Sandra R. Merchant DVM Diplomate ACVD
Dermatology Continuing Education Seminar
December 11, 2005
It is great to diagnose a "good" diseases like flea allergy dermatitis (FAD), scabies, and cutaneous adverse food reactions (CAFR) (or food "allergy") that are easily curable. Even if your patient has a "difficult" disease like atopic dermatitis (AD) that you cannot cure, with a detailed history, and dermatologic examination, you will be in a better position to control the disease, by determining all of the factors that are contributing to the pruritus (allergens, parasites, bacteria, yeast, etc.) and will be able to pursue the best treatments for all of these.
It is imperative that you establish a diagnosis, know the cause of the pruritus if possible, so that appropriate therapy can be selected. The basics are key and cannot be skipped. Signalment (age, breed), history (onset, seasonality, response to therapy, etc), physical findings (general and dermatologic examination) contribute fundamental clues to a logical list of differential diagnoses. Perpetuating or concurrent conditions must be treated specifically to assure getting your patient comfortable as quickly as possible. Every dog should be flea combed and fleas treated if found. A skin scraping and fungal culture allows you to identify and treat conditions that will respond rapidly to appropriate therapy. If you suspect sarcoptic mange, treat for this aggressively and early to remove this possibility from the picture. Secondary problems such as staphylococcal pyoderma, Malassezia dermatitis, or otitis (bacterial or yeast) must be identified and treated specifically. Once the "easy" things are managed, whatever pruritus is left is likely due to an allergy. It is here that a logical selection of anti-pruritic medication can occur. Hopefully, your client will allow a full diagnostic workup for the remaining allergic pruritus, but if not at least you are in a position to formulate a symptomatic treatment program
It is common to have secondary staphylococcal folliculitis or secondary Malassezia dermatitis associated with allergic dermatitis. It is very important to recognize and treat these secondary infections since Staphylococcus, and probably Malassezia as well, may exacerbate the patient’s allergic status and may in fact be a major cause of the patient’s pruritus. Failure to recognize this common complication may lead to complete failure in control of pruritus.
The pruritus of the allergy dog often responds (however not usually completely) to anti-bacterial therapy. Recommended antibiotics for recurrent Staphylococcal folliculitis and Staphylococcal hypersensitivity include the following: cephalexin, cefpodoxime (Simplicef), oxacillin, amoxicillin/clavulanic acid (Clavamox), clindamycin (Anaerobe), trimethoprim potentitated sulfonamides (Tribrissen), ormetoprim potentiated sulfonamide (Primor), enrofloxacin (Baytril), and marbofloxacin (Zeniquin.) Anti-microbial shampoo therapy with ethyl lactate or 2-4 % chlorhexidine shampoos, is also recommended to help manage recurrent pruritic pyoderma.
Yeast infection is also a common secondary complication. Malassezia dermatitis tends to be located in the same areas as classic atopic signs. The regular use of topical anti-yeast/anti-seborrheic therapy may be effective (miconazole, ketoconazole, selenium disulfide, acetic acid/boric acid, enilconazole or 3-4% chlorhexidine shampoos or rinses). Systemic anti-yeast medication may be warranted in severe cases (ketoconazole 5 mg/kg/day, fluconazole 5 - 10 mg/kg/day, itraconazole 5 mg/kg/day $). Maintenance therapy once the yeast dermatitis has been controlled include usually systemic anti-yeast therapy approximately twice weekly with ketoconazole or itraconazole.
When comparing a population of atopic dogs to a population of non-atopic dogs, flea allergy dermatitis will be more prevalent in the population of atopic dogs. This allergy must be controlled with strict avoidance. Controlling the flea allergy, because of the “summation effect,” may allow the atopic patient to become sub-clinical for its atopy. Infestation with other ectoparasites would also contribute to the “summation effect.”
Avoidance therapy is the most ideal approach to the management of the allergic patient. It is relatively easy to do in food allergy dogs, once the difficulty of making that diagnosis is overcome. Avoidance can seldom be satisfactorily achieved in atopy, since most atopic animals are sensitive to many allergens and most environmental allergens are ubiquitous. However, some patients can be improved by decreasing environmental exposure and some clients are willing to practice some control measures if given sufficient information.
The goal of environmental control measures is to minimize contact with allergens or irritants that precipitate or aggravate the clinical signs. Attention should be paid to where the pet sleeps or is left for hours during the day. Some airborne irritants can aggravate preexisting allergic reactions especially in those patients exhibiting signs of conjunctivitis, peri-ocular dermatitis and rhinorrhea. These irritants include cigarette smoke and chemical fumes from cleaning materials.
House dust is an important allergen for 35 to 100% of dogs tested, depending on the geographic region. It is a very important allergen in south LA and the gulf coast. The highest mite levels occur in the home during periods of high relative humidity. The mites are concentrated in areas of bedding, stuffed furniture and carpeted floors. The most successful control includes very strenuous efforts to minimize contact with these areas. This includes removal of carpeting, plastic covering of bedding, and regular washing and thorough drying of bedding. High efficiency vacuums or those with water traps and double filters reduce the allergens that become airborne during cleaning. In addition, stuffed toys should be avoided, the pet should not sleep on cushioned furniture and should be kept as much as possible in uncarpeted rooms, with frequent damp mopping of the areas most frequented by the patient.
Positive reactions to fungi/molds have been reported in 8 to 88% of dogs tested. Measures to decreased contact include avoiding rooms with high moisture level, (kitchen, bathroom, laundry room, basement), avoiding long-term storage of dry dog foods (may also have allergenic storage mites), storing dry dog foods in the freezer, decreasing the number of house plants and plant-derived material (burlap, wicker, bark, stored firewood, moldy mats), using a dehumidifier and keeping it clean and disinfected and cleaning with a chlorine bleach solution.
Pollen allergens are common with 17 to 85% reacting to grasses (summer), 17 to 64% reacting to trees (spring) and 23 to 86 % reacting to weeds (autumn). Pollen concentrations reach peaks early in the morning and at dusk. Measures to minimize contact include avoiding fields, keeping the grass in the garden cut short, rinsing or moist-toweling the patient after a trip into grassy and weedy sites, keeping the patient inside at dusk and dawn and while mowing the lawn, and using air conditioners and air filters. Keeping the animal indoors when high levels of pollen to which they react is in the air is helpful. This information can be found on the World Wide Web. One such site is http://www.pollen.com.
Antipruritic medications may be divided into general nonspecific, meaning that the treatment targets the symptom regardless of the cause, and specific therapy directed at the primary cause.
Systemic antipruritic medications for dogs with mild or limited seasonal signs might include antihistamines, sedatives, antidepressants, non-steroidal anti-inflammatory drugs, and essential fatty acids. Non-steroidal anti-inflammatory drugs find their best use with atopic pruritus. Although antihistamines and essential fatty acids are described as being the best choice for non-steroidal medical management of pruritus, response to these is unpredictable. What works great in one dog may not work well in another, and what works well for several months may suddenly appear not to work at all. It is important to advise your client of the variable response and give them a realistic level of expectation. Only 20 % of atopic dogs will respond with enough reduction in pruritus to use these therapies alone
Antihistamines block the classic inflammatory effects of histamine. They may also directly inhibit or stimulate mast cell secretion, may change the number, activity or both of helper or suppressor T lymphocytes, and may activate other cells such as the eosinophil that alter mast cell function.
There is a variety of classes of antihistamines (H1 blockers) and a great deal of individual variability in the response to antihistamines. (See table) It is worthwhile to try two or three different antihistamines, one from each class for two to three weeks each in evaluating the efficacy of antihistamine therapy. A common mistake made by owners (and human allergy sufferers) is to try to use antihistamines on a PRN basis. These drugs are much more effective when given before the allergy symptoms take hold. They will be most effective if used regularly as directed, starting just before the patient’s allergy season. Also, beware of TID drugs. Many owners cannot maintain this regimen and these drugs (notably, Benadryl and hydroxyzine) are not as effective given BID.
The major side effect of antihistamines is sedation; this may decrease after several days of treatment. Uncommonly, nervousness or tremors may be seen, especially at higher dosages. Increased efficacy may be expected when antihistamines are combined with fatty acid supplementation. Individual patients may develop antihistamine tachyphylaxis after a period of time. In these instances, a different antihistamine class should be evaluated.
There are many veterinary essential fatty acid (EFA) dietary supplements on the market. They are not all created equal. Some contain only omega 3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from marine fish oil or alpha linolenic acid from flax seed oil. Others contain primarily omega 6 fatty acids such as linoleic acid (LA) from vegetable oil, and gamma linoleic acid (GLA) from borage or evening primrose. Others contain both omega 3 and omega 6 fatty acids. Most contain a small amount of vitamins A, D and E. You must know what effect you wish to achieve before selecting a fatty acid supplement. For dry skin, products containing linoleic acid are best as LA is a fundamental fatty acid in the epidermal barrier. Its lack will lead to a dull coat and dry, flaky skin.
Omega 3 fatty acids (EPA. DHA) and GLA (and omega 6 fatty acid) are potentially useful in reducing pruritus because of their immunomodulatory effect. When used appropriately the omega 3 fatty acids, may modulate the formation of prostaglandins, thromboxanes and leukotrienes. In North America, n-3 fatty acids are used almost exclusively in allergy management. Diets rich in n-3 fatty acids can result in the incorporation of n-3 fatty acids into biological membranes, with a corresponding decrease in concentrations of n-6 fatty acids such as arachidonic acid. N-3 fatty acids are converted into a leukotriene B, prostaglandin E and thromboxane A that are less pro-inflammatory than the corresponding n-6 fatty acid isomers.
In this regard, the ratio of n-6 to n-3 fatty acids in the diet is important. In one study, a ratio of 5:1 to 10:1 n-6:n-3 fatty acids resulted in a decrease of the inflammatory leukotriene B4 after 6 weeks in the plasma and 12 weeks in the skin. Most diets are probably much higher in n-6 to n-3 than this ideal. For control of signs of atopy in the dog, dosing of n-3 fatty acids at 180 mg of EPA / 5 kg, used with a low-fat diet, was found to result in better control of the allergic symptoms. Fish oil supplements, to be useful in allergy management, should contain at least 90 mg EPA / capsule. The published clinical articles suggest a beneficial dose for EPA at 180 mg/ 10 lbs. Fatty acids are nutritional supplements and frequently require 6-8 weeks or more before significant clinical benefit is appreciated.
It should be noted that recently the ACVD Task force on canine atopy critically reviewed the evidence for or against the efficacy of FA in atopy and concluded that evidence is insufficient to recommend for or against their use.
Systemic glucocorticoids are often the symptomatic treatment of choice due to their low cost, rapid onset of action, and ease of administration. Glucocorticoids work at the nuclear level altering RNA and protein synthesis. Duration of action is related to potency, dose, and route of administration. Systemic effects include inhibiting phospholipase A (important in the arachidonic acid cascade and thus leukotriene and prostaglandin production), maintaining cell membrane integrity, stabilizing lysosomal membranes (steroids prevent release of preformed mediators), destroying lymphocytes (especially T cells), inhibiting antibody response, decreasing white blood cell chemotaxis and suppressing phagocytosis (impedes normal first line anti-microbial defense).
Glucocorticoids are the most effective treatment for non-complicated atopy, and also the drugs with the most serious side effects and potential for over-use. Uncomplicated atopy should be completely steroid responsive. Unfortunately, it is relatively uncommon to find an uncomplicated atopic patient and control of atopy with glucocorticoids is less than desirable in the face of secondary infection/seborrhea. The principles of use of glucocorticoids in atopy: Use as infrequently as possible, as low a dose as possible and never let the treatment be worse than the disease
Only short-acting glucocorticoids are recommended. The half-life must be shorter than the interval of dosing. Drugs that fulfill these criteria include prednisone, prednisone and methylprednisolone. Methylprednisolone has a slightly longer half- life than prednisolone and 4 mg of methylprednisolone equals 5 mg of prednisolone. This drug does not cause as much polydipsia. However, it is more expensive than prednisone or prednisolone.
Atopy patients that are to receive glucocorticoid therapy for longer than 2 weeks should be given prednisone on alternate days or less often. Dosages needed to control pruritus at the outset of therapy may be higher than the dosage needed for maintenance. Alternative day therapy does not eliminate all undesirable effects of glucocorticoids, but it does minimize adrenal suppression. It seems to be safer and more effective in small dogs than in large ones.
Clinical side effects of glucocorticoids affect every organ system. Inflammation is meant to be a protective mechanism and glucocorticoids do not differentiate the “good” from the “bad.” Infection is likely to be occult when inflammation is suppressed. Occult urinary tract infections are commonly seen in dogs on chronic glucocorticoid therapy. (45% in one study!) In addition, the most common cause of adult-onset generalized demodicosis is glucocorticoids. Other adverse effects of glucocorticoids include: polyuria, polydipsia, polyphagia; behavioral changes; iatrogenic hyperadrenocorticism; encouraging spread of infections or parasitic disease by altering skin microclimate and natural immune response (precipitates/ impedes resolution of pyoderma due to decreased neutrophil chemotaxis); gastrointestinal abnormalities; cutaneous atrophy; poor wound healing; calcinosis cutis. Glucocorticoids also interfere with performing or interpreting diagnostic tests (intradermal allergy tests, biopsies, endocrine evaluation, serum biochemical profiles) so timing their use and withdrawal is important.
The use of injectable glucocorticoids is almost never advisable in the treatment of allergy patients. With repositol forms of glucocorticoids, suppression of the pituitary adrenal axis far outlasts the anti-inflammatory duration of the drug. Some owners will report that oral medication in the dog does not work as well as injectable. Increasing the initial dose of the oral drug or changing to a different oral glucocorticoid can correct this problem.
An anti-inflammatory induction dose of prednisone/prednisolone is 1 -- 2 mg/kg/day for the dog. Use higher dosages for toy dogs and lower dosages for giant breeds. After the pruritus is controlled, the dosage is changed to an alternate day regimen and the dose is then decreased to the lowest possible level. There are a multitude of ways to decrease the dose from daily to every other day. One approach is to take the lowest daily dose that will control the symptoms and increase it by 50%. This dose is then given every other day. This dosage can then be adjusted down. The target dose for chronic maintenance therapy should be less than 0.5 mg/kg every other day. Some giant dogs will do better on a very low daily dose than on alternate day therapy. Dosages as low as 0.1 mg/kg per day can be effective in “pure” atopy. Patients on chronic maintenance therapy should be acceptably itchy, not completely itch free! Animals on chronic glucocorticoids supplementation should be monitored every three to four months with a bacterial culture and sensitivity of the urine. A CBC and chemistry panel should be evaluated once or twice yearly.
An antihistamine combined with an omega 3-containing fatty acid may result in reduced pruritus so that glucocorticoids are not needed. Antihistamines given twice a day alone or in combination with a fatty acid may allow prednisone to be given on alternate days. Temaril P (Pfizer: 5 mg trimeprazine with 2 mg prednisolone (1 tablet per 10 kg BW q24h for 3-5 days, then QOD) is a combination antihistamine/glucocorticoid that has been shown to be more effective in combination than either the antihistamine or prednisolone alone. Finally, the daily administration of an EFA may reduce the dose and frequency, it not the need for, glucocorticoids in the pruritic dog.
Phosphodiesterase (PDE) activity has been reported to be increased in dogs and people with atopic dermatitis. Increased PDE activity seems to be responsible for the deficient cAMP response in atopic people and dogs. In mast cells, macrophages, T lymphocytes eosinophils and keratinocytes, PDE-4 appears to be the predominant isoenyzme and is involved in cell activation and secretion. It plays a role in mediator release. The efficacy of an oral PDE-4 inhibitor was evaluated in 1999. The efficacy of arophylline at 1 mg/kg BID for 4 weeks was compared to prednisolone at 0.5 mg/kg BID x 7 days then SID x 7 days then EOD x 14 days. In all cases, there was progressive clinical improvement and no significant difference was noted among treatment. However, many dogs in the arophylline group experienced vomiting, diarrhea and anorexia.
Pentoxifylline (Trental®) is a phosphodiesterase inhibitor and has a number of anti-inflammatory effects: it decreases cytokine production (IL-1, IL-6, IL-12 and TNF-alpha) and the expression of adhesion cell molecules thus decreasing the accumulation of inflammatory cells at sites of allergen challenge (late phase cutaneous reaction at 4-6 hours). It may have its greatest efficacy in allergy because it is a phosphodiesterase inhibitor. Pentoxifylline suppresses contact allergy by suppression of TNF-alpha, which is considered an important mediator in delayed type hypersensitivity. To date, its use does not seem to decrease intradermal skin test reactivity. It has been tried with some success in canine atopics at 10 - 20 mg/kg TID. Side effects are rare and primarily consist of occasional vomiting. The tablets can be divided or ground and replaced into capsules by a compounding pharmacy for small dogs. The need to give TID limits usefulness, but it can be used SID when the slow-release 400 mg tablets do not need to be divided. The ACVD Task Force notes there is only fair evidence to support the recommendation of the use of pentoxifylline for treatment of canine atopic dermatitis.
Misoprostol (CytotecR ), is a PGE1 analogue. PGE elevated cyclic AMP, which in turn blocks the secretion of cytokines by Th1 cells. It also inhibits lymphocyte proliferation, granulocyte activation and synthesis of pro-inflammatory cytokines, which are thought to play a role in allergic reactions. In a study of 20 dogs misoprostol had good to excellent efficacy in diminishing the extent and or severity of cutaneous lesions in 61% of atopic dogs. It was given at 3 - 6 ug/kg orally three times daily. In most cases, misoprostol’s efficacy was seen after one week of continuous administration. Adverse side effects were observed in 33% of dogs and consisted of minor intermittent vomiting or diarrhea. In no case were the symptoms severe enough to justify discontinuation of the drug. In a second study, pruritus and skin lesions were significantly improved. This drug probably works by inhibiting the late phase reaction of the allergic response. It therefore may be more helpful to combine this drug with an antihistamine that will control the immediate phase allergic response. The Task Force on Canine Atopy notes there is fair evidence to support the recommendation of use of misoprostol for treatment of canine atopic dermatitis. The side effects incidence and the need to give TID may limit the usefulness of this drug.
Leukotrienes play an important role in inflammatory and allergic reactions. Numerous compounds with the specific property of inhibiting lipoxygenase enzymes or antagonizing leukotriene receptors have been developed in recent years. Zileuton is a 5-lipooxygenease inhibitor. It has been used for treatment of atopic dermatitis in people with good results. At oral doses ranging from 0.5 – 5 mg/kg, zileuton suppresses LTB4 synthesis in dogs. In a pilot study, zileuton used at 5 mg/kg TID decreased erythema but had no significant effect on pruritus. The ACVD Task Force on Canine Atopic Dermatitis notes at this time there is insufficient evidence to support the recommendation for or against the use of leukotriene inhibitors for treatment of canine atopic dermatitis.
Cyclosporine – Atopica (5 mg /kg q24h) is a calcineurin inhibitor with anti-pruritic and immunosuppressive properties. It binds to specific intracellular receptors in T lymphocytes and inhibits the synthesis of IL-2. It also inhibits cytokine secretion by keratinocytes. It decreases the number of Langerhans’ cells in the epidermis and inhibits the lymphocyte-activating function of these antigen-presenting cells. It inhibits skin mast cell counts, mast cell survival, mast cell secretory response after stimulation, mast cell histamine release, and prostaglandin production. It inhibits eosinophil survival, release of toxic granules, cytokine release and recruitment to the site of allergic inflammation. The anti-allergic effects of cyclosporine are similar to those of glucocorticoids.
Cyclosporine is still quite expensive but can be the drug to use in hyposensitization failures, and in dogs that have responded to no other anti-pruritic therapy. The drug should be given 2 hours before or after a meal to maximize its absorption. Unfortunately, some animals suffer gastrointestinal side effects including vomiting, loss of appetite, and diarrhea. These side effects can preclude its use in some animals, but may be overcome if the drug is given with food. Dogs do not seem to suffer either hepatic or renal toxic effects at this dose, but a base line CBC, biochemical profile, and urinalysis should be obtained before starting therapy. Cyclosporine should be given for 30 days before assessing response. If pruritus has been reduced 75% or more, many animals can be maintained on QOD or less often at an even smaller dose for maintenance therapy. Long-term use may lead to immunosuppression (secondary infections) and gingival hyperplasia and ??
Cyclosporine is metabolized by the cytochrome p450 enzyme system. Caution is in order if it is used concurrently with other drugs that are metabolized similarly. Ketoconazole is one such drug that has been used on purpose to be given concurrently with cyclosporine. In dogs who respond to cyclosporine, but whose signs return if the dose is reduced to every other day, ketoconazole can be added to the treatment to decrease cost. Five mg/kg/day given with the cyclosporine may allow the dose of cyclosporine to be cut in half or reduced to every other day or less.
Topical therapy is often used in addition to systemic anti pruritic medications. Shampoos, sprays and cream rinses can provide immediate relief of pruritus. Sometimes just cool water and a mild hypoallergenic shampoo will provide dramatic reduction is pruritus because the cleansing process has removed some of the offending substance (pollen, mold, contact irritant, etc). Antipruritic shampoos, cream rinses or sprays may contain colloidal oatmeal, pramoxine HCl, diphenhydramine HCl, hydrocortisone, dexamethasone, or triamcinolone along with moisturizers and essential fatty acids. Most shampoos only last as long as they are in contact with the skin and have little residual activity. As a group, sprays and cream rinses have a little longer course of action than shampoos because they are not rinsed off. It is often a trial and error event because individual response varies
It should be noted that an intact stratum corneum barrier is very important to the atopy patient. In fact, some theories about the pathogenesis of atopy focus on an inadequate lipid barrier against absorption of allergens as the primary problem in atopics! Also, atopic skin is over-reactive skin. Accordingly, topical therapy should be mild, non-irritating and should either not completely defat or “strip” the surface lipids or should restore the integrity of the surface lipid barrier. Shampoos should be emollient (ideally be formulated with spherulites or liposomes) or cream rinses or emollient sprays should be used in bathing atopics.
Topical antipruritic products in the formulation of gels, creams, lotions, sprays and ointments will be helpful in patients with localized areas of pruritus. In selecting a product for topical therapy, one must consider the vehicle the drug is combined with. For acute eruptions, the non-occlusive, non-irritating lotion, spray or gel form should be used, whereas creams and ointments are best used in chronic lesions. Ear products with glucocorticoids can be used on the skin.
Tacrolimus is another macrolide lactone that exhibits similar activity to cyclosporine A. It is proving very useful as a topical in human atopic dermatitis and has been studied in dogs, albeit at low application rates. It can be used to treat focal pruritic atopic dermatitis in the form of 0.1% ointment (Protopic), applied SID – BID. It is expensive however. A 30 gm tube costs approximately $60.
Is there failure to respond to appropriate therapy? First, reassess your diagnosis!
Has there been a change in the treatment protocol? Are the medications being used as prescribed?
Has a secondary infection developed (yeast or bacterial)?
Has the nature of the allergy changed (Food + fleas + ragweed season.)?
Has the patient developed a tolerance to the drug (Antihistamine/Steroid tachyphylaxis)?
Allergy is not curable at present. Our goal in allergy management is finding the safest, least expensive, least troublesome regimen for each allergy patient/owner. Combinations of many of the treatment options discussed are almost always needed for safe control of the signs of atopy. Only by trial and error with an individual patient, will the optimum therapy be formulated. THIS DOES NOT HAPPEN OVERNIGHT AND IS NOT BORN FROM ONE VISIT!!! Time and patience is the key.
Fatty Acids Many report that fatty acid therapy is more rewarding in feline allergy than it is in the dog, although no controlled trials have supported these observations. Dose recommendations for GLA/EPA are 500 mg daily.
Antihistamines There are no well-controlled trials. Again, more reported efficacy for the cat than the dog is the rule. Most consider chlorpheniramine (2 - 4 mg QD or BID) to be most effective. Others prefer clemastine, 0.34 - 0.68 mg daily. Cyproheptadine, 2 mg daily or BID, and hydroxyzine, 0.5 mg/kg BID are recommended, but are less satisfactory owing to behavior changes and excitability being frequent side effects.
Behavior Modification: Amitriptyline, 5 - 10 mg daily, fluoxetine 1 mg/kg QD, haloperidol, 1 -2 mg daily are used to control symptoms, especially in self-inflicted alopecia.
Glucocorticoids: Cats suffer fewer apparent side effects from chronic glucocorticoid usage and these drugs are used more commonly as the total management program in feline allergy. Methylprednisolone acetate is given 4 - 5 mg/ kg IM. This is used in cats with 1 -2 episodes of pruritus yearly or those that cannot be pilled. Prednisolone and prednisone are given 2 - 4 mg/kg BID then tapered to 5 mg q 48 hrs. Methylprednisolone oral is used at 80%of this dosage. Triamcinolone tablets are given .3 B .75 mg /kg QD, tapered to q 48 - 72 hrs. Dexamethasone phosphate IV injectable can be given orally at 0.1 0.2 mg/kg QD, tapered to .025 -- 1 mg q 48 -- 72 hours.
Side effects of chronic glucocorticoid usage in the cat include obesity, diabetes mellitus, alopecia, skin fragility and predisposition to infection.
Diphenhydramine (Ethanolamine) 2-4 mg/kg TID
Clemastine (Ethanolamine) 0.05-1 mg/kg BID
Dimenhydrinate (Ethanolamine) 8 mg/kg TID
Pyrilamine (Ethylenediamine) 1-2 mg/kg BID
Tripelennamine (Ethylenediamine) 1-1.5 mg/kg BID
Chlorpheniramine (Alkylamine) 0.2-0.8 mg/kg TID
Cetirizine 2.2 mg/kg BID
Brompheniramine (Alkylamine) 0.5 mg/kg B-TID
Hydroxyzine (Piperazine) 2-3 mg/kg TID
Promethazine (Phenothiazine) 0.2-1 mg/kg B-TID
Trimeprazine (Phenothiazine) 0.5-2 mg/kg B-TID
Cyproheptadine (Piperidine) 0.1-0.5 mg/kg BID
Azatadine (Piperidine) 1-2 mg/kg BID
Loratadine (Misc) .5 -1 mg/kg QD
Astemizole (Misc) 0.25-1 mg/kg QD
Terfenadine (Misc) 4-10 mg/kg BID
Doxepin (Not an antihist.) 1-2 mg/kg BID
Amitriptyline (Not an antihist.) 1-2 mg/kg Q-TID
Fluoxetine (Not an antihist.) 1 mg/kg Q
Dcyclosporine A 2-5 mg/kg QD or BID