Each tablet contains:
Triamcinolone 4 mg

Triamcinolone particularly acts as glucocorticoid and it has a potent anti-inflammatory effect, hormonal and metabolic effect like cortisone. Glucocorticoid activity leads to increased gluconeogenesis and decreased utilization of glucose in the tissues. Protein catabolism is accelerated and synthesis from dietary protein decreased, although the overall effect on nitrogen balance depends on other factor including diet, dose, and duration of treatment. Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Triamcinolone differs from naturally occurring glucocorticoids by having a greater anti-inflammatory and glycogen forming effect and diminished mineralocorticoid (salt-retaining) properties.

Triamcinolone is rapidly absorbed following an oral dose. Peak effects following oral administration occur within 1 - 2 hours. It is bound to plasma albumin to a much smaller extent than hydrocortisone. Triamcinolone crosses the placenta. The plasma half-life is approximately 5 hours and the biological half-life is 18-36 hours.

Treatment for the following conditions:

Endocrine disorders
Primary or secondary adrenocortical insufficiency (hydrocortisones or cortisones are the drugs of choice although synthetic analogs may be used in conjunction with mineralocorticoids where applicable, mineralocorticoid supplementation is of particular importance when treating this condition in infants); congenital adrenal hyperplasia; nonsuppurative thyroiditis; and hypercalcemia associated with cancer.

Rheumatic disorders
As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in psoriatic arthritis; rheumatoid arthritis (selected cases may require low-dose maintenance therapy); ankylosing spondylitis; acute and subacute bursitis; acute nonspecific tenosynovitis; and acute gouty arthritis.

Collagen diseases
For use during an exacerbation or as maintenance therapy in selected cases of systemic lupus erythematosus and acute rheumatic carditis.

Dermatologic diseases
Pemphigus, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, mycosis fungoides and severe psoriasis.

Allergic states
For the control of seasonal or perennial allergic rhinitis, bronchial asthma, contact dermatitis, atopic dermatitis, serum sickness, angioedema and urticaria when they are severe or incapacitating and intractable to adequate trials of conventional treatment.

Ophthalmic diseases
Severe, acute and chronic allergic and inflammatory processes involving the eye and its associated anatomic parts e.g., allergic conjunctivitis, keratitis, allergic corneal marginal ulcers, herpes zoster ophthalmicus, iritis and iridocyclitis, chorioretinitis, anterior segment inflammation, diffuse posterior uveitis and choroiditis, optic neuritis and sympathetic ophthalmia.

Respiratory diseases
Symptomatic sarcoidosis, Loeffler's syndrome not manageable by other means, berylliosis, fulminating or disseminated pulmonary tuberculosis when concurrently accompanied by appropriate antituberculous chemotherapy, pulmonary emphysema where bronchospasm or bronchial edema plays a significant role and diffuse interstitial pulmonary fibrosis (Hamman-Rich syndrome).

Hematologic disorders
Idiopathic and secondary thrombocytopenia in adults, acquired (auto-immune) hemolytic anemia, erythroblastopenia (RBC anemia) and congenital (erythroid) hypoplastic anemia.

Neoplastic diseases
For palliative management of leukemias and lymphomas in adults and acute leukemia in childhood.

Edematous states
To induce diuresis or remission of proteinuria in the nephrotic syndrome (non-uremic, the idiopathic type or that which is due to lupus erythematosus) and, in conjunction with diuretic agents, to induce diuresis in refractory congestive heart failure and in cirrhosis of the liver with refractory ascites.

Gastrointestinal diseases
To tide the patient over a critical period of the disease in ulcerative colitis, regional enteritis and intractable sprue.

Dental postoperative inflammatory reactions and tuberculous meningitis with subarachnoid block or impending block when concurrently accompanied by appropriate antituberculous chemotherapy.

Patients with systemic fungal infections.
Patients with a known hypersensitivity to the drug or any of its ingredients.

Dosage and administrations:
The initial dosage of triamcinolone tablets may vary from 4-48 mg/day depending on the specific disease entity being treated. In situations of lesser severity, lower doses will generally suffice while in selected patients, higher initial doses may be required.

The initial dosage should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period of time there is lack of satisfactory clinical response, the corticosteroid should be discontinued and the patient transferred to other appropriate therapy. It should be emphasized that dosage requirements are variable and must be individualized on the basis of the disease under treatment and the response of the patient.

For infants and children
The recommended dosage should be governed by the same considerations rather than by strict adherence to the ratio indicated by age or body weight. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small increments at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response is reached.

It should be kept in mind that constant monitoring is needed in regard to drug dosage. Changes in dose may be necessary if the clinical status changes, the patient's individual responsiveness changes or the patient is exposed to stressful situation not directly related to disease under treatment; it may be necessary to increase the dosage of the triamcinolone for a period of time consistent with the patient's condition. If after long-term therapy triamcinolone is to be stopped, it is recommended that triamcinolone be withdrawn gradually rather than abruptly. Hormone therapy is an adjunct to, and not a replacement for, conventional therapy.

To transfer patients from other corticosteroids:
Substitute triamcinolone 4 mg initially in place of each cortisone 25 mg, hydrocortisone 20 mg, prednisone 5 mg, prednisolone 5 mg, methylprednisolone 4 mg, dexamethasone 0.75 mg, betamethasone 0.6 mg and paramethasone 2 mg. Thereafter, dosage should be adjusted according to individual response.

Warnings and precautions:

  • Use in pregnancy and lactation:
  • Since adequate human reproduction studies have not been done with corticosteroids, the use of these drugs in pregnancy, nursing mothers or women of childbearing potential requires that the possible benefits of the drug be weighed against the potential hazards to the mother and the embryo, fetus or nursing infant.
  • Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
  • Patients who are receiving corticosteroid therapy are subjected to unusual stress, increased dosage of rapidly acting corticosteroids is indicated before, during, and after the stressful situation.
  • Corticosteroids may mask some signs of infection and new infections may appear during their use. There may be decreased resistance and inability to localize infection when corticosteroids are used. If an infection occurs during corticosteroid therapy, it should be promptly controlled by suitable antimicrobial therapy.
  • Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves and may enhance the establishment of secondary ocular infections due to fungi or viruses.
  • Salt and water retention as well as increased excretion of potassium can occur, although they are less likely to occur with the synthetic derivatives e.g., triamcinolone than with hydrocortisone or cortisone, except when they are used in large doses; dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.
  • Patient should not be vaccinated against smallpox while on corticosteroid therapy. Other immunization procedures should not be undertaken in patients who are on corticosteroids, especially on high dose because of possible hazards of neurological complications and a lack of antibody response.
  • The use of triamcinolone in patients with active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculous regimen.
  • If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary since re-activation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemotherapy.
  • High doses of triamcinolone may have a greater tendency to produce proximal myopathy.


  • As with all corticosteroids, patients should be observed for increased weight, edema, hypertension and excessive potassium excretion as well as less obvious signs of adrenocortical steroid untoward effects. A liberal protein intake is essential during prolonged therapy.
  • Drug-induced secondary adrenocortical insufficiency may be minimized by a gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy. Therefore, in any situation of stress (e.g., trauma, surgery or severe illness) occurring during that period, hormone therapy should be reinstituted. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should be administered concurrently.
  • There is an enhanced corticosteroid effect in patients with hypothyroidism and in those with cirrhosis.
  • Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
  • The lowest possible dose of corticosteroid should be used to control the condition being treated. A gradual reduction in dosage should be made when possible.
  • Psychic derangements may appear when corticosteroids are used. These may range from euphoria, insomnia, mood swings, personality changes and severe depression to frank psychotic manifestations. Existing emotional instability or psychotic tendencies may also be aggravated by corticosteroids.
  • Salicylates should be used cautiously in conjunction with corticosteroids in patients with hypoprothrombinemia.
  • Corticosteroids should be used with caution in patients with nonspecific ulcerative colitis if there is a probability of impending perforation, abscess or other pyogenic infection. Corticosteroids should also be used cautiously in patients with diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, renal insufficiency, hypertension, osteoporosis, acute glomerulonephritis, vaccinia, varicella, exanthema, Cushing's syndrome, antibiotic-resistant infections, diabetes mellitus, congestive heart failure, chronic nephritis, thromboembolic tendencies, thrombophlebitis, convulsive disorders, metastatic carcinoma and myasthenia gravis.
  • Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed.
  • Menstrual irregularities may occur and this possibility should be mentioned to female patients past menarche.
  • Triamcinolone, like other glucocorticoids, may aggravate diabetes so that higher dosages of insulin or hypoglycemic agents may become necessary.
  • Triamcinolone may also precipitate the manifestations of diabetes mellitus from a previously latent state. Continued supervision of the patient after termination of corticosteroid therapy is essential since there may be a sudden reappearance of severe manifestations of the disease for which the patient was treated.

Adverse reactions:
Patients should be watched closely for the following adverse reactions which may be associated with any corticosteroid therapy:

Fluid and electrolyte disturbance
Sodium retention, fluid retention, congestive heart failure in susceptible patients, potassium loss, hypokalemic alkalosis and hypertension.

Muscle weakness, fatigue, steroid myopathy, loss of muscle mass, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, pathologic fractures of long bones and spontaneous fractures.

Peptic ulcer with possible subsequent perforation and hemorrhage, pancreatitis, abdominal distention and ulcerative esophagitis.

Impaired wound healing, thin fragile skin, ptechiae and ecchymoses, facial erythema, increased sweating, subcutaneous fat atrophy, purpura, striae, hyperpigmentation, hirsutism, acneform eruptions and suppressed reactions to skin tests.

Convulsions, increased intracranial pressure with papilledema (pseudotumor cerebri) usually after treatment, vertigo, headache, neuritis or paresthesias and aggravation of preexisting psychiatric conditions.

Menstrual irregularities, development of the Cushingoid state, suppression of growth in children, secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress (e.g., trauma, surgery or illness), decreased carbohydrate tolerance, manifestations of diabetes mellitus from a previously latent state and increased requirements for insulin or oral hypoglycemic agents in diabetes.

Posterior subcapsular cataracts, increased intraocular pressure, glaucoma and exophthalmos.

Hyperglycemia, glycosuria and negative nitrogen balance due to protein catabolism.

Necrotizing angiitis, thrombophlebitis, thromboembolism, aggravation or masking of infections, insomnia, syncopal episodes and anaphylactoid reactions.

Drug interactions:
Potentially hazardous interaction
Combination of a corticosteroid with non-steroidal anti-inflammatory drug increases the risk of developing peptic ulcer and gastrointestinal hemorrhage.

Other significant interactions
Corticosteroids have been reported to antagonize neuromuscular blockade caused by pancuronium. The risk of hypokalemia may be increased if triamcinolone is given concurrently with sympathomimetics and theophylline, which lower plasma potassium and with potassium-losing diuretics, hypokalemia may also potentiate the effect of cardiac glycosides. The diabetogenic effect of corticosteroids will impair blood glucose control with insulin and oral hypoglycemic agents.

Accidental or intentional ingestion of a single excessive dose of a corticosteroid is unlikely to have serious results, but any symptoms that did occur would have to be treated symptomatically.

Presentation and registration number:
Box, 10 strips @ 10 tablets; DKL



Manufactured by:
PT Dexa Medica