Recurrent flank alopecia in a Tibetan terrier
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Recurrent flank alopecia in a Tibetan terrier
RJ BASSETT, GG BURTON and DC ROBSONMelbourne Veterinary Referral Centre, Glen Waverley, Victoria, 3150
Recurrent flank alopecia is described in a 2-year-old, male,neutered Tibetan Terrier with concurrent atopic dermatitis. Thediagnosis of recurrent flank alopecia was made after 3 consecu-tive years of localised, winter-onset alopecia. The diagnosis wasbased on history, compatible clinical signs and supportivehistopathology. The diagnosis was complicated by the presenceof concurrent pruritic dermatitis. To our knowledge this is thefirst report of recurrent flank alopecia in this breed.Aust Vet J 2005;83:276-279
ASIT Allergen specific immunotherapyRFA Recurrent flank alopeciaRR Reference rangeT4 ThyroxineTSH Thyroid stimulating hormone
RFA has been reported to occur in Airedales, Boxers,Bulldogs, Miniature Poodles, Miniature Schnauzers,Scottish Terriers, Doberman Pinschers, Bouvier deFlandres, Staffordshire Bull Terriers, French Bulldogs andAffenpinschers.1 The onset of alopecia occurs mostly between lateautumn and early spring and hair usually regrows spontaneouslywithin 3 to 4 months, but may take up to 14 months.1-4 Thealopecia may be bilateral or unilateral and can occur over thethoracolumbar and/or flank regions in irregular patterns.1,3-8 Thesize of the area affected can be quite variable. The affected skin isnot inflamed in the absence of secondary bacterial folliculitis. Theregrown hair may show colour and/or textural changes whencompared to the original hair coat.7,4,9 About 20% of dogs willexperience only one episode of alopecia while others show inter-mittent yearly recurrence.3,4,7 The alopecia does not necessarilyoccur in the same location each time.1
There are histopathological similarities between RFA and follic-ular dysplasia and therefore it is considered to be a localised formof follicular dysplasia.10 Typically there is follicular hyperkeratosisin follicles that are almost exclusively in telogen, however, inregressing lesions anagen follicles are present.11 Hair follicles canbe distorted and narrowed resembling a malformed foot or jelly-fish.6,10,12 Follicle walls may be undulating and the outer rootsheath, follicular lumen and sebaceous ducts usually containpigment clumps, although the degree of pigmentation variesbetween breeds.6,11,13 None of these changes alone is pathogno-monic for RFA.11-13
The aetiology and pathogenesis of this disease have not yet beenelucidated. In previous studies it has been found that dogssuffering from RFA are euthyroid, do not have hyperadrenocorti-cism and the reproductive and growth hormone status do notappear to be involved.3,5,6,9,14 Contributions of otherendocrinopathies have not yet been investigated, however, the
seasonal nature of the disease during the winter months suggeststhat photoperiod may play a role in the pathogenesis.5
Melatonin, produced in the pineal gland, is a messenger of lightdependent periodicity and acts at the level of the pars tuberalis ofthe pituitary. Decreased retinal day-length exposure results inincreased melatonin production and has an inhibitory effect onprolactin.15 There have been many studies to show involvementof prolactin in seasonal hair loss in mammals including the mink,cashmere goats, red deer, Siberian hamsters, Djungarian hamsters,blue foxes, meadow voles, sheep and horses.16-21 Although studiesinto the hormonal regulation of hair growth in non-seasonalspecies have not been extensive, a single study showed thatprolactin is involved in hair growth in the mouse, a non-seasonalspecies.22 To date there have been no extensive investigations intothe regulation of hair growth cyclicity in dogs with RFA.
Melatonin has been used in an attempt to stimulate hair growthin dogs with RFA.7 The efficacy of oral melatonin for treatmentof RFA is difficult to evaluate as there can be spontaneous hairregrowth.1,3,4 The exact mechanism of action of melatonin is notknown. In a study performed by Carter et al, no melatonin recep-tors were identified in the canine skin and it was suggested thatthe effect on hair growth may be via mechanisms other thandirect action on hair follicles.23 It may have effects within centralnervous system to alter secretion of melatonin stimulatinghormone or prolactin or both.2
Case reportA 2-year-old neutered male Tibetan Terrier was presented in thesecond month of spring with generalised pruritus, otitis externaand a 4-month history of localised dorsolumbar alopecia with aninflammatory bacterial folliculitis. A free T4 (8.4 pmol/L, RR 5.5to 25 by chemiluminescence) and endogenous TSH (< 0.03ng/mL, RR < 0.50) were performed by the referring veterinarianand found to be within the normal reference range.
First year of presentationAt presentation a thorough clinical examination was performedand there were no clinical signs to suggest underlying hypera-drenocorticism. A trichogram from the alopecic region revealedfractured hairs with both anagen and telogen bulbs. The dog wastreated with cephalexin (22 mg/kg twice daily) and ketoconazole(5 mg/kg once daily) on the basis of cytological examination oflesions. This produced a reduction of pruritus and new hairgrowth. Food hypersensitivity was ruled out with a food elimina-tion diet performed for 6 weeks with a novel protein and carbohy-drate source, and a diagnosis of atopic dermatitis was made.Intradermal skin testing showed positive reactions and ASITcommenced 9 weeks after presentation. Six weeks of cyclosporinwas prescribed at 5 mg/kg daily for symptomatic control ofpruritus. Complete hair regrowth was not observed until after thecessation of cyclosporin at the end of the first month of summer.
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Second year after presentationThe following year in the second month of winter, a small patchof non-inflammatory alopecia developed on the right cranialdorsolumbar area, in the same site as the previous year. This timethe dog had been on ASIT for 6 months and pruritus was inter-mittently high, but manageable, on non-steroidal symptomatictherapy without cyclosporin. The alopecic area enlarged slightlyover the ensuing 9 weeks. A trichogram revealed anagen hairbulbs and broken hair shafts and the alopecic area was consideredto be due to self-trauma. No further investigation of the alopeciawas performed. Over a 4-week period during the second monthof summer, the dog was given prednisolone for management ofpruritus that gradually tapered from 0.5 mg/kg daily to 0.1 mg/kgevery 2 to 3 days. By this time all hair had regrown.
Third year after presentationBy the first month of winter, there was a recurrence of a smallnon-inflammatory, hyperpigmented, alopecic patch that haddeveloped on the right caudal dorsolumbar region. At this time,the dog had been on ASIT for 19 months. Pruritus was minimaland intermittent, but controlled with 0.1 to 0.2 mg/kg pred-nisolone every second day, but occasionally every day. Atrichogram from the alopecic region revealed all telogen hairswith tapering tips, in contrast to a trichogram taken from anormal haired region revealing anagen hair bulbs. Hair that hadregrown in the previously affected area was of a darker colour incomparison to the hair colour prior to any onset of alopecia(Figures 1 and 3). A biopsy was recommended at this stage as itwas noted that the alopecia had recurred for 3 consecutive years inthis region, but was declined by the owner. Prednisolone was thenreduced to 0.2 mg/kg twice weekly and within the followingmonth, the alopecia progressed to involve both flanks anddorsolumbar area, extending cranially to the thoracolumbarregion. By the end of winter prednisolone had been stopped,there was minimal hair growth and approval for biopsy was given.
Histopathological examination, performed by one of the authors(GB), of biopsies from the areas of new hair growth and theperiphery of the lesion revealed a minimal perivascular masto-cytic, lymphocytic superficial dermatitis, and mild lymphocyticexocytosis, with mild follicular hyperkeratosis. Some follicles inthe periphery of the lesion showed mild undulation in the folliclewall. Anagen hair bulbs were present and adnexal glands showed nopathological changes (Figure 4).
In the biopsy sections from the alopecic area, the mainhistopathological change was marked follicular hyperkeratosis, allfollicles were in telogen, a few follicles were empty and showedluminal pigment clumping (Figure 5), mild undulating folliclewalls, moderate perifollicular fibrosis and several Civatte bodies inthe follicular walls. Adnexal glands were normal.
Recurrent flank alopecia was diagnosed as a cause for the recur-rent alopecic region, on the basis of these histopathologicalchanges and the recurrent nature of the disease. Treatment withoral melatonin was commenced at the end of winter at 3 mg twicedaily for 6 weeks, but had minimal effect on hair growth. Haircontinued to grow during late summer, without any melatonintherapy, and had almost completely regrown by the end ofsummer (Figure 2). The atopic dermatitis remained controlled onASIT.
DiscussionThe diagnosis of RFA in this case was based on seasonally recur-rent regional alopecia in the lumbar region with hyperpigmenta-
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Figure 1. Third year of recurrent flank alopecia in a Tibetan Terrier(now 3-years-old). Note the different colour of regrown haircompared to the original coat colour on the legs and neck.
Figure 2. Hair almost completely regrown, spontaneously in thethird year, 7 months after onset of alopecia (in the first month ofwinter).
Figure 3. Dorsal view of the same dog and time as in F