xerostomia
Triamcinolone (Nasacort® AQ; Kenalog®) Adverse Reactions
NOTE: Prolonged systemic administration of physiologic replacement dosages of corticosteroid therapy usually does not cause adverse effects. The severity of the adverse effects associated with prolonged administration of pharmacological dosages of corticosteroids increases with the duration and frequency of therapy. Short-term administration of large doses typically does not cause adverse effects, but long-term administration can lead to adrenocortical atrophy and generalized protein depletion.
Possible adverse nasopharyngeal effects following oral or nasal inhalation of triamcinolone include flushing, xerostomia (dry mouth), nasal dryness, rash (unspecified), cough, dysphonia (hoarseness), tongue, mouth, and nasal irritation, and dysgeusia. Nasal septum perforation has been reported rarely in patients receiving aerosolized intranasal glucocorticoids. Bronchospasm may occur after administration of inhaled corticosteroids. If there is an immediate increase in wheezing following dosing of an inhaled corticosteroid, treatment with a fast-acting inhaled bronchodilator should be initiated immediately and corticosteroid inhalation therapy discontinued. Alternative treatment should be instituted.
Pharmacologic doses of systemic corticosteroids administered for prolonged periods can result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. Systemic absorption of topical triamcinolone is minimal in adults, but theoretically could cause systemic adverse reactions, especially if applied to a large surface area and/or if occlusive dressings are used. Generally, HPA suppression is not observed with inhaled triamcinolone alone, but is theoretically possible at high doses. Additionally, use of inhaled corticosteroids with systemic corticosteroids could increase the likelihood of HPA suppression compared to a therapeutic dose of either one alone. Exogenously administered corticosteroids exert a negative feedback effect on the pituitary, inhibiting the secretion of adrenocorticotropin (ACTH). This results in a decrease in ACTH-mediated synthesis of endogenous corticosteroids and androgens by the adrenal cortex. The severity of secondary adrenocortical insufficiency varies among individuals and is dependent on the dose, frequency, time of administration, and duration of therapy. Systemic administration drug on alternate days may help to alleviate this adverse effect. Patients with HPA suppression will require increased doses of corticosteroid therapy during periods of physiologic stress. Acute adrenal insufficiency and even death can occur with abrupt discontinuation of therapy. Discontinuation of prolonged oral corticosteroid therapy should be gradual, since HPA suppression can last for up to 12 months following cessation of therapy. Patients may continue to need supplemental corticosteroid treatment during periods of physiologic stress or infectious conditions, even after the drug has been discontinued. A withdrawal syndrome unrelated to adrenocortical insufficiency can occur following sudden discontinuance of corticosteroid therapy. This syndrome includes symptoms such as anorexia, lethargy, nausea/vomiting, headache, fever, arthralgia, myalgia, exfoliative dermatitis, weight loss, and hypotension. These effects are believed to be due to the sudden change in corticosteroid concentration rather than to low corticosteroid levels. HPA axis suppression and increased intracranial pressure have been reported in children receiving topical corticosteroids. Increased intracranial pressure with papilledema (i.e., pseudotumor cerebri) has also been reported with parenteral therapy and after withdrawal of glucocorticoid therapy.
Prolonged corticosteroid therapy can result in manifestations of Cushing’s syndrome. Cushing’s syndrome is characterized by truncal obesity, moon face, acne vulgaris, abdominal striae, increased blood pressure, decreased carbohydrate tolerance, protein catabolism, psychiatric disturbances, and skeletal changes, menstrual irregularity including amenorrhea or dysmenorrhea, and hirsutism.
Because of retardation of bone growth, children receiving prolonged systemic corticosteroid therapy may have growth inhibition. Controlled clinical trials have shown that intranasal or orally inhaled corticosteroids may also cause growth inhibition in pediatric patients. Growth inhibition has been observed in the absence of laboratory evidence of hypothalamic-pituitary-adrenal (HPA) suppression, suggesting that growth velocity is a more sensitive indicator of systemic corticosteroid exposure in pediatric patients. With orally inhaled corticosteroids, the mean reduction in growth velocity is approximately one centimeter per year (range 0.3 - 1.8 cm per year) and appears to be related to the dose and duration of exposure. The long-term effects of this reduction in growth velocity, including the impact on final adult height, are unknown. To minimize the effects of intranasal corticosteroids, each patient should be titrated to the lowest effective dose.
Glucocorticoids are responsible for protein metabolism, and prolonged therapy can result in a negative nitrogen balance and various musculoskeletal manifestations including myopathy (myalgia, muscle wasting, muscle weakness), impaired wound healing, bone matrix atrophy (osteoporosis), bone fractures such as vertebral compression fractures or fractures of long bones, and avascular necrosis of femoral or humoral heads. These effects are more likely to occur in older or debilitated patients. Glucocorticoids interact with calcium metabolism at many sites, including decreasing the synthesis by osteoblasts of the principle proteins of bone matrix, malabsorption of calcium in both the nephron and the gut, and reduction of sex hormone concentrations. Although all of these actions probably contribute to glucocorticoid-induced osteoporosis, the actions on osteoblasts are the most important. Glucocorticoids do not modify vitamin D metabolism. Postmenopausal women, in particular, should be monitored for signs of osteoporosis during corticosteroid therapy. Intra-articular injections of corticosteroids can cause Charcot-like arthropathy, calcinosis, and post-injection flare. Atrophy at the site of injection has been reported following administration of soluble glucocorticoids. Tendon rupture has also been reported.
Adverse GI effects associated with long-term corticosteroid administration include nausea/vomiting and anorexia with subsequent weight loss. Appetite stimulation with weight gain, diarrhea, constipation, abdominal pain, esophageal ulceration, esophagitis, gastritis, and pancreatitis also have been reported. Peptic ulcers with possible subsequent GI bleeding and GI perforation have been reported. Although it was once believed that corticosteroids contributed to the development of peptic ulcer disease, in a review of 93 studies of corticosteroid use, the incidence of peptic ulcer disease was not found to be higher in steroid recipients compared to control groups. While most of these studies did not utilize endoscopy, it is unlikely that corticosteroids contribute to the development of peptic ulcer disease. Elevated hepatic enzymes and hepatomegaly have occurred after parenteral administration. Hepatic enzyme elevations are usually reversible upon corticosteroid discontinuation.
Topical preparations of triamcinolone may be associated with local adverse effects and skin irritation including acneiform rash, allergic contact dermatitis, erythema, folliculitis, hypertrichosis, miliaria, perioral dermatitis, pruritus, skin atrophy, skin hypopigmentation, telangiectasia, and xerosis. Various adverse dermatologic effects reported during systemic corticosteroid therapy include skin atrophy, diaphoresis, facial erythema, petechiae, ecchymosis, and easy bruising. Hypersensitivity reactions may manifest as allergic dermatitis, urticaria, and/or angioedema. Post-marketing reports of anaphylactoid reactions have been rarely associated with the use of triamcinolone inhalation aerosol. Paresthesias (burning or tingling) in the perineal area may occur following IV injection of corticosteroids. Parenteral corticosteroid therapy has also produced hypertrichosis, anaphylactoid reactions; anaphylaxis; angioedema; urticaria; rash (unspecified); skin hypopigmentation; skin hyperpigmentation; scarring; acne; contact dermatitis; xerosis; increased sweating; ecchymoses; petechiae; striae; thin, fragile skin; and other types of injection site reaction (e.g., erythema, edema, induration, delayed pain or soreness, subcutaneous and cutaneous atrophy, and sterile abscesses).
In general, excessive use of systemic or topical corticosteroids can lead to impaired wound healing. Triamcinolone should not be applied directly on or near healing wounds. Skin ulcer may develop in patients with markedly impaired circulation who use topical corticosteroids.
Corticosteroid therapy (systemic or topical) can mask the symptoms of infection resulting in secondary infections; corticosteroids should not be used with an active infection unless adequately controlled by antiinfective agents. Oral candidiasis (thrush) occurs frequently with oral inhalation corticosteroid therapy. The incidence or course of acute viral or bacterial infection, however, is probably minimally affected by inhaled corticosteroids in immunocompetent individuals. Immunosuppression is most likely to occur in patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily), systemic corticosteroid therapy for any period of time, particularly in conjunction with corticosteroid sparing drugs (e.g., troleandomycin) and/or concomitant immunosuppressant agents; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods may also be at risk. Corticosteroid-induced immunosuppression may result in activation of latent viral (e.g., herpes) or bacterial (e.g., tuberculosis) infections and should not be used in patients with an active infection except when appropriate antiinfective therapy is instituted concomitantly.
Prolonged administration of glucocorticoids also can result in edema and fluid retention due to sodium retention; electrolyte disturbances (hypokalemia, hypokalemic metabolic alkalosis, hypernatremia, hypocalcemia); and hypertension. In a review of 93 studies of corticosteroid use, hypertension was found to develop 4 times as often in steroid recipients compared to control groups. Congestive heart failure can occur in susceptible patients.
Prolonged corticosteroid therapy can result in hyperglycemia and aggravation of diabetes mellitus in susceptible patients. In a review of 93 studies of corticosteroid use, the development of diabetes mellitus was determined to occur 4 times more frequently in steroid recipients compared to control groups. Insulin or oral hypoglycemic dosages may require adjustment.
Adverse neurologic effects have been reported during prolonged corticosteroid administration and include headache, insomnia, vertigo, restlessness, ischemic peripheral neuropathy, seizures, neuritis, and EEG changes. Mental disturbances, including depression, anxiety, euphoria, personality changes, and psychosis have also been reported; emotional lability and psychotic problems can be exacerbated by corticosteroid therapy. Arachnoiditis, meningitis, paresis, and paraplegia have occurred after intrathecal administration.
Although corticosteroids are used to treat Graves’ ophthalmopathy, ocular effects such as exophthalmos, posterior subcapsular cataracts, retinopathy, or ocular hypertension, can result from prolonged use of corticosteroids and could result in glaucoma, or ocular nerve damage including optic neuritis. Temporary or permanent visual impairment, including blindness, has been reported with corticosteroid administration by several routes of administration including intranasal. Secondary fungal and viral infections of the eye can be exacerbated by corticosteroid therapy. Inhaled corticosteroid therapy has been associated with the development of cataracts in adults. The risk of cataracts increases with long-term and high-dose inhaled corticosteroid use. The mechanism of corticosteroid-induced cataract formation is uncertain but may involve disruption of sodium-potassium pumps in the lens epithelium leading to accumulation of water in lens fibers and agglutination of lens proteins. Ocular hypertension and cataracts leading to visual impairment have also occurred following prolonged application of corticosteroids to the skin around the eye. Post-marketing reports of cataracts and glaucoma have been rarely associated with the use of triamcinolone inhalation aerosol.
Hypercholesterolemia, atherosclerosis, fat embolism, thrombosis, thromboembolism, and phlebitis, specifically, thrombophlebitis have been associated with corticosteroid therapy. Thrombocytopenia has occurred in several patients receiving prolonged, high-dose corticosteroid therapy. Palpitations, sinus tachycardia, glossitis, stomatitis, urinary incontinence, and urinary urgency have been rarely reported. Corticosteroids may also decrease serum concentrations of vitamin C (ascorbic acid) and vitamin A, which may rarely produce symptoms of vitamin A deficiency or vitamin C deficiency.
Tolerance may occur with the prolonged use of topical corticosteroid formulations. This may explain the dramatic responses noted initially by patients early in topical corticosteroid treatment and an apparent diminished response with time. Tolerance is reversible and may be attenuated by interrupted or cyclic schedules of application of triamcinolone creams or ointments for chronic dermatologic conditions.
[ Last revised: 2/23/2006 9:31:00 AM ]
References
. Conn HO, Poynard T. Corticosteroids and peptic ulcer: meta-analysis of adverse events during steroid therapy. J Intern Med 1994;236:619 - 32.
. Hanania NA, Chapman KR, Kesten S. Adverse effects of inhaled corticosteroids. Am J Med 1995;98:196 - 207.
. Cumming RG, Mitchell P, Leeder SR et al. Use of inhaled corticosteroids and the risk of cataracts. N Engl J Med 1997;337:8 - 14.
. Reid IR. Preventing glucocorticoid-induced osteoporosis. N Engl J Med 1997;337:420 - 1.
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