Description

Overview of Psoriasis CTS Cream

Dosage Strength of Psoriasis CTS Cream

Coal Tar Solution / Triamcinolone Acetonide / Salicylic Acid / Urea 5/0.16/5/10% 30 mL Pump

Coal Tar Solution

Coal tar is indicated for the symptomatic management of pruritus and irritation caused by dandruff, seborrheic dermatitis, atopic dermatitis, eczema, and psoriasis. Treatment with coal tar and UV light or sunlight can be beneficial because of its photosensitizing action. Official USP coal tar preparations include crude coal tar, coal tar topical solution, and coal tar ointment. Crude coal tar is produced as a byproduct secondary to the destructive distillation of coal, and it can be further refined into coal tar topical solution or ointment. Commercially available preparations that are not officially recognized by USP and do not have specifications for composition include coal tar extract and distillate. Application of crude coal tar preparations may be aesthetically displeasing to the patient; however, further refined products are believed by many clinicians to be therapeutically inferior. It has been suggested that the variability in refining processes may be responsible for differences in therapeutic response to coal tar preparations. Coal tar was in use prior to 1938 and approved by the FDA at its inception.

Triamcinolone Acetonide

Triamcinolone is a synthetic glucocorticoid that is considered slightly more potent than prednisone when given orally. Triamcinolone has little mineralocorticoid activity and is therefore not used systemically to manage adrenal insufficiency unless a more potent mineralocorticoid is administered concomitantly. Triamcinolone is commercially available in nasal, parenteral, topical, and intravitreal injection formulations. Oral and respiratory formulations of triamcinolone were previously available but are no longer marketed in the U.S. Triamcinolone injections are commonly used for intra-articular use when such therapy is indicated. The nasal spray is used to manage symptoms of seasonal and perennial allergies. Topical preparations for corticosteroid-responsive dermatoses are considered to be of medium or high potency.

Salicylic Acid

Salicylic acid is a topical keratolytic agent. It is used to remove excess keratin in hyperkeratotic skin disorders such as common and plantar warts, psoriasis, seborrheic dermatitis, calluses, and corns. Salicylic acid also is used to treat acne. Salicylic acid works by causing desquamation of the horny layer of skin. Prolonged or repeated daily use over large areas of skin may result in salicylism, especially in children and patients with renal or hepatic impairment. This drug was approved by the FDA in 1939.

Urea

Urea (also known as carbamide) is available as topical formulations and a powder for oral solution. It is used topically to treat dry skin (xerosis) and for destruction and dissolution of dystrophic nails due to onychomycosis. As an oral agent, urea is an osmotic diuretic and is used for the treatment of hyponatremia, particularly due to SIADH.

Coal Tar Solution

Coal tar exhibits keratoplastic and mild irritant activity. Coal tar may decrease the quantity and size of epidermal cells produced and inhibit mitosis, possibly through removal of oxygen in the skin. Shampoo and soap preparations may exert their action through absorption into the epidermis and enhancement of scale removal. It has been suggested that a reaction similar to that following exposure to sunlight can occur in the epidermis through interaction between the peroxides in coal tar and epidermal sulfhydryl groups. Subsequently, epidermal proliferation may be decreased. Coal tar preparations are also believed to possess antipruritic, antiseptic, astringent, antifungal, vasoconstrictive, and photosensitizing properties. Coal tar is reportedly carcinogenic in humans, inducing skin cancer primarily in the anogenital region, following prolonged exposure to coal tar in industrial settings. It is unlikely that patients treated acutely for dermatologic conditions are at an increased risk for developing skin cancer. Nevertheless, this risk should be considered during prolonged treatment periods.

Triamcinolone Acetonide

Corticosteroids exhibit anti-inflammatory, antipruritic, and vasoconstrictive properties. At the cellular level, corticosteroids induce peptides called lipocortins. Lipocortins antagonize phospholipase A2, an enzyme which causes the breakdown of leukocyte lysosomal membranes to release arachidonic acid. This action decreases the subsequent formation and release of endogenous inflammatory mediators including prostaglandins, kinins, histamine, liposomal enzymes and the complement system.

Early anti-inflammatory effects of topical corticosteroids include the inhibition of macrophage and leukocyte movement and activity in the inflamed area by reversing vascular dilation and permeability. Later inflammatory processes such as capillary production, collagen deposition, keloid (scar) formation also are inhibited by corticosteroids. Clinically, these actions correspond to decreased edema, erythema, pruritus, plaque formation and scaling of the affected skin.

In the treatment of asthma, corticosteroids block the late phase allergic response to allergens. Mediators involved in the pathogenesis of asthma include histamine, leukotrienes (slow releasing substance of anaphylaxis, SRS-A), eosinophil chemotactic factor of anaphylaxis (ECF-A), neutrophil chemotactic factor (NCF), cytokines, hydroxyeicosatetraenoic acids, prostaglandin-generating factor of anaphylaxis (PGF-A), prostaglandins, major basic protein, bradykinin, adenosine, peroxides, and superoxide anions. Different cell types are responsible for release of these mediators including airway epithelium, eosinophils, basophils, lung parenchyma, lymphocytes, macrophages, mast cells, neutrophils, and platelets. Corticosteroids inhibit the release of these mediators as well as inhibit IgE synthesis, attenuate mucous secretion and eicosanoid generation, up-regulate beta-receptors, promote vasoconstriction, and suppress inflammatory cell influx and inflammatory processes. Clinical effects in asthma include a reduction in bronchial hyperresponsiveness to allergens, a decreased number of asthma exacerbations, and an improvement in FEV-1, peak-flow rate, and respiratory symptoms. Since corticosteroid effects take several hours to days to become clinically noticeable, they are ineffective for primary treatment of severe acute bronchospastic attacks or for status asthmaticus. Inhaled corticosteroids have no bronchodilatory properties.

Salicylic Acid

Salicylic acid exhibits keratolytic action by dissolution of intercellular cement substance causing desquamation of the horny layer of skin.

Urea

Topically, urea promotes the uptake of water by the stratum corneum by allowing it to have a high water-binding capacity. This promotes hydration in dry skin and a mild keratolytic action in hyperkeratotic skin.

When used systemically, urea is an osmotic diuretic agent. Urea creates an osmotic gradient across the blood-brain barrier that promotes water flow out of the brain. As the urea gradient across the blood-brain barrier is diminished, it is replaced by an increase in serum sodium concentration that prevents plasma water from reentering the brain. This osmotic effect will persist as long as a gradient exists between the tissues and the blood; as urea diffuses into the tissues, the effect is diminished. Administration of large doses of urea will increase the osmotic pressure of the glomerular filtrate, inhibit the reabsorption of water and solutes in the renal tubule, and induce diuresis.

Coal Tar Solution

Coal tar preparations should not be applied to patients with skin abrasion or skin that is inflamed, broken, or infected because exacerbation of the condition can occur and systemic absorption of the drug can be enhanced.

Sunlight (UV) exposure should be avoided for at least 24 hours following application of coal tar preparations, unless otherwise directed by a physician, because a photosensitivity reaction can occur. In addition, development of cutaneous viral infections is possible following UV light exposure.

Coal tar prescription products are classified as FDA pregnancy risk category C; non-prescription products are not assigned a risk rating. Adequate studies in humans of the risks to the fetus have not been conducted. In one retrospective study in which pregnancy outcome data were gathered using a patient questionnaire among women with psoriasis or dermatitis, 19% of pregnancies without coal tar exposure (n = 59) resulted in spontaneous abortion and 5% in a congenital disorder compared to 26% of pregnancies with coal tar exposure (n = 23) resulting in spontaneous abortion and 4% in a congenital disorder. Until conclusive pregnancy outcome data become available, these agents should be used during pregnancy only when clearly needed. Coal tar preparations should only be considered for use during pregnancy when moisturizers and emollients are ineffective for symptom control. The effect of coal tar preparations during labor and delivery is unknown.

Manufacturer recommendations for breast-feeding mothers are not available. It is not known whether coal tar is distributed into breast milk and there is no information available on the effects of coal tar preparations on a nursing infant. Coal tar shampoos are generally compatible with use during breast feeding, as most of the agent is rinsed off during bathing and skin contact time is low. Other coal tar skin preparations should be used with caution; alternatives recommended include general emmollient and humectant lotions and baths. In one case of a mother applying coal tar ointment to her entire body except for face and breasts, the pyrene metabolite was detected in all of the nursing infant’s urine samples. Because the mother’s breast milk contained no detectable pyrene and only low levels of the pyrene metabolite, the authors speculated that the infant obtained the pyrene via skin-to-skin or skin-to-mouth contact with the mother and metabolized it.17 If coal tar skin treatment is deemed necessary during lactation, the smallest amount of lotion, foam or oil possible should be used to treat the affected areas. The infant’s skin should not come into direct contact with treated areas of the mother’s skin. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.

Triamcinolone Acetonide

Prolonged administration of pharmacological doses of systemic corticosteroids or topical preparations (resulting in systemic absorption) may result in hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing’s syndrome in some patients. Adrenal suppression and increased intracranial pressure have been reported with the use and/or withdrawal of various corticosteroid formulations in pediatric patients. Inhaled triamcinolone should be used with caution when substituting the drug for oral corticosteroid therapy; deaths due to adrenal insufficiency have been reported in asthmatic patients during and following such a transfer. Acute adrenal insufficiency and even death may occur following abrupt discontinuation of systemic therapy. In addition, a withdrawal syndrome unrelated to adrenocortical insufficiency may occur following sudden discontinuation of corticosteroid therapy. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid concentrations. Withdraw prolonged systemic corticosteroid therapy (duration of treatment more than 2 weeks) gradually. HPA suppression can last for up to 12 months following cessation of systemic therapy. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid. HPA-suppressed patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as post-surgical stress, acute blood loss, or infectious conditions, even after the corticosteroid has been discontinued. Encourage patients currently receiving chronic corticosteroid therapy or who have had corticosteroids discontinued within the last 12 months to carry identification advising the need for administration of corticosteroids in situations of increased stress. Conditions that increase systemic absorption of topical corticosteroids include use over large surface areas, prolonged use, use in areas where the epidermal barrier is disrupted (i.e., skin abrasion), and the use of an occlusive dressing. Pediatric patients may absorb proportionally larger amounts of topical corticosteroids compared to adults due to a larger skin surface to body mass ratio and, therefore, may be at increased risk of systemic adverse reactions. Evaluate patients receiving large doses of triamcinolone applied to a large surface area periodically for evidence of HPA axis suppression and/or manifestations of Cushing’s syndrome. If these effects are noted, attempt withdrawal of the drug, a reduction in the frequency of application, or substitution of a less potent corticosteroid. Non prescription intranasal corticosteroids should not be used for greater than 2 months in pediatric patients without oversight of a healthcare provider. If signs of HPA suppression occur with the use of intranasal corticosteroids, the drug should be slowly discontinued. Additionally, clearance of corticosteroids is decreased in patients with hypothyroidism and increased in hyperthyroidism.

Potential adverse effects of chronic corticosteroid therapy should be weighed against the clinical benefits obtained and the availability of other treatment alternatives. Prolonged systemic corticosteroid therapy can lead to osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humoral heads, and pathologic fractures of long bones secondary to decreased bone formation, increased bone resorption, and protein catabolism in any patients. A high-protein diet may alleviate or prevent the adverse effects associated with protein catabolism. The elderly, post-menopausal, and pediatric patients may be more susceptible to the effects on bone. Chronic systemic triamcinolone therapy may cause growth inhibition in pediatric patients due to hypothalamic-pituitary-adrenal axis suppression and inhibition of bone growth. Corticosteroids should be titrated to the lowest effective dose. Because bone development is critical in pediatric patients, monitoring is warranted in patients receiving high-dose or chronic corticosteroid treatment. Growth inhibition may also occur with intranasal or topical triamcinolone due to systemic absorption, particularly in susceptible patients or when used in high doses or for prolonged periods of time. Use of the lowest effective dose is recommended to minimize the occurrence of systemic adverse effects. Monitor growth routinely.

Do not use high doses of corticosteroids such as triamcinolone hexacetonide for the treatment of traumatic brain injury. An increase in early mortality (at 2 weeks) and late mortality (at 6 months) was noted in patients with head trauma who were determined not to have other clear indications for corticosteroid treatment; in the trial, patients received methylprednisolone hemisuccinate.

Corticosteroids such as triamcinolone are not recommended for use by patients with cerebral malaria. Systemic corticosteroid therapy can mask the symptoms of infection and should not be used in cases of viral infection, fungal infection, or bacterial infection that are not adequately controlled by antiinfective agents. Although the manufacturers state that systemic triamcinolone is contraindicated in patients with systemic fungal infections, most clinicians believe that systemic corticosteroids can be administered to these patients as long as appropriate antiinfective therapy is administered simultaneously.

Patients receiving immunosuppressive doses of systemic corticosteroids should be advised to avoid exposure to viral infections (i.e., measles or varicella) because these diseases may be more serious or even fatal in immunosuppressed patients. Pediatric patients dependent on systemic corticosteroids should undergo anti-varicella-zoster virus antibody testing. The incidence or course of acute viral or bacterial infection are probably minimally affected by inhaled triamcinolone. Application of topical corticosteroids to areas of infection, including dermatologic fungal infection, and cutaneous or systemic viral infection (e.g., herpes infection, measles, varicella), should be initiated or continued only if the appropriate antiinfective treatment is instituted. If the infection does not respond to the antimicrobial therapy, the concurrent use of the topical corticosteroid should be discontinued until the infection is controlled. Use ophthalmic triamcinolone acetonide injectable suspension (Triesence or Trivaris) with caution in patients with ocular herpes infection because of possible corneal perforation. Corticosteroids should not be used in active ocular herpes infection.

Topical corticosteroids, such as triamcinolone, should not be used to treat acne vulgaris, acne rosacea, or perioral dermatitis as they may exacerbate these conditions.

Topical corticosteroids may delay the healing of non-infected wounds, such as venous stasis ulcers. Use topical triamcinolone preparations with caution in patients with markedly impaired circulation or peripheral vascular disease; skin ulceration has been reported in these patients following topical corticosteroid use.

As with any long-term topical treatment of the nasal cavity, patients using triamcinolone intranasally over several months or longer should be examined periodically for possible changes in the nasal mucosa. Further, because of the inhibitory effect of corticosteroids on wound healing, patients who have experienced recent nasal septal perforation or ulcer, nasal surgery, or nasal trauma should not use a nasal corticosteroid until healing has occurred.

Topical corticosteroids should be used for brief periods, or under close medical supervision in patients with evidence of preexisting skin atrophy. Elderly patients may be more likely to have preexisting skin atrophy secondary to aging. Purpura and skin lacerations that may raise the skin and subcutaneous tissue from deep fascia may be more likely to occur with the use of topical corticosteroids in older adult patients. Use of lower potency topical corticosteroids also may be necessary in some patients.

Topical corticosteroids should be used with caution in patients with diabetes mellitus. Exacerbation of diabetes may occur with systemic absorption of the topical corticosteroid. Use of topical corticosteroids may further delay healing of skin ulcers in diabetic patients.

Topical use of triamcinolone during pregnancy should also be approached with caution. Topical corticosteroids, including triamcinolone, should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Guidelines recommend mild to moderate potency topical agents over potent corticosteroids, which should be used in short durations. Fetal growth restriction and a significantly increased risk of low birthweight has been reported with use of potent or very potent topical corticosteroids during the third trimester, particularly when using more than 300 grams. Corticosteroids are generally teratogenic in laboratory animals when administered systemically at relatively low dosage levels. The more potent corticosteroids have been shown to be teratogenic after dermal application in laboratory animals.

Triamcinolone therapy usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (< 2 weeks); low to moderate dose; long-term alternate day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); or administration topically (skin or eye), by aerosol, or by intra-articular, bursal or tendon injection. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live-virus vaccines. In general, patients with severe immunosuppression due to large doses of corticosteroids should not receive vaccination with live-virus vaccines. When cancer chemotherapy or immunosuppressive therapy is being considered (e.g., for patients with Hodgkin’s disease or organ transplantation), vaccination should precede the initiation of chemotherapy or immunotherapy by >= 2 weeks. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy. In patients who have received high-dose, systemic corticosteroids for >= 2 weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.

According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities (LTCFs); the need for continued use of a glucocorticoid, with the exception of topical or inhaled formulations, should be documented, along with monitoring for and management of adverse consequences with intermediate or longer-term systemic use.

Monitor patients with renal disease or renal impairment for signs of edema, weight gain, or serum electrolyte abnormalities. Triamcinolone may increase salt and water retention and increase the excretion of potassium and calcium. Dietary salt restriction or potassium supplementation may be necessary.

Use triamcinolone with caution in patients with hepatic disease. An enhanced corticosteroid effect may occur due to increased drug metabolism in patients with cirrhosis.

Salicylic Acid

Salicylic acid preparations are contraindicated in patients who have previously exhibited salicylate hypersensitivity.

Topical salicylic acid preparations in concentrations greater than 6% are contraindicated in patients with diabetes mellitus and other conditions of poor blood circulation such as peripheral vascular disease. Do not use these preparations on moles, birthmarks, warts with hair growing from them, genital warts, or warts on the face or mucous membranes.

Prolonged use of salicylic acid over large areas, especially in children and patients with renal impairment or hepatic disease may increase the risk for development of salicylism. In such patients, limit the treated area and closely monitor the patient for signs of salicylate toxicity such as nausea, vomiting, dizziness, loss of hearing, tinnitus, lethargy, hyperpnoea, diarrhea, and psychic disturbances. When the potential for toxicity is present, advise patients not to apply occlusive dressings, clothing or other occlusive topical products such as petrolatum-based ointments to prevent excessive systemic exposure to salicylic acid. Concomitant use of other drugs which may contribute to elevated serum salicylate levels (e.g., oral aspirin and other salicylate containing medications, such as sports injury creams) should be avoided. Discontinue use of salicylic acid if salicylic acid toxicity occurs and treat appropriately.

The potential for Reye’s syndrome should be considered with administration of salicylic acid products in children and adolescents with varicella or influenza.

Avoid accidental exposure of salicylic acid products to the eyes, lips, mucus membranes and inflamed or broken skin as increased absorption may occur. If unintended mucus membrane or ocular exposure occurs, thoroughly rinse affected areas with water.

Urea

Most topical formulations of urea are classified as either FDA pregnancy category B or C. The topical suspension and solution are classified as pregnancy risk B; while the topical paste, shampoo, and nail lacquer are in category C. Depending on the manufacturer, the cream, lotion, emulsion, foam, and gel formulations can be either B or C. Urea topical ointment is not included in the pregnancy category rating. It is not known if topical administration of urea can cause fetal harm when administered to a pregnant woman. Urea should only be administered during pregnancy if clearly needed.

It is not known if urea is excreted in human milk. According to the manufacturer, caution should be exercised when urea is administered to a nursing woman. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.

Coal Tar Solution

Coal tar prescription products are classified as FDA pregnancy risk category C; non-prescription products are not assigned a risk rating. Adequate studies in humans of the risks to the fetus have not been conducted. In one retrospective study in which pregnancy outcome data were gathered using a patient questionnaire among women with psoriasis or dermatitis, 19% of pregnancies without coal tar exposure (n = 59) resulted in spontaneous abortion and 5% in a congenital disorder compared to 26% of pregnancies with coal tar exposure (n = 23) resulting in spontaneous abortion and 4% in a congenital disorder. Until conclusive pregnancy outcome data become available, these agents should be used during pregnancy only when clearly needed. Coal tar preparations should only be considered for use during pregnancy when moisturizers and emollients are ineffective for symptom control. The effect of coal tar preparations during labor and delivery is unknown.

Triamcinolone Acetonide

Systemic triamcinolone use should be approached with caution during pregnancy and should be used during pregnancy only when the anticipated benefit outweighs the potential fetal risk. Complications, including cleft palate, still birth, and premature abortion, have been reported when systemic corticosteroids, including triamcinolone, were administered during pregnancy in animal studies. If systemic triamcinolone must be used chronically during pregnancy, the potential risks should be discussed with the patient. Infants born to women receiving large doses of systemic corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary. Caution is also recommended with the use of inhaled and respiratory triamcinolone. Low-dose inhaled corticosteroids are considered first line therapy for control of mild persistent asthma during pregnancy. Data on the use of medium to high dose inhaled corticosteroid use during pregnancy are limited. However, dose titration may be considered for those with moderate to severe persistent asthma, preferably using budesonide. Budesonide is preferred over other inhaled corticosteroids due to availability of more safety information during pregnancy. However, there are no data to indicate safety concerns with other inhaled corticosteroids, and maintaining a previously established treatment regimen may be more beneficial to the patient. Selection of any pharmacologic treatment for asthma control during pregnancy should include the specific needs of the patient, based on an individual evaluation, and consideration of the potential benefits or risks to the fetus. Topical use of triamcinolone during pregnancy should also be approached with caution. Topical corticosteroids, including triamcinolone, should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Guidelines recommend mild to moderate potency topical agents over potent corticosteroids, which should be used in short durations. Fetal growth restriction and a significantly increased risk of low birthweight has been reported with use of potent or very potent topical corticosteroids during the third trimester, particularly when using more than 300 grams. Corticosteroids are generally teratogenic in laboratory animals when administered systemically at relatively low dosage levels. The more potent corticosteroids have been shown to be teratogenic after dermal application in laboratory animals.

Salicylic Acid

There are no adequate and well-controlled studies in pregnant women. Salicylic acid products should only be used during pregnancy if the potential benefit to the mother outweighs the potential risk to the fetus.

Urea

Most topical formulations of urea are classified as either FDA pregnancy category B or C. The topical suspension and solution are classified as pregnancy risk B; while the topical paste, shampoo, and nail lacquer are in category C. Depending on the manufacturer, the cream, lotion, emulsion, foam, and gel formulations can be either B or C. Urea topical ointment is not included in the pregnancy category rating. It is not known if topical administration of urea can cause fetal harm when administered to a pregnant woman. Urea should only be administered during pregnancy if clearly needed.

Coal Tar Solution

Manufacturer recommendations for breast-feeding mothers are not available. It is not known whether coal tar is distributed into breast milk and there is no information available on the effects of coal tar preparations on a nursing infant. Coal tar shampoos are generally compatible with use during breastfeeding, as most of the agent is rinsed off during bathing and skin contact time is low. Other coal tar skin preparations should be used with caution; alternatives recommended include general emollient and humectant lotions and baths. In one case of a mother applying coal tar ointment to her entire body except for face and breasts, the pyrene metabolite was detected in all of the nursing infant’s urine samples. Because the mother’s breastmilk contained no detectable pyrene and only low levels of the pyrene metabolite, the authors speculated that the infant obtained the pyrene via skin-to-skin or skin-to-mouth contact with the mother and metabolized it. If coal tar skin treatment is deemed necessary during lactation, the smallest amount of lotion, foam or oil possible should be used to treat the affected areas. The infant’s skin should not come into direct contact with treated areas of the mother’s skin. Consider the benefits of breastfeeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breastfeeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.

Triamcinolone Acetonide

There are no available data on the presence of triamcinolone in human milk following systemic, inhaled, or nasal administration, the effects on the breast-fed infant, or the effects on milk production. Reviewers and an expert panel consider inhaled and oral corticosteroids acceptable to use during breast-feeding. Low-dose inhaled corticosteroids are considered first line therapy for control of mild persistent asthma during lactation. Due to greater availability of data, budesonide is the preferred agent in this population. However, there are no data to indicate safety concerns with other inhaled corticosteroids and maintaining a previously established treatment regimen may be more beneficial to the patient. It is not known whether topical administration of triamcinolone could result in sufficient systemic absorption to produce detectable quantities in breast milk. However, most dermatologists stress that topical corticosteroids can be safely used during lactation and breast-feeding. If applied topically, care should be used to ensure the infant will not come into direct contact with the area of application, such as the breast. Increased blood pressure has been reported in an infant whose mother applied a high potency topical corticosteroid ointment directly to the nipples. Consider the benefits of breastfeeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breastfeeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.

Salicylic Acid

It is not known whether topically applied salicylic acid is excreted into breastmilk. According to the manufacturer, salicylic acid should not be used during breast-feeding. However, if the drug is used by nursing mothers, care should be taken to avoid application to the skin of the breast during lactation; oral ingestion by the infant could be harmful. Consider the benefits of breastfeeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.

Urea

It is not known if urea is excreted in human milk. According to the manufacturer, caution should be exercised when urea is administered to a nursing woman. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.

Coal Tar Solution

Prolonged periods of coal tar application can result in dermatitis that can be severe. A contact dermatitis can develop, with the latter increasing in severity with increasing concentrations of the drug.

Application of coal tar over an extended period can result in an asymptomatic, chronic folliculitis. This reaction generally subsides following discontinuance of treatment or reduction in the frequency of application. The occurrence of folliculitis can be reduced by: avoiding application to areas with hair, if possible; shortening treatment length; and avoiding occlusion of treated areas.

Triamcinolone Acetonide

Pharmacologic doses of systemic corticosteroids, such as triamcinolone, administered for prolonged periods can result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. 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. Systemic absorption of topical corticosteroids can also produce reversible HPA suppression with possible adrenocortical insufficiency after withdrawal of treatment. Percutaneous absorption of triamcinolone is dependent on many factors including the vehicle, the integrity of the epidermal barrier, duration of use, and use of an occlusive dressing. Children may be more susceptible to systemic toxicity from equivalent doses due to their larger skin surface to body mass ratios. Manifestations of adrenocortical insufficiency in children include low plasma cortisol concentrations and absence of response to adrenocorticotropin (ACTH) stimulation. HPA axis suppression has been reported in children receiving topical corticosteroids. Increased intracranial pressure has also been reported in children receiving topical corticosteroids. Increased intracranial pressure with glucocortiocoids usually occurs after treatment. Clinical signs of increased intracranial pressure include bulging fontanelle, head pain/ache, and bilateral papilledema (i.e., pseudotumor cerebri). Patients applying triamcinolone to a large surface area or to areas under occlusion should be evaluated periodically for evidence of HPA axis suppression (using the ACTH stimulation test, A.M. plasma cortisol test, and urinary free cortisol test). To minimize risk of HPA axis suppression, discontinue therapy when control is achieved. If no improvement is seen within 2 weeks, reassessment of diagnosis may be necessary. If HPA axis suppression is noted, an attempt should be made to withdraw the drug, reduce the frequency of application, or substitute a less potent corticosteroid. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid. Exogenously administered corticosteroids exert a negative feedback effect on the pituitary, inhibiting the secretion of 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 appetite loss, lethargy, nauseousness, head pain/ache, fever, joint pain, muscle pain, exfoliative dermatitis, loss of weight, and hypotension. These effects are believed to be due to the sudden change in corticosteroid concentration rather than to low corticosteroid levels.

Adverse GI effects associated with long-term triamcinolone administration include nausea, vomiting and anorexia with subsequent weight loss. Appetite stimulation with weight gain, diarrhea, constipation, abdominal pain and/or distention, esophageal ulceration, hiccups, gastritis, and pancreatitis also have been reported. Among intranasal triamcinolone recipients, diarrhea (3% vs. 1.3% with placebo), upper abdominal pain (4.7% vs. 0.8% with placebo), and dyspepsia (3.4% vs. 1% with placebo) were noted. 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.

Corticosteroid therapy including triamcinolone can mask the symptoms of infection and should generally be avoided during an acute viral, fungal, or bacterial infection. The incidence or course of acute viral or bacterial infection, however, is probably minimally affected by inhaled or nasal corticosteroids in immunocompetent individuals. The most common potentially infectious-related adverse reactions with nasal triamcinolone use (more than 2% incidence) were flu-like syndrome and bronchitis. Influenza or a flu-like syndrome was reported in 8.4% of pediatric patients treated with intranasal triamcinolone in clinical trials. Localized candidiasis of the nasal mucosa and pharynx occurs frequently with intranasal corticosteroid therapy. If such an infection develops, the corticosteroid should be discontinued and appropriate local or systemic therapy initiated. It is recommended that patients using an intranasal or inhaled corticosteroid for several months or longer be examined periodically for evidence of infection. Leukocytosis is a common physiologic effect of systemic corticosteroid therapy and may need to be differentiated from the leukocytosis that occurs with inflammatory or infectious processes. Immunosuppression from corticosteroids 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 the 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 anti-infective therapy is instituted concomitantly. Patients receiving immunosuppressive doses of corticosteroids should be advised to avoid exposure to measles or varicella (chickenpox) and, if exposed to these diseases, to seek medical advice immediately. Monitoring systemic corticosteroid recipients for signs of an opportunistic fungal infection is recommended, as cases of oropharyngeal candidiasis have been reported. Development of Kaposi’s sarcoma has also been associated with prolonged administration of corticosteroids; discontinuation of the corticosteroid may result in clinical improvement. Topically applied corticosteroids can be absorbed in sufficient amounts to produce systemic effects, especially if used in excessive dosage, over large body surface areas, for prolonged periods, or with occlusive dressings. In the presence of dermatological infections, institute the use of an appropriate antifungal or antibacterial agent. If a favorable response does not promptly occur, discontinue the topical corticosteroid until the infection has been adequately controlled.

The following adverse reactions (listed in decreasing order of occurrence) are reported with topical corticosteroids such as triamcinolone and may occur more often when used with an occlusive dressing: skin irritation (including burning), pruritus, xerosis (dry skin), folliculitis, hypertrichosis, acneiform rash/eruptions, skin hypopigmentation, perioral dermatitis, maceration of the skin or oral mucosa, secondary infection, skin atrophy, atrophy of the oral mucosa, striae, and miliaria. Erythema, telangiectasia, purpura, and maculopapular rash may also occur. A rash (unspecified) was noted in 2.5% of intranasal triamcinolone recipients as compared with 1.7% of placebo recipients. Although skin atrophy usually occurs after prolonged use of topical corticosteroids, this effect may occur even with short-term use on intertriginous or flexor areas, or on the face. If irritation develops, discontinue topical corticosteroids and institute appropriate therapy. The anti-inflammatory activity of topical corticosteroids may also mask manifestations of infection. In the presence of dermatological infections, institute the use of an appropriate antifungal or antibacterial agent. If a favorable response does not promptly occur, discontinue the corticosteroid until the infection has been adequately controlled. Various adverse dermatologic effects reported during systemic corticosteroid therapy include skin atrophy, diaphoresis, acne vulgaris, striae, hirsutism, acneiform rash, alopecia, xerosis, lupus-like symptoms, perineal pain and irritation, purpura, rash (unspecified), telangiectasia, facial erythema, petechiae, ecchymosis, and easy bruising. Hypersensitivity reactions may manifest as allergic dermatitis, urticaria, anaphylactoid reactions, and/or angioedema. Post-marketing reports of anaphylactoid reactions have been rarely associated with the use of triamcinolone inhalation aerosol. Burning or tingling in the perineal area may occur following IV injection of corticosteroids. Parenteral corticosteroid therapy has also produced skin hypopigmentation, skin hyperpigmentation, scarring, and other types of injection site reaction (e.g., 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. Use of intranasal triamcinolone is not recommended until healing has occurred for patients who have experienced recent nasal septal ulcers, nasal surgery, or trauma. Skin ulcer may develop in patients with markedly impaired circulation who use topical corticosteroids.

Prolonged administration of triamcinolone 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. In a study, an increased risk of heart failure was observed for medium-dose glucocorticoid use as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. Medium exposure was defined as less than 7.5 mg daily of prednisolone or the equivalent given orally, rectally, or parenterally.

Prolonged triamcinolone therapy can result in hyperglycemia, glucosuria (glycosuria), 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. Systemic absorption of topical corticosteroids has produced hyperglycemia and glucosuria in some patients. Percutaneous absorption of hydrocortisone is dependent on many factors including the vehicle, the integrity of the epidermal barrier, duration of use, and use of an occlusive dressing. Children may be more susceptible to systemic toxicity from equivalent doses due to their larger skin surface to body mass ratios. Insulin or oral hypoglycemic dosages may require adjustment.

Adverse neurologic effects have been reported during prolonged triamcinolone administration and include insomnia, vertigo, restlessness, amnesia and memory impairment, increased motor activity, impaired cognition, paresthesias, ischemic peripheral neuropathy, malaise, ischemic peripheral neuropathy, seizures, neuritis, and EEG changes. Mental disturbances, including depression, anxiety, euphoria, personality changes, emotional lability, delirium, dementia, hallucinations, irritability, mania, mood swings, schizophrenic reactions, withdrawn behavior, and psychosis have also been reported; emotional lability and psychotic problems can be exacerbated by corticosteroid therapy. Arachnoiditis, meningitis, paresis, paraplegia, and sensory disturbances have occurred after intrathecal administration. Spinal cord infarction has been reported after epidural administration.

Ocular effects such as corneal perforation, posterior subcapsular cataracts, retinopathy, or ocular hypertension can result from prolonged use of systemic corticosteroids and could result in glaucoma or ocular nerve damage including optic neuritis. Temporary or permanent visual impairment including blurred vision and blindness has been reported with corticosteroid administration by several routes of administration. If injectable systemic steroid therapy is continued for more than 6 weeks, monitor intraocular pressure. Evaluate any patient who develops visual impairment or changes in vision during corticosteroid therapy for ocular hypertension or other ocular adverse effects. Postmarketing reports of cataracts and glaucoma have been rarely associated with the use of triamcinolone inhalation aerosol or intranasal sprays. 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 have also occurred following prolonged application of topical corticosteroids to the skin around the eye. Triamcinolone use may reduce host resistance to infection. Secondary fungal and viral infections of the eye (ocular infection) can be masked or exacerbated by corticosteroid therapy. Investigate the possibility of fungal infection if patients have persistent corneal ulceration. After intravitreal injection with triamcinolone acetonide injectable suspension (Triesence or Trivaris), monitor patients for ocular hypertension and endophthalmitis. Increases in intraocular pressure, lasting up to 6 months, and cataract progression have been observed in 20% to 60% of patients after treatment. Appropriate monitoring and management of intraocular pressure and optic nerve head perfusion are needed. Monitoring may consist of a check for perfusion of the optic nerve head immediately after the injection, tonometry within 30 minutes following the injection, and biomicroscopy between 2 and 7 days after the injection. The increased intraocular pressure caused by triamcinolone is usually managed by topical glaucoma therapy, but patients may require aggressive non-topical treatment. After intravitreal injection, infectious culture-positive endophthalmitis was reported at a rate of 0.5%, and infectious and noninfectious endophthalmitis was present in less than 2%. Instruct patients to immediately report any symptoms suggestive of endophthalmitis. Less common reactions occurring in up to 2% of patients receiving intravitreal triamcinolone include exophthalmos, hypopyon (leukocytosis in the anterior chamber of the eye), blurring and transient discomfort upon injection, retinal detachment, optic disc vascular disorder, ocular inflammation, ocular hemorrhage, and visual impairment (including vitreous floaters).

Hypercholesterolemia, atherosclerosis, fat embolism, sinus tachycardia, palpitations, bradycardia, syncope, vasculitis, necrotizing angiitis, thrombosis, thromboembolism, and phlebitis, specifically, thrombophlebitis have been associated with triamcinolone therapy. Glucocorticoid use appears to increase the risk of cardiovascular events such as myocardial infarction, left ventricular rupture (in persons who recently experienced a myocardial infarction), angina, angioplasty, coronary revascularization, stroke, transient ischemic attack, cardiomegaly, arrhythmia exacerbation and ECG changes, hypertrophic cardiomyopathy (in premature infants), congestive heart failure and pulmonary edema, cardiac arrest or cardiovascular death. As determined from observational data, the rate of cardiovascular events was 17 per 1,000 person-years among 82,202 non-users of glucocorticoids. In contrast, the rate was 23.9 per 1,000 person-years among 68,781 glucocorticoid users. Furthermore, the rate of cardiovascular events was 76.5 per 1,000 person-years for high exposure patients. After adjustment for known covariates by multivariate analysis, high-dose glucocorticoid use was associated with a 2.56-fold increased risk of cardiovascular events as compared with nonuse. At the beginning of the study, patients were at least 40 years of age and had not been hospitalized for cardiovascular disease. High glucocorticoid exposure was defined as at least 7.5 mg daily of prednisolone (or equivalent) given orally, rectally, or parenterally whereas medium exposure was defined as less than the above dosage by any of the 3 routes. Low-dose exposure was defined as inhaled, topical, or nasal usage only.

Tolerance may occur with the prolonged use of topical triamcinolone formulations. Tolerance is usually described as a decreased acute vasoconstrictive response to the agent after a period of days to weeks. 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.

Cases of elevated hepatic enzymes (usually reversible upon discontinuation) and hepatomegaly have been associated with corticosteroid receipt such as triamcinolone.

Allergic contact dermatitis with topical corticosteroids such as triamcinolone is usually diagnosed by observing a failure to heal. Appropriate diagnostic patch testing may help with the diagnosis.

Dizziness and anemia have been reported with corticosteroid use such as triamcinolone. Corticosteroids may decrease serum concentrations of vitamin C (ascorbic acid) and vitamin A, which may rarely produce symptoms of vitamin A deficiency or vitamin C deficiency. Some loss of folic acid may also be caused by corticosteroid use; glossitis may be noted.

Salicylic Acid

Prolonged and repeated daily use over large areas, especially in children and patients with significant renal or hepatic impairment increases the potential for development of salicylism.

Topical application of salicylic acid is generally well tolerated, but may result in skin irritation including transient stinging, burning, or pruritus. Excessive erythema, peeling of the skin, and scaling may also occur, particularly if used on open skin lesions. Advise patients to discontinue use and consult a physician if excessive burning, stinging, or peeling occurs.

Topical over-the-counter (OTC) acne products, including salicylic acid, have been associated with rare but serious and potentially life-threatening hypersensitivity reactions. These reactions may occur within minutes to a day or longer after use of the product. Instruct patients to stop using topical acne products if they experience signs of anaphylactoid reactions such as throat tightness; difficulty breathing; feeling faint; or swelling of the eyes, face, lips, or tongue. The product should also be discontinued in patients who develop urticaria or pruritus. Based on the information reported to the FDA, it is uncertain whether the reactions are caused by the active ingredients benzoyl peroxide or salicylic acid, the inactive ingredients or a combination of both. When initiating therapy with an OTC topical acne product, advise patients to apply a small amount to one or two small affected areas for 3 days and monitor for signs of a hypersensitivity reaction. If no discomfort occurs, the instructions on the Drug Facts label may be followed.

Urea

Skin irritation (i.e., stinging, burning, or itching) may occur after topical application of urea products; the irritation is usually transient and normally subsides after discontinuation of the medication.

Mild GI upset and unpleasant taste have been reported with oral urea. Rapid administration of larger doses by nasogastric tube may cause vomiting and diarrhea. Other adverse reactions observed with oral urea include headache, hypernatremia, and hypokalemia.

Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.

1.Compound W (salicylic acid 17%) package insert. Tarrytown, NY: Prestige Brands; 2013 Mar.
2.Compound W gel (salicylic acid 17% gel) package insert. Tarrytown, NY: Prestige Brands; 2013 April.
3.Hydrisalic gel (salicylic acid 17%) package insert. Farmingdale, NY: Pedinol Pharmacal Inc.; 2011 Nov.
4.Virasal (salicylic acid 27.5%) package insert. Vernon Hills, IL: Elorac, Inc.; 2011 Jan.
5.Salex 6% (salicylic acid) cream and lotion package insert. Bridgewater, NJ: Valeant Pharmaceuticals North America LLC; 2019 Jan.
6.Salacyn 6% (salicylic acid 6%) cream or lotion package insert. Miami, Fl: Stratus Pharmaceuticals Inc.; 2010 Nov..
7.Salitech (salicylic acid 5% lotion) package insert. Peoria, AZ: Solutech Pharmaceuticals; 2016 Dec.
8.Salisol (salicylic acid 23% topical solution) package insert. Peoria, AZ: Solutech Pharmaceuticals; 2016 Dec.
9.Urea powder for oral solution product information. Accessed March 9, 2018; Available on the world wide web at: http://www.ure-na.com.
10.Schimmer B, Parker K. Adrenocorticotropic hormone; adrenocortical steroids and their synthetic analogs; inhibitors of the synthesis and actions of adrenocortical hormones. In: Hardman JG, Limbird LE, Molinoff PB, et al., eds. Goodman and Gilman’s the Pharmacological Basis of Therapeutics, 10th edition. New York: McGraw Hill, 2001;1649-1674.
11.Barnes PJ. Anti-inflammatory actions of glucocorticoids: molecular mechanisms. Clin Sci (Lond). 1998;94(6):557-572.
12.National Asthma Education and Prevention Program Expert Panel 3. Expert panel report 3: guidelines for the diagnosis and management of asthma. Bethesda (MD): National Institutes of Health. National Heart, Lung, and Blood Institute; 2007 Aug. NIH Publication No. 07-4051.
13.Salvax 6% foam (salicylic acid) package insert. Newtown, PA: Quinnova Pharmaceuticals, Inc.; 2009 Apr.
14.Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: Expert Panel Recommendations. Am J Med 2013;126:S1-S42.
15.Sterns RH, Silver SM, Hix JK. Urea for hyponatremia?. Kidney Int 2015;87:268-270.
16.Franssen ME, van der Wilt GJ, de Jong PC, et al. A retrospective study of the teratogenicity of dermatological coal tar products. Acta Derm Venereol 1999;79:390-1.
17.Scheepers PT, van Houtum JL, Anzion RB, et al. Uptake of pyrene in a breast-fed child of a mother treated with coal tar. Pediatr Dermatol 2009;26:184-7.
18.Bond DW, Charlton CPJ. Benign intracranial hypertension secondary to nasal fluticasone propionate. BMJ 2001;322 (7291):987.
19.Patradoon-Ho P, Gunasekera H, Ryan MM. Inhaled corticosteroids, adrenal suppression and benign intracranial hypertension. Med J Aust 2006;185:279-280
20.Triamcinolone acetonide ointment package insert. Melville, NY: E. Fougera & Co., 2011 Oct.
21.Azmacort (triamcinolone acetonide) package insert. North Chicago, IL: Abbott Laboratories; 2007 Sept.
22.Kenalog-40 (triamcinolone acetonide) injection package insert. Princeton, NJ: Bristol-Myers Squibb Company; 2018 Mar.
23.Shulman DI, Palmert MR, Kemp SF. Adrenal insufficiency: still a cause of morbidity and death in childhood. Pediatrics 2007;119(2):e484-494.
24.Triamcinolone acetonide cream package insert. Melville, NY: E. Fougera & Co.; 2011 Sept
25.Nasacort AQ (triamcinolone acetonide) nasal spray package insert. Bridgewater, NJ: Sanofi-aventis U.S. LLC; 2013 July.
26.Nasacort Allergy 24HR (triamcinolone acetonide) OTC nasal spray package insert. Chattanooga, TN: Chattem, Inc., a wholly-owned subsidiary of Sanofi-Aventis; 2016 Sept.
27.Zilretta (triamcinolone acetonide extended-release injectable suspension). Burlington, MA: Flexion Therapeutics, Inc.; 2019 Dec.
28.Hengge UR, Ruzicka T, Schwartz RA. Adverse effects of topical glucocorticosteroids. J Am Acad Dermatol 2006;54:1-15.
29.Morley KW, Dinulos JG. Update on topical glucocorticoid use in children. Curr Opin Pediatr 2012;24(1):121-128
30.Hanania NA, Chapman KR, Kesten S. Adverse effects of inhaled corticosteroids. Am J Med 1995;98:196-207.
31.Kenalog (triamcinolone acetonide) topical aerosol package insert. Jacksonville, FL: Ranbaxy; 2011 July.
32.Triesence (triamcinolone acetonide injection for ophthalmic use) package insert. Fort Worth, TX: Alcon Laboratories, Inc.; 2018 Dec.
33.Murase JE, Heller MM, Butler DC. Safety of dermatologic medications in pregnancy and lactation: Part I. Pregnancy. J Am Acad Dermatol. 2014;70:401.e1-14. Review.
34.The American Geriatrics Society 2019 Beers Criteria Update Expert Panel. American Geriatrics Society 2019 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc 2019;00:1-21.
35.Health Care Financing Administration. Interpretive Guidelines for Long-term Care Facilities. Title 42 CFR 483.25(l) F329: Unnecessary Drugs. Revised 2015.
36.Zilretta (triamcinolone acetonide extended-release injectable suspension). Burlington, MA: Flexion Therapeutics, Inc.; 2019 Dec.
37.Curad mediplast (salicylic acid 40%) package insert. Mundelein, IL: Medline Industries, Inc.; 2013 Feb.
38.Urea 40 Gel/Lotion package insert. Port St. Joe, FL: Kylemore Pharmaceuticals; 2009 Dec.
39.Urea cream, 40% package insert. Montvale, NJ: Ascend Laboratories, LLC; 2012 Mar.
40.Aristospan (triamcinolone hexacetonide) 5 mg/ml injection package insert. Princeton, NJ: Sandoz Inc.; 2014 Apr.
41.NAEPP Working Group Report on Managing Asthma During Pregnancy. Recommendations for Pharmacologic Treatment-Update 2004. NIH Publication No. 05-3279. Bethesda, MD: U.S. Department of Health and Human Services; National Institutes of Health; National Heart, Lung, and Blood Institute, 2004
42.Scheepers PT, van Houtum JL, Anzion RB, et al. Uptake of pyrene in a breastfed child of a mother treated with coal tar. Pediatr Dermatol 2009;26:184-7.
43.Greenberger PA, Patterson R. The management of asthma during pregnancy and lactation. Clin Rev Allergy 1987;5:317-24.
44.Ellsworth A. Pharmacotherapy of asthma while breastfeeding. J Hum Lact 1994;10:39-41.
45.Butler DC, Heller MM, Murase JE. Safety of dermatologic medications in pregnancy and lactation: Part II. Lactation. J Am Acad Dermatol. 2014;70:417.e1-10. Review.
46.Conn HO, Poynard T. Corticosteroids and peptic ulcer: meta-analysis of adverse events during steroid therapy. J Intern Med 1994;236:619-32.
47.Abramson N, Melton B. Leukocytosis: basic of clinical assessment. Am Fam Physician 2000;62:2053-60.
48.Shoenfeld Y, Gurewich Y, Gallant LA, et al. Prednisone-induced leukocytosis. Influenced of dosage, method and duration of administration on the degree of leukocytosis. Am J Med 1981;71:773-8.
49.Prednisone tablet package insert. Salisbury, MD: Cadista Pharmaceuticals Inc.; 2016 Mar.
50.Wei L, MacDonald TM, Walker BR. Taking glucocorticoids by prescription is associated with subsequent cardiovascular disease. Ann Intern Med 2004;141:764-70.
51.Kenalog-10 (triamcinolone acetonide) injection package insert. Princeton, NJ: Bristol-Myers Squibb Company; 2018 Jun.
52.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.
53.Trivaris (triamcinolone acetonide injectable suspension) package insert. Irvine, CA: Allergan, Inc.; 2008 Jun.
54.Food and Drug Administration MedWatch. Over-The-Counter Topical Acne Products: Drug Safety Communication – Rare But Serious Hypersensitivity Reactions. Retrieved June 25, 2014. Available on the World Wide Web http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm402722.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery
55.Urea 40% Mousse package insert. Charleston, SC: Innocutis Holdings LLC; 2011 Dec.
56.Soupart A, Coffernils M, Couturier B, et al. Efficacy and tolerance of urea compared with vaptans for long-term treatment of patients with SIADH. Clin J Am Soc Nephrol 2012;7:742-747.
57.de Sola-Morales O, Riera M. Urea for management of the syndrome of inappropriate secretion of ADH: A systematic review. Endocrinol Nutr 2014;61:486-492.
58.Decaux G, Genette F. Urea for long-term treatment of syndrome of inappropriate secretion of antidiuretic hormone. Br Med J (Clin Res Ed) 1981;283:1081-1083.

Reviews

There are no reviews yet.


Be the first to review “Psoriasis CTS Cream”

General Inquiries

There are no inquiries yet.