Pigmentary Incontinence Research Articles

Idiopathic eruptive macular pigmentation

A 23-year-old, dark-skinned man presented at the dermatology department with pigmented macules over the trunk and proximal thighs of 2 months’ duration. He reported that the number of lesions had increased progressively for a few weeks and then remained stable. Skin examination showed oval brown macules and patches, 5–40 mm in diameter, involving mainly the anterior trunk and proximal thigh, but also the neck and dorsum (Fig. 1). The lesions were asymptomatic. There was no previous history of an inflammatory process, erythema, scaling, or drug intake. The mucous membranes, palms, and soles were clear. The pigmentation was not influenced by sunlight. Darier's sign (urticaria or erythema around the macules after scratching or rubbing of the lesions) was absent. The previous use of emollients, keratolytics, and topical antifungal agents did not alter the aspect of the lesions. The results of physical examination and routine laboratory tests (blood cell count, blood chemistry) were normal. Venereal Disease Research Laboratory (VDRL) test and direct skin examination and culture for fungus were negative. A biopsy specimen was obtained from a pigmented macule. The histologic study showed hyperkeratosis and acanthosis, epidermal basal layer pigmentation with an irregular distribution, focal mild lymphohistiocytic infiltrate in the papillary dermis and dermal–epidermal junction, and discrete pigmentary incontinence (2-4). The mast cell population was normal. A further biopsy 1 year later showed similar findings. Figure 1Open in figure viewerPowerPoint Multiple brown macules involving the trunk Figure 2Open in figure viewerPowerPoint Mild inflammation in the papillary dermis and dermal–epidermal junction with focal lichenoid changes (hematoxylin and eosin, ×40) Figure 3Open in figure viewerPowerPoint Mild inflammation in the papillary dermis. Melanin pigmentation with an irregular distribution in the epidermal basal layer (hematoxylin and eosin, ×250) Figure 4Open in figure viewerPowerPoint Detail of the epidermal basal layer showing irregular melanin pigmentation; there are a few extravasated red cells and a melanophage in the papillary dermis (hematoxylin and eosin, ×400) After 3 years of follow-up, mild spontaneous fading occurred in some of the trunk lesions, but most remained unchanged.

Dyschromatosis universalis hereditaria: Two cases

Dyschromatosis universalis hereditaria is a rare genodermatosis reported initially and mainly in Japan. However, subsequent cases have been reported from other countries. We describe two Tunisian cases of dyschromatosis universalis hereditaria in a 3-year-old and a 3-month-old girl. They presented to our department with asymptomatic progressive mottled pigmentation over the trunk and limbs, which had been noted since birth and had become more noticeable with age. Palms and soles were also affected in the first case. The two patients did not have any systemic or other cutaneous illness. They were born to healthy, second-degree consanguineous parents (case 1) and non consanguineous parents (case 2), following an uneventful pregnancy. No family members had a similar appearance. Physical examination revealed numerous, generalized, hyperpigmented macules interspersed with spotty de-pigmented macules. Hair, nails, teeth, and mucosae were normal. Systemic examination did not reveal abnormalities. Histological exam revealed basal layer hypermelanosis with pigmentary incontinence in some areas. So based on those findings a clinical diagnosis of DUH was made and the patients were followed up in our department for periodic general evaluation of their skin. After a follow up of 12 months, the first child didn't develop other lesions, but palms and soles were also involved in the second case.

Visual Diagnosis

1. Lopa Shah, MD* 2. Gita Balakumar, MD* 1. *University of Nevada School of Medicine, Las Vegas, Nev A 3-week-old girl presents to the clinic for a persistent rash that has been present since birth. Following an uncomplicated term gestation, the infant was born by cesarian section due to prolonged dilation and failure to progress. She weighed 3.2 kg. A rash was noted at birth on her left lower extremity, and her parents were reassured that the rash would resolve. However, the rash now extends over both lower extremities. The mother has not applied any creams, lotions, or topical medications to the infant’s skin. The family history is noncontributory; there is no history of nervous system or skin disorders. The infant is well-appearing, comfortable, and afebrile. She weighs 3.54 kg (25th percentile). Skin examination reveals red, hyperpigmented streaks and plaques on the upper part of her lower extremities (Fig. 1), with occasional vesicles distributed linearly (Fig. 2). An accessory nipple is noted on the right chest wall. The infant is active, there is no evidence of scratching, and her muscle strength and tone are normal for age. The remaining physical findings are normal. Figure 1. Red, hyperpigmented streaks and plaques on left lower extremity. Figure 2. Vesicles on left lower extremity. A complete blood count demonstrates: hemoglobin, 12.5 g/L (125 g/L); white blood cell count, 46.3×103/mcL (46.3×109/L) with 14% neutrophils, 2% bands, 33% lymphocytes, 44% eosinophils, and 1% myelocytes; and platelet count, 560.0×103/mcL (560.0×109/L). Peripheral blood smear reveals a slight normochromic, normocytic anemia with erythropenia, normal red cells with a few teardrop cells, moderately increased number of platelets, and a mild-to-moderate increase of white blood cells with relative and absolute eosinophilia. A clinical diagnosis is made. The presence of vesicular and hyperpigmented linear skin lesions since birth, their distribution over lines of Blaschko, and the laboratory finding of …

532‐nm and 1064‐nm Q‐switched Nd:YAG laser therapy for reduction of pigmentation in macular amyloidosis patches

Macular amyloidosis is a primary form of skin amyloidosis with deposition of small to moderate amyloid material in the upper dermis and mild pigmentary incontinence with resultant clinical hyperpigmentation. To determine the efficiency of Q-switched Nd:YAG laser (532 and 1064 nm) in reducing the pigmentations due to skin macular amyloidosis. A prospective, side by side, controlled, clinical trial study was designed. Twenty subjects with clinical diagnosis and pathology confirmation of macular amyloidosis were treated with Q-switched Nd:YAG laser: 532 nm in a part of their plaques and with 1064 nm in another part of their plaques. Assessment of efficiency was done by colorimetric scores based on Mexameter measurement and also digital photographs before laser therapy and 8 weeks after treatment. Mexameter-based data analysis showed that the two lasers (Q-switched 532 and 1064 Nd:YAG) are effective in reducing the degree of macular amyloidosis patches pigmentation, and 532 nm is meaningfully more effective than 1064 nm in this matter. Photograph-based analysis showed that 90% of cases treated by 532 nm had good or very good response, and for the 1064 nm-treated patches, 60% of cases had the good or very good response. The results of study showed the net positive effect of Q-switched Nd:YAG laser, either 532 nm or 1064 nm, in pigment reduction of macular amyloidosis patches, but the 532-nm laser was more effective than 1064 laser.

Poikilodermatous mycosis fungoides

A 60‐year‐old woman presented with a 10‐year history of pruritic patch lesions that had originated on her breast and progressed over the years to involve the lower part of the abdomen. Different cutaneous biopsies were obtained during this period revealing a superficial chronic dermatitis. She had been treated previously with intermittent cycles of medium‐strength topical steroids. This regimen was of only temporary benefit and progression of the skin lesions had occurred over the last year. The patient's medical history was otherwise unremarkable.Physical examination revealed atrophic red–brown skin with telangiectasia predominantly located on the breast (Fig. 1). Clinical examination also revealed various red‐to‐brown scaly plaques affecting the lower part of the abdomen.Representative clinical appearance with reticulate pigmentation, atrophy, scaling, and telangiectasiaimageTwo skin biopsies were obtained from the breast and the abdomen. Routine hematoxylin and eosin staining of the breast area revealed an atrophic epidermis covered by a scale of hyperkeratosis and parakeratosis. Scattered intraepidermal atypical lymphocytes were observed. In the dermis, there was a superficial band‐like infiltrate of atypical lymphocytes sparing the dermo‐epidermal interface. Pigmentary incontinence and dilated capillaries were present within the superficial dermis (Fig. 2). All of these findings were compatible with the poikilodermatous variant of cutaneous T‐cell lymphoma (CTCL). Plaques affecting the lower part of the abdomen showed clinical features of classic mycosis fungoides (MF), and histology revealed an epidermis with acanthosis, a dense band‐like infiltrate within the upper dermis, and a prominent epidermotropism with intraepidermal collections of lymphocytes. Immunohistochemical analysis of both biopsies identified the cells as CD2+, CD3+, CD4+, CD8–. Further detailed examination did not reveal any visceral or lymph node involvement.Biopsy specimen of the breast. (A) Atrophic epidermis and a superficial band‐like infiltrate (hematoxylin and eosin; original magnification, ×40). (B) Scattered intraepidermal atypical lymphocytes and melanophages within the superficial dermis (hematoxylin and eosin; original magnification, ×200)imageWhen topical mechlorethamine had no significant effect, psoralen plus UV‐A (PUVA) phototherapy was started at 0.5 J/cm2 twice weekly. After 20 treatments (cumulative dose, 143.5 J/cm2), the lesions had disappeared, leaving slight postinflammatory hyperpigmentation. No maintenance treatment was required and the patient remained in complete remission during a 14‐month follow‐up period.

Miz1 is required for hair follicle structure and hair morphogenesis

Previous work has implicated the Myc-binding transcription factor Miz1 in the control of keratinocyte proliferation and in the cellular response to TGFbeta. Miz1 is expressed in basal keratinocytes of the interfollicular epidermis and in hair follicles. Here we have conditionally knocked out the POZ/BTB transactivation domain of Miz1 in keratinocytes using a keratin 14 (K14)-Cre mouse deleter strain. K14Cre(+)/Miz1(lox/lox) mice have rough fur as a result of altered hair follicle orientation, irregular hair pigmentation and disturbed hair fiber structure. A regional thickening of the epidermis at the hair funnel orifice was accompanied by suprabasal proliferation, indicating a delayed exit of keratinocytes from the cell cycle. In addition, the catagen of the hair cycle was delayed in K14Cre(+)/Miz1(lox/lox) mice and intrafollicular keratinocyte proliferation was increased. In aged K14Cre(+)/Miz1(lox/lox) animals, the number of hair follicles remained unchanged but the number of visible hairs, especially of zigzag hairs, was reduced and a pigmentary incontinence into the dermis developed. Our data show that Miz1 is involved in controlling proliferation and differentiation in hair follicles and in hair fiber morphogenesis.

VOGT-KOYANAGI-HARADA-LIKE SYNDROME IN A GERMAN SHEPHERD DOG

A 6-year-old male dog was presented with a one-year history of vision loss, alopecia, and generalized depigmentation of the skin and hair. Op hthalmic signs were the first symptoms, described a s conjunctivitis (whites of the eye, and rimgo red) b y owners. After that, the skin and hair changes fol lowed within three months. Clinical examination confirmed diffus e generalized depigmentation, hair loss, and blindn ess. Ophthalmic examination indicated depigmentation of the mucocutaneous junctions of the superior and inf erior eyelids, mild conjunctival hyperemia, and congestio n of the episcleral vessels. Menace and pupillary l ight reflexes were decreased. The main aspect was a milk y blue surface on the eyes balls and bilateral cata ract. No complete ophthalmologic exam was performed. The complete blood count did not show significant changes. Skin scrapings collected from affected areas (alope cic and depigmented) showed an absence of bacteria, fungi or mites. Skin-punch biopsies of depigmented skin from the face and thoracic region were were placed in 1 0% buffered formalin for fixation, sectioned in paraff in, and stained with hematoxylin and eosin (H&E) and Trichrome Masson. The conclusion of histopathology was histiocytic lichenoid interface dermatitis with marked pigmentary incontinence. Such findings, associated with clinical and ophthalmic signs, suggested uveodermatologic or VKH-like syndrome. In addition, epidermal atrophy was noted but are considered a secondary lesion of treatment with anti-inflammator y drugs (SAID). Biochemical and serologic analyzes had elucidated no other cause for the ocular and skin l esions.

Confluent and reticulated papillomatosis successfully treated with amoxicillin

Conflicts of interest: none declared. Sir, Further to the recently published experience of the Mayo Clinic in the treatment of confluent and reticulated papillomatosis (CRP),1 we report a case of CRP treated successfully with amoxicillin. Confluent and reticulated papillomatosis is an unusual skin disorder originally described by Gougerot and Carteaud. It consists of a scaly, macular and papular eruption typically affecting the seborrhoeic areas of young adults. As the name suggests, lesions become confluent in the centre, coalescing to form a reticulated pattern at the periphery of affected areas. We describe a 29‐year‐old female who initially presented in 2004 with a 4‐year history of an asymptomatic eruption affecting the axillae, mons pubis, submammary (Fig. 1) and inguinal folds. She had been treated unsuccessfully with topical steroids and antifungal agents. Differential diagnoses included a fungal eruption, pityriasis versicolor, Darier's disease and Dowling–Degos disease (reticulate pigmented anomaly of the flexures) but these were excluded by investigations; skin scrapings for mycology were negative and a skin biopsy showed mild chronic inflammation in the upper dermis with some mild pigmentary incontinence. Wood's light examination was unremarkable. A skin swab and culture of skin scrapings on chocolate agar were negative. Following clinical and histological correlation a diagnosis of CRP was made.

Imiquimod as an antiaging agent

Topical imiquimod therapy has proven to be effective for a variety of infectious, neoplastic, and inflammatory dermatologic diseases. Several published reports have validated the benefit of imiquimod therapy for actinic keratoses and superficial melanoma and nonmelanoma skin cancers. There is, however, limited evidence demonstrating the use of topical imiquimod application as an antiaging treatment. We examined the effectiveness of imiquimod 5% cream in the treatment of photoaging by evaluating pretreatment and posttreatment biopsy specimens and documenting the histologic changes. This study represents an extension of an earlier project in our department in which patients with biopsy-proven lesions of lentigo maligna (LM) were recruited from a university dermatology service, a hospital, and referrals from private practitioners for an open-labeled efficacy trial with daily topical application of 5% imiquimod for 3 months. Biopsy of clinically affected skin was carried out on all patients before and after treatment. Using a semiquantitative method, biopsy specimens were analyzed for changes in the dermal collagen table (solar elastosis vs papillary dermal fibroplasia). Additional parameters analyzed included epidermal changes (atrophy vs acanthosis, melanin content, and hypergranulosis) and inflammatory effects (epidermal and dermal cell populations along with presence of pigment incontinence). Variables were compared using paired Wilcoxan rank sums. Of 26 evaluable patients who completed 3 months of daily application, 24 (>92.3%) showed a significant increase in papillary dermal fibroplasia (P < .0001) with associated reduction in solar elastosis (P = .0036). Other noteworthy findings were restoration of normal epidermal thickness (P = .0073) and melanization (P < .0001). This study only evaluates the effect of imiquimod in the lesional skin of LM. It is not known whether the results are applicable to nonlesional, photoaged skin. Topical imiquimod appears to induce reparative changes to the epidermis and the dermal collagen table in chronically sun-damaged skin associated with LM, indicating its potential use as an antiaging treatment. These findings need to be confirmed in photodamaged skin not associated with LM.

A Case of Interface Perianal Dermatitis in a Dog: Is This an Unusual Manifestation of Lupus Erythematosus?

Discoid lupus erythematosus (DLE) is a well-known autoimmune disorder described in dogs and humans. In dogs, DLE is considered the second most common immune-mediated dermatitis and is usually localized to the nasal planum. DLE does not evolve to generalized disease, however lesions may spread to the bridge of the nose and less commonly may extend to periocular region, pinnae, distal limbs, and mucocutaneous junctions (lips, oral cavity, and genital region). A 4-year-old male Bavarian Mountain Scenthound developed a chronic, erosive, cutaneous lesion located exclusively in the perianal region without facial skin involvement. Clinical signs included erythema, depigmentation, severe alopecia, crusting, and ulceration. Histologically, the hallmarks of the changes were an interface dermatitis consisting of plasma cells, lymphocytes, neutrophils, and macrophages, hydropic degeneration of basal cells, few apoptotic cells in the basal layer, pigmentary incontinence, and a focal thickening of the basement membrane, which was characterized by linear deposition of IgG. Despite the unusual localization the lesion was diagnosed as DLE based on the characteristic histologic and immunohistologic features. Following diagnosis, corticosteroid therapy resulted in a complete resolution of perianal lesions.

Unilateral uveitis in a dog with uveodermatologic syndrome

A 7-year-old Siberian Husky-type dog with heterochromia irides was evaluated because of signs of pain associated with the right eye. Unilateral panuveitis, iris bombé, and secondary glaucoma were detected in the right eye. Tear production was low bilaterally. Facial and truncal poliosis and vitiligo were also evident; skin biopsy specimens were obtained from the nasal planum. Uveodermatologic syndrome was diagnosed on the basis of histopathologic findings of a lichenoid interface dermatitis and pigmentary incontinence within the dermis. Immunohistochemical analysis was performed on skin samples retrospectively, and findings were inconclusive. Treatment involved topical (ocular) and oral administration of corticosteroids, oral administration of azathioprine, and topical (ocular) administration of a carbonic anhydrase inhibitor and a lacrimostimulant. The secondary glaucoma was refractory to treatment, and the right eye was enucleated. Uveodermatologic syndrome was confirmed via histologic examination of ocular tissues. The left eye remained free of inflammation 16 months after the initial diagnosis. The periocular skin and skin of the nose partially regained pigment, but the hair did not. Some breeds in which uveodermatologic syndrome has been reported (eg, Siberian Huskies, Old English Sheepdogs, Australian Shepherds, and Shetland Sheepdogs) often have heterochromia irides. This case highlights the fact that dogs with asymmetric uveal pigmentation may have unilateral ocular changes; therefore, uveodermatologic syndrome should not be excluded as a differential diagnosis on the basis of unilateral clinical signs.

Diltiazem Induces Severe Photodistributed Hyperpigmentation

Diltiazem hydrochloride is a commonly prescribed benzothiazepine calcium channel blocker for the treatment of cardiovascular disease. Recently, 8 cases of diltiazem-induced photodistributed hyperpigmentation occurring predominantly in elderly African American women were reported. Here, we report occurrence for the first time in a light-skinned African American woman and a Hispanic woman. We also report this finding in an African American man. Biopsy specimens of hyperpigmented areas were obtained for histopathologic evaluation and marker studies. Photospectrometry analysis for diltiazem was performed to analyze the photoabsorption properties of this drug. Routine laboratory examination results were normal in all patients. Serologic test results for antinuclear antibodies, including Sjögren antibodies anti-Ro (SS-A) and anti-La (SS-B), were negative. Histopathologic analysis of the skin biopsy specimens revealed a sparse lichenoid infiltrate, prominent pigmentary incontinence, and numerous melanophages in the dermis. There was no increase in dermal mucin suggestive of lupus. The mononuclear cells in the specimens were strongly positive for CD3, weakly positive for CD68, and either weakly positive or negative for CD79a. All specimens were negative for Alcian blue staining. Photospectrometry analysis of diltiazem showed an absorption range within the UV-B spectrum. Photospectrometry analysis revealed diltiazem could demonstrate a photosensitizing effect within the UV-B range. Discontinuation of therapy with diltiazem is the most effective modality in resolving hyperpigmentation. Avoidance of sun exposure and consistent use of sunscreens and sun-protective clothing are indicated for patients undergoing diltiazem therapy.

Docetaxel-induced recall dermatitis on previous laser treatment sites

Sir, Chemotherapy‐induced ‘recall’ is a phenomenon whereby the administration of a chemotherapeutic agent induces an inflammatory reaction in a previous injury site.1–3 The most well‐known recall phenomenon is radiation recall, and there is no previous report of a chemotherapy‐induced recall reaction on a laser‐induced wound.1–3 A 45‐year‐old female presented in August 2002 with intermittent headache, ataxia, vertigo and vomiting, followed by sudden loss of consciousness. Brain magnetic resonance imaging revealed multiple brain tumours at the right cerebellum, right occipital and left parietal lobes. The patient underwent excision of the right cerebellar tumour and was found to have a metastatic adenocarcinoma. Chest computed tomography (CT) study disclosed multiple nodules in the right lung field and the patient was diagnosed as having nonsmall‐cell lung cancer with multiple brain metastases. Whole brain radiotherapy with the dosage of 3000 cGy in 15 fractions was administered during September and October 2002, and all the neurological symptoms subsided. The patient was also treated with four courses of gemcitabine 1000 mg m−2 (on days 1, 8 and 15) plus cisplatin 90 mg m−2 (on day 15) from November 2002 to March 2003. In November 2003, the chest CT study revealed progression of the disease, and the patient was then treated with docetaxel 40 mg m−2 on days 1, 8 and 15. No obvious skin side‐effect was ever noted until the first infusion of the third cycle. The patient found two well‐defined, erythematous, slightly scaling, infiltrative plaques with tingling and pruritic sensations, which had developed on both cheeks 2 days after that infusion. The skin lesions were worse after the second and third infusions of that cycle (Fig. 1). An incision skin biopsy was performed on the left cheek lesion; this revealed epidermal dysmaturation with frequent dyskeratotic keratinocytes, basal vacuolar changes and pigment incontinence, which were compatible with the effects of chemotherapeutic agents (Fig. 2).

Novel autosomal recessive progressive hyperpigmentation syndrome

We present a family of Iraqui origin with three siblings affected by a novel type of progressive hyperpigmentation syndrome. The generalized initially diffuse, later disseminated hyperpigmentation started in early infancy and increased during childhood. It also affected palms and soles, and the face but spared the cheeks. Additional features were dry, itchy and sunlight sensitive skin, dystrophy of toe nails, hair loss, and myopia, but normal sweat glands. Light and electron microscopy showed signs of pigment incontinence and compound melanosomes as well as fibrillar bodies. The occurrence of this entity in affected siblings from a consanguineous mating suggests autosomal recessive inheritance. Extensive review of the literature showed no previous report with this distinct combination of clinical and microscopic findings.

Lesões de pele em bovinos com doença granulomatosa sistêmica associada ao pastoreio de ervilhaca (Vicia spp.)

Descrevem-se as lesões cutâneas macroscópicas em 10 e histológicas em 8 vacas afetadas por doença granulomatosa sistêmica associada ao pastoreio de ervilhaca (Vicia spp.). Em todos os casos, as lesões cutâneas eram caracterizadas por múltiplas áreas coalescentes de alopecia, liquenificação e descamação. Os locais mais atingidos pela lesão de pele foram: cabeça e pescoço (10/10), tronco (4/10), períneo (3/10) e mama (2/10). Em todos os 8 casos avaliados histologicamente, as lesões se caracterizavam por dermatite perivascular superficial granulomatosa de intensidade variável. Outros achados histológicos incluíram dermatite perivascular profunda (1/8), perifoliculite (2/8), foliculite mural (3/8), hiperqueratose ortoqueratótica compacta (6/8), erosões (1/8), úlceras (2/8), microabscessos de Munro (8/8), crostas serocelulares (1/8), espongiose (4/8), degeneração hidrópica (5/8), acantólise (1/8), corpúsculos de Civatte (2/8), exocitose linfoplasmocitária (6/8), edema superficial (6/8), incontinência pigmentar (2/8), basofilia (6/8) e mineralização distrófica do colágeno (2/8), tumefação do núcleo das células endoteliais (8/8) e ectasia de glândulas sudoríparas (8/8).

Pigmentary Mosaicism of Hyperpigmented Type in Two Sisters

A 17-year-old girl and her 15-year-old sister presented with progressively increasing streaks of reticulate hyperpigmented macules arranged in a whorled pattern over the trunk and extremities (Figure), which appeared soon after birth. The face, palms, soles, eyes, and mucous membranes were spared. Both parents were unrelated Saudis. There was no history of any preceding eruption or any associated systemic abnormality, except for recurrent oral ulcers in both patients for several years. The younger one also had one episode of genital ulcers. Dermatological examination of both parents and the patients' three brothers and one sister were normal with no history of oral ulceration. Examination revealed few aphthous ulcers in either cases, but no joint or eye symptoms. Pathergy testing in both cases was negative. Ophthalmological examination and consultation revealed no signs of Behcet's disease. Routine blood tests did not show any abnormalities. Skin biopsies were taken from pigmented and normal skin in both patients. Histopathological examination of pigmented skin in both cases revealed basal cell hyperpigmentation with pigmentary incontinence. Similar features but in milder form were seen in the biopsies of normal skin in both cases.

Melasma on the Nape of the Neck in a Man

Sir, We report a 47-year-old man with light brown macular pigmentation on the nape of his neck (Fig. 1). It was asymptomatic and had developed gradually over 2 years. He worked outdoors as a pipe fitter on an oilrig module; however, he denied exposure at this site because he always wore a shirt with a collar that covered the affected area. However, on further questioning it transpired that he spent most of the day with his head bent forward. This reproducibly exposed the area of pigmentation with a sharp cut off inferiorly at the level of his collar. He used various shampoos, aftershaves and shower gels, but none was applied directly to that area. His skin was otherwise normal and there was no family history of abnormal pigmentation. Woods lamp examination showed the pigmentation extending onto the sides of his neck. Skin biopsy of the light brown pigmentation of the nape of the neck showed a normal epidermis with increased basal pigmentation and normal numbers of melanocytes. These findings are consistent with an epidermal type of melasma. Melasma is an acquired hypermelanosis of the skin most commonly seen in women. Pigment may be epidermal, dermal or mixed type (1). The usual distribution patterns are centro-facial, malar or mandibular facial skin, although it has been described on the forearms in association with hormone replacement therapy (2). High oestrogen states, sunlight exposure, familial tendency and photosensitizing agents have been aetiologically implicated (3). Melasma is recognized in men although the contribution of hormone dysregulation in this group is uncertain (4, 5), and the influence of sunlight and photosensitizing agents may be more relevant. The differential diagnosis for pigmentation at this site includes Riehl’s melanosis, Berloque dermatitis and poikiloderma of Civatte. Riehl’s melanosis typically involves the face with a brownish-grey pigmentation; biopsy might be expected to show interface change and liquefaction basal cell degeneration with a moderate lymphohistiocytic infiltrate, melanophages and pigmentary incontinence in the upper dermis. It is usually associated with cosmetic use and may be considered synonymous with pigmented allergic contact dermatitis of the face (6, 7). Berloque dermatitis is considered to be caused by a photoirritant reaction to bergapentin; it may affect the sun-exposed areas of the face, neck and arms. There is usually an early inflammatory phase followed by hyperpigmentation. Histology may show an irritant response in the acute phase; however, older pigmented lesions show increased number and size of melanosomes, melanocyte hypertrophy with arborization of dendrites (8, 9). Poikiloderma of Civatte consists of a reticulate reddish-brown pigmentation, atrophy and telangiectasia typically affecting the lateral aspect of the cheeks and neck, and is most often seen in women. The aetiology is unknown but photosensitizing chemicals in perfumes and cosmetics have been implicated. Histology shows moderate thinning of the stratum malpighii, hydropic degeneration of basal cells and effacement of the rete ridges. In the upper dermis there is a band-like infiltrate of lymphocytes and histiocytes; there may also be pigmentary incontinence (10). We are not aware of any previous reports of melasma at this site. We feel that this unusual distribution of melasma in a man may result in part from UV exposure and it may be that intermittent exposure to UV is more relevant than constant exposure, as the skin of the face and hands are spared. We also suspect that this may not be a rarity, but may pass unnoticed by patient and physician.

An immunohistochemical study of uveodermatologic syndrome in two Japanese Akita dogs

Ocular and cutaneous tissues from two Japanese Akita dogs with uveodermatologic syndrome (UVD) were subjected to immunohistochemical analysis. Light microscopic examination of the globes confirmed the presence of panuveitis of different severity in each case. The infiltrate was primarily granulomatous with prominent perivascular lymphoid aggregates. Melanophages were present throughout the affected areas, and there were scattered plasma cells. Immunohistochemistry using CD79a, CD3, MAC387 and MHC class II markers indicated that there were relatively few T lymphocytes and that most lymphocytes were of the B-cell lineage. The two skin biopsies examined also appeared to represent different stages of cutaneous pathology. The biopsy from one case was consistent with the reported features of skin lesions of canine UVD syndrome, including granulomatous dermatitis with extensive T-cell infiltration extending into the epidermis. In contrast, the skin lesion from the second case showed less inflammation, more pigmentary incontinence and evidence of dermal fibrosis. There was no immunoglobulin or complement deposition at any level within the cutaneous or ocular lesions. The findings of these two cases suggest that the skin lesions of these two dogs with UVD syndrome were mediated by T cells and macrophages (Th1 immunity), whereas the ocular lesions were more consistent with a B cell and macrophage response (Th2 immunity). This is, however, a preliminary investigation and these features may not be the same for all cases of UVD syndrome.

Drug‐Induced Follicular Lupus‐Like Eruption

A 51‐year‐old female presented with agminate flesh‐colored, slightly hyperkeratotic papules, 3–5 mm in diameter, on her upper back and to a lesser extent on the upper chest, neck and forehead. The papules were centered around the hair follicles and several showed mild perifollicular erythema. Clinical impression was keratosis pilaris with an unusual distribution or follicular mucinosis. Medications included hydrochlorothiazide (HCTZ), begun several months previously, along with potassium supplements. Histologic findings revealed mild interface dermatitis with rare individually necrotic keratinocytes and mild pigment incontinence, a superficial and mid perivascular and periappendageal lymphocytic infiltrate with marked dermal mucin deposition and extravasated erythrocytes. No definitive basement membrane thickening was present. Laboratory investigation revealed antinuclear antibodies at 1:640; anti‐double stranded DNA and anti‐histone antibody titers were normal. Following discontinuance of HCTZ and addition of topical steroids, her eruption slowly resolved. Taken together, these findings are those of a new cutaneous manifestation of a drug‐induced lupus‐like eruption. We have named it drug‐induced follicular lupus‐like eruption to reflect the drug‐induced counterpart of the newly described follicular lupus erythematosus.

Ultrastructural characterization of the distribution of melanin and epidermal macrophages in photodamaged skin.

We examined the characteristics of melanin distribution, the possible mechanisms underlying the histological incontinence of pigment, and the significance of epidermal macrophages in photodamaged skin. We used electron microscopy to compare and quantitate melanin distribution in various types of cells and structures, to qualitatively observe associations of melanin granules with melanophages, and to examine morphological differences of epidermal macrophages in sun-exposed versus sun-protected facial skin. Melanin-containing cells (such as Langerhans' cells) and melanin-containing structures (such as colloid bodies) in photodamaged skin were more numerous than in sun-protected skin, in proportion to differences in melanocyte density and in epidermal melanin content. Although the precise mechanism(s) of histological incontinence of pigment in photoaging skin appear to be very complicated, it is certainly one of the morphological hallmarks of photodamaged facial skin, and the degeneration of keratinocytes (noted by their electron-lucent properties), a feature characteristic of photoaging, contributes to that process. Furthermore, the increased numbers of epidermal macrophages in sun-exposed skin may be associated with photoaging processes (probably through their phagocytic function) as well as alterations of the cutaneous immune system.