recurrent flank alopecia in a tibetan terrier

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 de

Flandres, 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.

ClinicalClinicalClinicalClinical

276 Australian Veterinary Journal Volume 83, No 5, May 2005

CASE REPORT

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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-


277Australian Veterinary Journal Volume 83, No 5, May 2005

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 Figure 2. Thedarker coat colour of regrown hair is more obvious in this view -note the lighter original colour of the coat more cranially.

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been reported to occur in the Tibetan Terrier. Careful considera-tion was given to possible influences of prednisolone on hairgrowth. During the second year, the dog was on steroidal anti-pruritic therapy (prednisolone at 0.1 to 0.2mg/kg per week) buthair regrew during this time. This dose of prednisolone continuedin the following months into mid-winter when the third episodeof alopecia occurred in the same region. A trichogram at this timerevealed anagen hairs on the head region and on histologicalexamination there were anagen bulbs. Based on this apparent lackof effect of prednisolone on hair growth in this case, and absenceof corticosteroid changes histologically (that is, atrophic epithe-lium, sebaceous gland atrophy),10,11 it was concluded that thealopecia developed independent of prednisolone therapy.

During the first episode of alopecia, cyclosporin was given andthe alopecia resolved soon after cessation of this therapy.Consideration was given to possible effects of cyclosporin on hairgrowth, as hirsutism has been noted as a side effect of cyclosporinin dogs.24 However, as hair regrew after cessation of cyclosporin,it was suspected that growth of hair was independent ofcyclosporin.

Melatonin was given for a 6-week period after diagnosis of RFA(late winter), however, there was no noticeable hair growth. Haircompletely regrew by the end of summer. Melatonin has beenused experimentally to stimulate hair growth in RFA, caninepattern baldness, alopecia X and follicular dysplasias.2 7 In thiscase, melatonin failed to induce hair growth, which has beenpreviously reported.2 Early studies have considered melatonin tobe successful as a prevention of the onset of alopecia in dogs withRFA, if given in the 2 months prior to the usual onset ofalopecia.7

During the winter months, dogs may be exposed to an artificiallyextended photoperiod which may be the stimulus for prolactinsecretion and inhibition of melatonin secretion, and for thisreason melatonin has been used to stimulate hair growth.4 Therecommended dose is 3 to 6mg every 8 to 12 hours for a 4 to 6week period.1,2,4,7 Side effects recorded in humans includehypotension, sleep disorders and abdominal pain.2 Althoughthese side effects have not been reported in the dog, it should benoted that melatonin can alter sex hormones levels, and thereforeshould be avoided in breeding dogs.25 In this case, as melatoninwas only given after alopecia occurred, it could not have inducedalopecia via any alteration of adrenal sex hormones.

ConclusionRFA has not been previously reported to occur in the TibetanTerrier. This case describes a Tibetan Terrier with atopicdermatitis diagnosed with concurrent RFA that demonstratedspontaneous hair regrowth.

References1. Scott DW, Miller Jr, WH, Griffin CE. Muller and Kirk’s Small AnimalDermatology. 6th edn, Saunders, Philadelphia, 2001;890-893.2. Rees CA. New drugs in veterinary dermatology. Vet Clin N Am: Small AnimPract 1999;29:1449-1460.3. Daminet S, Paradis M. Evaluation of thyroid function in dogs suffering fromrecurrent flank alopecia. Can Vet J 2000;41:699-703.4. Paradis M. Melatonin therapy for canine alopecia. In: Bonagura JD. Kirk’sCurrent Veterinary Therapy XIII, Saunders, Philadelphia, 2000:546-549.5. Curtis CH, Evans H, Lloyd DH. Investigation of the reproductive and growthhormone status by idiopathic recurrent flank alopecia. J Small Anim Pract1996;37:417-422.6. Miller MA, Dunstan RW. Seasonal flank alopecia in Boxers and AiredaleTerriers: 24 cases (1985-1992). J Am Vet Med Assoc 1993;203:1567.7. Paradis M. Melatonin in Canine Alopecia: Fourth World Congress of Veterinary

tion, apparent spontaneous resolution and histopathologicalchanges. The anagen bulbs present in this case probably reflectedthe timing of the biopsy when hair was beginning to regrow. Thedermal inflammatory changes were consistent with atopicdermatitis.10, 11 The histopathology and recurrent nature of thedisease ruled out any other causes of alopecia, such as adrenal sexhormone alopecia, alopecia X and alopecia areata.

In this case of RFA, the clinical presentation was initiallymisleading due to the inflammatory alopecia and self-trauma in adog with atopic dermatitis. In addition, RFA had not previously


278 Australian Veterinary Journal Volume 83, No 5, May 2005

Figure 4. Histological section of cross section of a follicle, showingtelogen follicles, follicular hyperkeratosis, normal adnexal glandsfeatures that are all consistent with RFA. Haematoxylin & eosin,x100.

Figure 5. A closer view of a cross section of a follicle in Figure 4.There is pigment clumping in the follicular lumen, a feature consis-tent of RFA. Haematoxylin & eosin, x400.


Dermatology: Clinical Program Proceedings, San Francisco, California, 2000:52-59.8. Waldman L. Seasonal flank alopecia in Affenpinschers. J Small Anim Pract1995;36:272-273.9. Scott DW. Seasonal flank alopecia in ovariohysterectomized dogs. Cornell Vet1990;80:187-195.10. Gross TL, Ihrke PJ, Walder EJ. Veterinary dermatopathology: A macroscopicand microscopic evaluation of canine and feline skin disease. Mosby Year Book,St Louis, 1992:302-306.11. Yager JA, Wilcock BP. Colour atlas and text of surgical pathology of the dogand cat. Wolfe Publishing/Mosby Year Book Europe Ltd, London, 1994:228.12. Rothstein E, Scott DW, Miller WH Jr, Bagladi MS. A retrospective study ofdysplastic hair follicles and abnormal melanisation in dogs with follicular dysplasiasyndromes or endocrine skin disease. Vet Dermatol 1998;9:235-241.13. Bagladi MS, Scott DW, Miller WH Jr. Sebaceous gland melanosis in dogs withendocrine skin disease or follicular dysplasia: a retrospective study. Vet Dermatol1996;7:85-90.14. Duncan MJ, Goldman BD. Hormonal regulation of the annual pelage colorcycle in the Djungarian hamster, Phodopus sungorus. II. Role of prolactin. J ExpZool 1984;230: 97-103.15. Stankov, B, Moller B, Lucini V, Capsoni S, Fraschini F. A carnivore species(Canis familiaris) expresses circadian rhythm in peripheral blood and melatoninreceptors in the brain. Eur J Endocrinol 1994; 131:191-200.16. Allain D, Ravault JP, Panaretto BA, Rougeot J. Effects of pinealectomy onphotoperiodic control of hair follicle activity in the Limousine ram: possible relation-ships with plasma prolactin levels. J Pineal Res 1986;3: 25-32.

17. Badura LL, Goldman BD. Prolactin-dependent seasonal changes in pelage:role of the pineal gland and dopamine. J Exp Zool 1992;261: 27-33.18. Badura LL, Goldman BD. Anterior pituitary release of prolactin is inhibited byexposure to short photoperiod. J Neuroendocrinol 1997;9: 341-345.19. Smale L, Lee TM, Nelson RJ, Zucker I. Prolactin counteracts effects of shortday lengths on pelage growth in the meadow vole, Microtus pennsylvanicus. J ExpZool 1990;253:186-188.20. Smith AJ, Mondain-Monval M, Simon P et al. Preliminary studies of the effectsof bromocriptine on testicular regression and the spring moult in a seasonalbreeder, the male blue fox (Alopex lagopus). J Reprod Fertil 1987;81:517-524. 21. Thompson DL Jr, Hoffman R, DePew CL. Prolactin administration to season-ally anestrous mares: Reproductive, metabolic and hair-shedding responses. JAnim Sci 1997;75:1092-1099.22. Craven AJ, Ormandy CJ, Robertson FG et al. Prolactin signaling influencesthe timing mechanism of the hair follicle: Analysis of hair growth cycles in prolactinreceptor knockout mice. Endocrinology 2001;142: 2533-2539.23. Carter AW, Thoday KL, Hill PB et al. Failure to detect melatonin receptors incanine skin. Proceedings of the 17th ESVD-ECVD Congress in VeterinaryDermatology, Copenhagen, Denmark 2001:180.24. Mouatt JG. Cyclosporin and ketoconazole interaction for the treatment of peri-anal fistulas in the dog. Aust Vet J 2002;80: 207-211.25. Ashley PF, Frank LA, Schmeitzel LP, Bailey EM, Oliver JW. Effect of oralmelatonin administration on sex hormone, prolactin and thyroid hormone concen-trations in adult dogs. J Am Vet Med Assoc 1999;215: 1111-1115.

(Accepted for publication 6 August 2003)


279Australian Veterinary Journal Volume 83, No 5, May 2005

Handbook of Veterinary Neurology, 4th edn. Lorenz MD and Kornegay JN. Elsevier Saunders, Marrickville, 2004, 468 pages. Price$117.70. ISBN 0 7216 8986 8.

This textbook is an updated version of a tried and tested neurology text that is written for veterinary practitioners and students. It is organ-ised into two parts. The first part is called ‘Fundamentals’ and includes chapters on taking a history and performing a neurological exam-

ination, neurolocalisation, micturition including micturition disorders, and diagnostic tests. The second part is based on presenting problemsand includes eleven chapters on different problems. These problem oriented chapters start with a discussion of lesion localisation followedby a description of relevant diseases in terms of pathogenesis, clinical signs, diagnosis and treatment. There is a useful appendix of speciesand breed specific diseases at the end of the book.

This book has several strengths. Firstly, it covers both large and small animal clinical neurology, and therefore has wide appeal. The problemspecific chapters in the second part of the book make it easy for veterinarians to research presenting problems, and the inclusion of algo-rithms, tables and appendices make it a very useful reference text. The book has been indexed well and so searching for a disease whenunsure which chapter it would be described in does not pose a problem. The logical flow of the entire book enables veterinary students tolearn about neurology as a specialty. The learning experience is enhanced by clear figures of relevant neuroanatomy and the inclusion ofcase studies at the end of each chapter. These cases are well thought out to illustrate the points discussed in each chapter and are veryuseful to anyone wanting to test their knowledge of neurology.

Updating this excellent book is a difficult task, and this version is not that different from the two previous versions. Although some newlydescribed diseases have been included, there are relatively important diseases that have been omitted. For example, there is no mention ofWest Nile virus causing encephalitis in horses. As this virus is an important human pathogen that has recently spread across the UnitedStates of America, this particular omission is surprising. Another example of a disease that has come to the forefront of veterinary neurologybut has not made it into this book is the Chiari-like malformation in Cavalier King Charles Spaniels. The information on common diseaseshas also not been updated as much as might be expected. For example, there is a large body of new literature on the treatment andoutcome of acute intervertebral disc herniations that has not been included. Similarly, the chapter on seizures is not up to date with respectto terminology, breeds of dog that have proven primary (inherited) epilepsy and antiepileptic drugs. Although little more is known about thepathogenesis of degenerative myelopathy in German Shepherd dogs, there have been several new publications that have evaluated avariety of proposed causes that were not mentioned. Finally, chapter 4 (Confirming a Diagnosis) does not yet reflect the revolution that hasoccurred with the advent of accessible magnetic resonance imaging (MRI). More space should be dedicated to the description of MRI andobsolete diagnostic tests such as ventriculography, cavernous sinus venography and intracranial thecography could be removed.

Veterinarians and veterinary students have been using this book since 1983 and it continues to be an extremely useful, clear, informativeand instructive text. This version has been updated to include some of the more recently diagnosed diseases, but it is not radically differentfrom the previous versions and is not, in this reviewer’s opinion, completely up to date. It therefore probably does not merit replacing the thirdversion with this fourth version. However, it is very competitive when compared with other neurology text books available, and can berecommended as a clearly written, well-illustrated textbook that provides excellent instruction in large and small animal neurology.

N Olby

Dr Olby is an assistant professor of neurology and neurosurgery at North Carolina State University College of Veterinary Medicine. She recently co-edited thethird edition of the BSAVA Manual of Canine and Feline Neurology.

BOOK REVIEW


recurrent flank alopecia in a tibetan terrier

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