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Hair follicle infundibula have a similar lymphocytic interface and mural folliculitis [ 8 ]. Pigment dispersal to dermal macrophages pigmentary incontinence is often not a feature or is very mild, likely due to breed coat coloration and the tendency for lesions to occur in poorly- or non-pigmented skin.
The thickening of the basement membrane zone and superficial dermal fibrosis are uncommon, which is attributable to the subacute nature of the disease, but they can occur in persistent lesions Fig. Cell-rich lesions dominate biopsies but very mild lymphocytic dermal infiltrates or even cell-poor areas of lesions can occur that lack a subepidermal, band-like lichenoid , dermal infiltrate of lymphocytes Fig.
Cell-poor areas of lesions can lead to confusion with juvenile dermatomyositis, which is seen often in the same breeds [ 8 ]. Dermatomyositis presents with lesions of ischemic dermatopathy i. If the intrabasal level of epidermal clefts is not recognized Fig. Occasionally superficial epidermal apoptosis with lymphocytic satellitosis might erroneously suggest the diagnosis of erythema multiforme and its morphologically related conditions [ 29 ].
Neutrophilic inflammation is common in lesions that progress to ulcers and support the development of secondary bacterial infection. Histopathology of canine vesicular cutaneous lupus erythematosus. Marked basal keratinocyte apoptosis has caused a secondary cleft vesiculation through the epidermal basal cell layer, which is typical of the disease.
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In one of the two largest case series [ 22 ], detailed information on mononuclear cell immunophenotyping was reported. T-lymphocytes expressing CD3 were found in epidermal sections of all 11 dogs examined. The other epithelial leukocytes were identified as CD1-positive Langerhans cells. In the superficial dermis, infiltrating cells consisted of an approximately equal population of alpha-beta T-lymphocytes expressing CD4 or CD8-alpha and CD1-positive dermal dendritic cells. Rare CDpositive B-lymphocytes were detected in the superficial dermis. In contrast, gamma-delta T-cells were not identified in either the epidermis or dermis.
Basal keratinocytes expressed high levels of ICAM-1 and low levels of class II major histocompatibility complex molecules signifying their activated state. Indirect immunofluorescence did not reveal anti-basement membrane circulating IgG autoantibodies in the serum of five dogs with VCLE [ 22 ]. Similarly circulating antinuclear IgG autoantibodies were not detected in the serum of any of 11 dogs with VCLE using human Hep2 cells as a substrate [ 22 ].
The first case series provided detailed information on the post-treatment outcome in 11 dogs with VCLE [ 23 ]. Lesions have also been shown to respond to the immunosuppressant mycophenolate mofetil in one rough collie with VCLE, as the introduction of this drug led to the complete remission of skin lesions after the discontinuation of oral glucocorticoids [ 27 ]. More recently, the benefit of calcineurin inhibitors, which had been previously reported in two dogs with VCLE [ 24 , 26 ], was confirmed in 11 additional patients [ 28 ]. In all dogs, treatment was initiated with sun avoidance, oral glucocorticoids and oral ciclosporin at a median dosage of 5.
While relapses of clinical signs were common when the dosage of ciclosporin was lowered, the long-term remission of signs was possible with calcineurin inhibitors, either alone or in combination.
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These observations suggest that calcineurin inhibitors might be the drug category of choice to treat canine VCLE. One brief case report [ 31 ], one series of five cases [ 32 ] and a book chapter [ 33 ] constituted the early descriptions of this rare disease.
In , we reviewed the histopathological and immunological characteristics of eight dogs with this disease, and proposed the name exfoliative cutaneous lupus erythematosus ECLE [ 7 ]. Clinical, histopathological and immunological data from 25 dogs with ECLE were later collated and described in more detail [ 34 ]. At this time, there is insufficient information on canine ECLE to appropriately assess the incidence and prevalence of this disease in dogs.
It appears to have a worldwide distribution.
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A large pedigree analysis of purebred GSHPs and experimental mating studies established that this disease was transmitted on an autosomal recessive manner [ 35 ]. A single nucleotide polymorphism on the CFA 18 chromosome was found to perfectly segregate with the trait in dogs [ 35 ]. Interestingly, ECLE has been diagnosed also in several Magyar viszlas living in western Europe [ 36 , 37 ]; this observation is noteworthy, as viszlas share a common ancestry with GSHPs [ 37 ]. Adding the cases from the largest case series [ 34 ] to those of the genome-wide association study [ 35 ] yielded 45 GSHPs already reported with ECLE: there were 26 females and 19 males with a female-to-male ratio of 1.
Follicular casts were noted in one third of patients Fig. Recently seen GSHPs with ECLE were found to also exhibit irregular and polycyclic patches and plaques with dyspigmentation and some scarring personal observations; Fig. In this form of canine CCLE, skin lesions typically affect the muzzle, pinnae and dorsal trunk and then progress to involve the limbs, sternum and ventral abdomen. Generalized skin lesions are found in most dogs, while crusting, with or without an underlying ulceration, was recorded in one fourth of patients in the largest series of GSHPs [ 34 ].
In one dog of that report, ulcers were so extensive that they resulted in bacterial septicemia. Clinical characteristics of canine exfoliative cutaneous lupus erythematosus in German shorthaired pointers. This observation, as well as the presence of typical histological changes of CLE in these dogs, raises the suspicion that some of the viszlas reported with sebaceous adenitis might have had, in fact, ECLE.
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Clinical characteristics of canine exfoliative cutaneous lupus erythematosus in Magyar viszlas. A generalized peripheral lymphadenomegaly was reported in one-third of GSHPs with ECLE [ 34 ]; lymph node enlargement was also described in other reports [ 31 , 32 , 38 ]. Many GSHPs with ECLE eventually develop signs suggestive of arthralgia, which manifests as a stiff gait, lameness or an arched back [ 34 , 38 , 39 ] In one report, all six dogs were infertile, with azoospermia and irregular or arrested cycles in females [ 38 ].
While rare GSHPs with ECLE have mild anemia, fluctuating thrombocytopenia is seen more commonly in these dogs [ 34 , 38 ]; serum biochemistry and urinalysis usually do not exhibit consistent changes, except for hyperglobulinemia seen occasionally [ 34 , 38 ]. Fine needle aspirate material from enlarged peripheral lymph nodes was submitted for cytological evaluation in one GSHP with lymphadenomegaly, and it revealed lymphoid hyperplasia.
Spinal radiographs, myelogram and cerebrospinal fluid analysis and stifle and hock joint aspirates were performed in dogs suffering from intermittent arthralgia, but they failed to identify any underlying abnormality [ 34 ]. The largest compilation of dogs with ECLE confirms previous information regarding the histopathology of this disease [ 34 ].
In this study, microscopic examination revealed a cell-rich interface dermatitis Fig. Typical of cell-rich interface lesions, the apoptosis of basal keratinocytes was accompanied by moderate to marked lymphocytic exocytosis in the lower epidermis Fig.
Cutaneous lupus erythematosus: new insights into pathogenesis and therapeutic strategies
In addition, biopsies of most dogs had mild lymphocytic exocytosis and keratinocyte apoptosis in the upper epidermis. Diffuse orthokeratotic hyperkeratosis was a notable feature of most biopsies and was usually moderate Fig. Histopathology of canine exfoliative cutaneous lupus erythematosus. Sebaceous glands are absent in this biopsy, as is reported in some cases. Telogen hair follicles can also be affected not shown.
Cutaneous Lupus Erythematosus | Dermatology | JAMA Dermatology | JAMA Network
Sebaceous glands were also affected. These latter features can lead to confusion with primary sebaceous adenitis. In addition, anti-sebaceous gland IgG antibodies were also detected in these dogs. Circulating anti-epidermal basement membrane antibodies were not observed, however. Immunohistochemical staining confirmed the predominance of CD3-bearing T lymphocytes in the lower epidermis, superficial dermis, in the infundibulum of hair follicles and around sweat glands [ 34 ].
These CD3-positive T lymphocytes infiltrated sebaceous glands and their associated ducts in samples collected from two dogs. The review of published reports has yielded inconsistent information on the treatment and outcome of this disease. Hydroxychloroquine, an first-line antimalarial drug used in human CCLE, appeared to slow down the clinical progression in some dogs with ECLE; in contrast, high-dose ciclosporin reportedly was not able to halt lesion worsening [ 38 ]. As the response to immunomodulators is heterogeneous in human CCLE variants [ 40 ], the use of high-dose oral glucocorticoids and adjunctive immunosuppressive regimens need to be investigated on an individual patient basis [ 34 , 38 , 39 ].
Taking into account all GSHPs with ECLE for which a long-term outcome has been reported [ 31 , 32 , 34 , 38 , 39 ], over half of dogs are eventually euthanized for their lack of disease response to therapy. Collating the signalment of all published cases of canine MCLE yielded pertinent information. Altogether, females appear nearly twice over-represented with a female-to-male ratio of 1. Odds ratios for breed, sex or age predispositions for the development of MCLE cannot be estimated, as dogs come from multiple continents North and South America, Japan, Europe , and a reference population therefore is not available.
The owners of dogs with MCLE often report perimucosal ulcerative skin lesions with vocalization suggesting pain why defecating or urinating. In the largest case series, most dogs had two or more areas affected, and the lesions were usually symmetrically distributed [ 9 ]. Clinical characteristics of canine mucocutaneous lupus erythematosus. Crusts are present when lesions extend into haired skin. Hyperpigmentation can be seen often around ulcerative lesions or at the site of previous ones, thus leaving a figurate or reticulated pattern [ 9 , 41 , 42 , 43 , 44 , 45 , 46 ].
Pruritus is normally absent or mild, but pain is described when defecating and urinating or when touching the lesions; systemic signs have not been reported [ 9 , 41 , 42 , 43 , 44 , 45 , 46 ]. In the largest case series, and per inclusion criteria, skin biopsies contained a cell-rich lymphocytic interface dermatitis with basal keratinocyte damage i.
This pattern was often patchy, or in limited areas, sometimes only being observed at close proximity to an ulcer margin. Interface dermatitis commonly extended to the infundibula of hair follicles Fig. Basement membrane thickening was found to be multifocal, patchy to diffuse Fig. Pigmentary incontinence varied from mild to marked. Plasma cells were present in all cases Fig. Erosions and ulcers were common but granulation tissue was limited and fibrosis scarring was not seen. Occasional suprabasal keratinocyte apoptosis was noted in half of the cases, but suprabasal lymphocytic satellitosis, when present, was always mild.
Not surprisingly, for a perimucosal ulcerative disease, lesions of concurrent bacterial infection were common, including neutrophilic crusting, pustules, perifolliculitis and folliculitis, as well as presence of bacteria in surface exudates. Such infection will complicate the histological diagnosis and the successful treatment of pyoderma is warranted prior to biopsy. Histopathology of canine mucocutaneous lupus erythematosus. Positive ANA titers were rarely found, however.
Acute Cutaneous Lupus
The skin lesions of canine MCLE appear to respond best to immunosuppressive dosages of oral glucocorticoids [ 9 , 41 , 42 , 43 , 44 , 45 , 46 ]. The complete remission of signs is generally obtained within one month of treatment induction [ 9 ]. A combination of a tetracycline antibiotic, with or without niacinamide, appears beneficial either alone or as adjunctive combination in some dogs [ 9 , 41 , 45 ].
In most patients, the tapering of oral glucocorticoids leads to the prompt relapse of skin lesions, which will undergo remission once the dosage is re-escalated again. The usefulness of adding additional immunosuppressive drugs e. Among the several variants of human chronic CLE e. In , Griffin and colleagues reported clinical, histopathological and immunological characteristics of two dogs with localized facial lesions that were diagnosed as being affected with the canine counterpart of human DLE [ 1 ]. In these two dogs, the nasal-predominant dermatitis was associated with microscopic focal interface dermatitis, basement membrane thickening and a superficial lymphocytic and plasmacytic dermatitis.
Since then, there were three large case series describing dogs with nasal skin-predominant DLE lesions [ 2 , 3 , 4 ], two of them including some of the same cases [ 2 , 4 ].