Overdose & Contraindications


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.


Contraindicated in patients with hypercalcemia, abnormal sensitivity to the effects of vitamin D, and hypervitaminosis D.

Clinical Pharmacology


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.

Medication Guide



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