SOLITARY TRUNCAL POROKERATOTIC ECCRINE OSTIAL AND DERMAL DUCT NEVUS IN A SIXTY-YEAR-OLD MAN

A sixty-year-old white man presented with a 2 × 1.5 cm lesion on his right buttock. The lesion had been present for several years, but had not been present when the patient was a child. No other family members reported having similar lesions. His past medical history was unremarkable. By history, the lesion was slowly growing, but was neither painful nor pruritic. On examination, a well defined pink nodule was noted on his right buttock. The surface of the lesion had a crateriform appearance with verrucous edges. A shave biopsy was performed.
Histopathology : The specimen was cut into four pieces and sections stained with hematoxylin and eosin were examined. A low power view (Fig. 1) shows an epidermis with considerable hyperkeratosis and several focal areas of parakeratosis that fill epidermal dilated eccrine ducts. Higher magnification (Fig. 2) reveals, that these foci of parakeratosis resemble the cornoid lamellae seen in porokeratosis of Mibelli. Figure 2 also reveals that the process originates within the eccrine duct. Higher magnification demonstrates the porokeratotic column arising from dyskeratotic keratinocytes that lack a granular layer (Fig. 3). An inflammatory infiltrate consisting of lymphocytes and histiocytes is present in the underlying dermis with accentuation directly under the cornoid lamellae.     

Annular atrophic lichen planus

A 30-year-old woman presented with a 1-year history of a pruritic eruption on the extremities, characterized by several annular plaques. The patient had been treated unsuccessfully with medium-potency topical steroids. The lesions had an erythematous papular border with an atrophic center (width, 1-4 cm) (Fig. 1). No oral, genital, or nail lesions were observed. A skin biopsy from one of the plaques was performed. Histopathologic examination of the raised border showed hyperkeratosis of the stratum corneum, focal thickening of the granular layer, basal liquefaction degeneration of the epidermis, and a band-like subepidermal infiltration with numerous Civatte bodies. In the center of the lesion, the epidermis became thinner (Fig. 2). Elastic fibers were reduced or absent in the papillary dermis. The patient was treated with high-potency topical steroids for 2 months with clinical improvement.     

An unusual melanocytic lesion associated with eccrine duct fibroadenomatosis and syringoid features

The intimate association of nevomelanocytic nevi with eccrine ducts commonly seen in congenital nevi was emphasized by Mishima, who described as eccrine-centered nevi those lesions characterized by nevomelanocytic cells predominantly proliferating around and within the eccrine sweat duct walls. However, there were no changes in the overlying epidermis, dermis, or eccrine acrosyringeal or dermal duct proliferation in these lesions. We present the case of a 16-year-old boy with a 1-year-history of a 0.6-cm diameter single tan papule on the right heel, clinically thought to be a Spitz nevus. Histopathologic examination revealed a compound nevomelanocytic nevus associated with epidermal hyperplasia, thin anastomosing cords of acrosyringeal epithelium extending within the dermis, and eccrine ductal proliferation in a syringoma-like pattern associated with a dense fibrous stroma. Features that distinguish our case from eccrine-centered nevus are that the latter lacks epidermal and eccrine duct hyperplasia and a dense fibrous stroma. The location of the lesion on the heel in our case suggests the possibility that the pathologic changes observed could result from repetitive trauma.     

Syringotropic melanoma: a variant of melanoma with prominent involvement of eccrine apparatus and risk of deep dermal invasion

We report 7 cases which can be regarded as a syringotropic melanoma-a unique presentation of melanoma defined as melanoma spreading within the eccrine apparatus into the reticular dermis and/or subcutaneous tissue deeper than any (if present) associated invasive melanoma. Six patients were females, and 1 was a male. Their ages ranged from 32 to 85 years old (average 63). The lesions showed a wide site distribution, occurring on the extremities (4), trunk (2), and head and neck (1). Five melanomas were superficial spreading type; 1 was acral lentiginous type; 1 was unclassified. Four lesions (57%) invaded from within eccrine apparatus at a depth and anatomical level greater than that of an adjacent conventional invasive melanoma arising from the surface epidermis. In 1 lesion, which presented clinically as a pigmented macule, deep dermal syringocentric invasive tumor was the only site of invasion and tumorigenic growth. Thus, this variant of melanoma carries a significant risk of syringocentric deep dermal invasion, which may be unsuspected clinically but must be detected on histological examination to provide the most accurate prognosis and staging information.     

Carcinomatous transformation of eccrine syringofibroadenoma

BACKGROUND: While squamous cell carcinoma and pseudocarcinomatous hyperplasia have been documented as pre-existing lesions in cases of reactive eccrine syringofibroadenoma (ESFA), to the best of our knowledge carcinoma occurring in a solitary ESFA has not yet been reported. We present one such case in a 91-year-old female who had a dome-shaped, reddish tumor on the extensor side of the left forearm. METHODS: We review the histopathological, immunophenotypical and ultrastructural findings of this tumor, including the keratin expression profile. RESULTS: Histopathologically, long, branching, anastomosing, thin and thick strands of small cuboidal epithelial cells were extending from the surface epidermis into the dermis. In the center of the tumor, there were irregular-shaped nests of atypical tumor cells invading downward into the dermis. Ultrastructurally, duct-like lumina lined with cuboidal tumor cells were present in the epithelial cords. From these findings, the present case was diagnosed as solitary eccrine syringofibroadenocarcinoma (ESFAC). Keratin expression studies revealed that cells of the thick strands, except for the luminal and basal cells, were positive for differentiation-specific keratins, keratins 1 and 10, and that cells of the thin strands were positive for keratins 5 and 14. CONCLUSIONS: Histopathological, immunophenotypical and ultrastructural evidence, as well as the pattern of keratin expression, suggest differentiation of the present malignant tumor towards the eccrine dermal duct. This case is the first reported case of ESFAC as far as we know.     

Atrophoderma of moulin with preceding inflammation

A 16-year-old Vietnamese man presented to the Dermatology Clinic with a 10-year history of bizarre brown patches, which initially started as red asymptomatic "bumps" on the trunk, upper and lower extremities, and face. His past medical history was significant for hypothyroidism and idiopathic urticaria. He was on Eltroxin for hypothyroidism. The family history was noncontributory. Physical examination revealed two types of lesion: erythematous, well-circumscribed papules in a linear configuration along with linear hyperpigmented atrophic patches following Blaschko's lines were noted on the lower extremities (Fig. 1), right upper extremity, right flank (Fig. 2), and right jawline. Initial biopsies taken from the papular lesions on the right thigh and right elbow revealed the following changes. The first biopsy showed a slightly thinned epidermis with prominent dilated blood vessels in the superficial dermis. There also appeared to be a slight increase in the amount of collagen in the deep dermis. The findings were reported as in keeping with "epithelial atrophy." The second biopsy from the lesion on the right elbow revealed an acanthotic epidermis. The granular layer was absent in several areas and there was marked overlying parakeratosis. In the dermis, there was a heavy perivascular lymphocytic infiltrate. The appearances were consistent with a psoriasiform dermatitis (Fig. 3). A biopsy taken from the left thigh approximately 18 months later showed slight irregular acanthosis with dermal edema, dilated blood vessels, and a patchy lymphocytic infiltrate. The appearances were compatible with mild inflammation.     

Tissue estimation of protein gene product 9.5 (PGP 9.5) expression and apoptosis in vitiligo

Background  Vitiligo is probably the end result of different interacting processes.
Objective  To determine the possible roles of neural and apoptotic mechanisms in the pathogenesis of vitiligo.
Methods  Fifty-six biopsies from 28 patients with generalized vitiligo (28 from depigmented lesional areas and 28 from clinically nondepigmented skin at the periphery of the same areas) were examined; the panaxonal marker neuropeptide protein gene product 9.5 (PGP 9.5) and apoptosis were investigated using immunohistochemistry.
Results  Statistically significant differences were detected in the numbers of PGP 9.5-positive nerve fibers/axons in the papillary dermis between the center and periphery of the lesions (i.e. increased at the center in comparison with the periphery). A statistically significant inverse association was found between PGP 9.5 immunostaining in the dermis at the lesion center and the duration of the disease. When apoptosis and PGP 9.5 expression were compared, there was an identical distribution of PGP 9.5-positive nerve fibers/axons and apoptotic cells in the epidermis (i.e. basal in the lesion center; diffuse at the lesion periphery).
Conclusions  There is a possible connection between the neural and apoptotic pathogenetic theories of vitiligo.     

Increased nerve growth factor and its receptors in atopic dermatitis: an immunohistochemical study

Evidence suggests that neurotrophins may regulate certain immune functions and inflammation. In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in early lesions of atopic dermatitis (AD). In AD involved skin, strong NGF-immunoreactive (IR) cells were observed in the epidermis. In some cases, a huge number of infiltrating cells with stronger NGF immunoreactivity was seen mainly in the dermal papillae. Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis. In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity. The p75 NGFr-IR nerve fibre profiles were increased (900 per mm²; p<0.001) compared to normal [the involved skin also differed from the uninvolved skin (p<0.05)] in the dermal papillae. These nerve fibres were larger, coarser and branched, some of them terminated at p75 NGFr-IR basal cells, and also revealed a stronger fluorescence staining than the controls or the uninvolved skin. In normal healthy volunteers and AD uninvolved skin, the NGF immunoreactivity was weak in the basal layer of epidermis. Only a few trkA positive cells were seen in the basal layer of the epidermis and upper dermis. The IR epidermal basal cells revealed a striking patchy arrangement with strong p75 NGFr immunostaining in the peripheral part of the cells, and short and thick NGFr-IR nerve fibre profiles appeared as smooth endings scattered in the dermis including the cutaneous accessory organs. Using NGF and p75 NGFr double staining, both immunoreactivities showed a weak staining in the epidermis and dermis in normal and uninvolved skin. In the involved dermis of AD, the intensity of p75 NGFr-IR nerves was stronger in areas where there were also increased numbers of NGF-IR cells. These findings indicate that NGF and its receptors may contribute to the neurohyperplasia of AD.     

Papillary eccrine adenoma: immunohistochemical studies of keratin expression

Despite various studies, there are serious disagreements about the cellular differentiation of papillary eccrine adenoma. In the present study, 2 specimens of papillary eccrine adenoma were analyzed by immunohistochemical techniques, using a panel of monoclonal antibodies against keratins, to elucidate its differentiation. Histopathologically, the tumor was composed of multiple tubular structures lined by two or more layers of epithelial cells. The luminal cells of the tubules were flattened or cuboidal. The former were noted in large dilated tubules. The latter were usually observed in small-to-moderate-sized tubules, and formed intra-luminal papillary projections in some tubules. Immunohistochemically, there were two kinds of cuboidal cells in the luminal layers of the tubules. Most of the large dilated tubules and some of the small-to-moderate-sized tubules expressed immunophenotypes similar to those of the eccrine dermal duct. The other tubular structures, including the small tubules resembling those of syringoma, expressed immunophenotypes similar to those of the transitional portions between the dermal ducts and the secretory segments of eccrine glands. From the above comparative studies, papillary eccrine adenoma is considered to differentiate towards the dermal duct and the transitional portions between the dermal ducts and the secretory segments of eccrine glands.     

Eccrine angiomatous hamartoma

A 50-year-old Korean man had an erythematous patch on the left side of his chest since birth ( Fig. 1 ). We first regarded this lesion as nevus flammeus because of the resemblance of the lesion to an erythematous patch that blanched with pressure. Physical examination revealed an 8×5 cm erythematous patch with a central profuse sweating zone surrounded by a flame-like non-sweating zone ( Fig. 2 ). The patch was sharply demarcated from the normal skin. Sweating was evoked by physical exercise or emotional stress. There was no history of pain or tenderness for the lesion. The patient had no history of any other vascular disease. Histopathologic examination of the central zone showed an increased number of eccrine glands in the mid and deep dermis. Some dilated vascular channels that were not associated with the eccrine glands were present in the upper dermis and subcutaneous tissue ( Fig. 3 ). Immunohistochemical stain with anti-factor VIII-related antigen showed reactivity on the endothelia of the vascular elements which were not associated with eccrine glands in the upper dermis. Histopathologic examination of the surrounding zone showed non-specific findings, except for the dilated vascular channels in the upper dermis.

Figure 1 Open in figure viewer PowerPoint (A) hyperhidrotic erythematous patch on the left side of the chest     

Eccrine tubular adenoma--a histopathological, histochemical, and ultrastructural study

A case of eccrine tubular adenoma on the dorsum of the right foot is presented. Histopathologically, in the central nodule of the tumor, the whole dermis was involved and the tumor islands were connected to the epidermis; in the rest of the lesion, tumor islands were observed in the upper dermis. The tumor islands were composed of cystic or alveolar structures and cell masses possessing multiple lumina. Tubules were surrounded by two or more layers of epithelium forming papillations projecting into the lumen. There were only a few basaloid islands and no sclerotic strands. The tumor cells were well differentiated. Acid mucopolysaccharides were seen in the stroma. Histochemically, phosphorylase and acid phosphatase reacted moderately. Succinic dehydrogenase gave a weak reaction and β-glucuronidase was negative in tumor cells. Ultrastructurally, intracellular ducts with numerous microvilli, periluminal filamentous zones, and many multivesicular dense bodies surrounded by a limiting membrane were observed. Keratohyalin granules were absent. Based on these findings, the tumor reported here was considered to be an adenoma differentiating toward the eccrine duct. Some aspects resembled tubular apocrine adenoma, syringoma and basal cell tumor with eccrine differentiation, but they were most similar to papillary eccrine adenoma.     

ULTRASTRUCTURAL CHANGES IN ACQUIRED PERFORATING DERMATOSIS

We performed ultrastructural studies of skin lesions in seven adults with acquired perforating dermatosis. Three of the patients had diabetes mellitus and two were undergoing hemodialysis. Lesions in an early stage showed exocytosis of inflammatory cells and alteration of elastic fibers. Lesions in an intermediate stage featured discontinuities of the basement membrane and aggregates of electron-dense material lateral to the perforated focus, together with dermal edema, scattered macrophages, and densely aggregated collagen fibers that focally filled the papillary dermis. Later-stage lesions showed fibroblasts in the dermis and degenerated elastic fibers within transepidermal channels. In most cases there was a single large epidermal channel lined by flattened epithelial cells, and containing a variety of cellular and extracellular materials. Small "secondary" channels without abnormal keratinization were also observed within the epidermis. The findings suggest that altered keratinization is limited to the immediate vicinity of well-formed transepidermal channels, and that exocytosis of inflammatory cells and alterations of elastica are early and possibly key changes in lesion development. The unexpected discovery of hair fragments in one case suggests that curled hairs may play a role in the pathogenesis of some cases of acquired perforating dermatosis.     

T cell subsets and macrophages in lichen planus. In situ identification using monoclonal antibodies and histochemical techniques

Skin lesions from 6 patients with lichen planus were studied for the presence of T cells and T cell subsets using monoclonal antibodies and indirect immunoperoxidase technique. Small numbers of Leu-2a-reactive suppressor-cytotoxic cells were present early in the basal cell layer in 2 patients with recent lesions. The analysis of T cell subsets revealed the predominance of anti-pan-T-cell (Leu-1)- and Leu-3a-reactive helper-inducer cells in 4 patients with older active lichen planus lesions. Significant numbers of suppressor-cytotoxic cells were observed in the papillary dermis and within the epidermis associated with hydropic degeneration of the basal cell layer. Activated T lymphocytes with focal acid phosphatase activity, together with activated histiocytes-macrophages with strong diffuse activity of acid phosphatase and non-specific esterase, were identified in the dermis and within the epidermis. These findings suggest that a cytotoxic immune process directed against the basal cell layer of the epidermis is the dominant pathogenic event in lichen planus.     

Transient bullous dermolysis of the newborn

A black male newborn delivered by cesarean section developed large bullae on his extremities and in other friction areas soon after birth. No significant family history was obtained. The bullae healed rapidly, leaving hypopigmentation but no scars or milia. Occasional new lesions continued to appear for four months but not after. Reexamination 12 months later showed a normal healthy infant with only residual hypopigmentation in some of the previously involved areas. Histologic and electron microscopic examinations revealed a subepidermal bulla that was ultrastructurally a subbasal lamina separation. Collagenolysis and damage to the anchoring fibrils were found to be responsible for this separation. Perifollicular collagen sheath was also damaged, but periductal collagen of eccrine duct was intact. Keratinocytes in the lower epidermis showed large, dilated rough endoplasmic reticulum (RER), which contained electron-dense stellate bodies. The contents of these RER vacuoles were discharged into the papillary dermis through the rupture of the basal lamina. The number and size of RER vacuoles in the lower epidermis correlated with the severity of collagenolysis in the underlying papillary dermis. The outer root sheath keratinocyte in the upper hair follicle contained RER vacuoles, but the eccrine duct keratinocyte did not. We suspected that the RER vacuoles contained proteolytic enzymes, which were responsible for the collagenolysis.     

Immunopathological studies on rosacea

Seven patients with papulo-pustular rosacea were investigated with immunofluorescence (IF) techniques. Indirect IF has been performed also with antibodies eluted from circulating lymphoid cells. Besides confirming the data in the literature on the positivity of the basal zone, anticollagen antibodies were found, and eluted antinuclear antibodies were detected against nuclei of cells in the epidermis and dermis, namely, scattered dermal, endothelial and eccrine duct cells.     

Lichen planopilaris.

P, a 20-year-old laborer displayed initial symptoms of the disease in question when he was 10 years old. Initially he had an asymptomatic progressive loss of hair on the scalp. A couple of years later he had mild to moderate pruritis, and the appearance of slate-blue eruptions on the scalp and elsewhere on the body. This resulted in a complete loss of hair on the vault of the scalp, which led him to seek specialist opinion. Skin surface examination revealed the presence of grayish-blue acuminate follicular papules, disposed singly and in groups (plaques). The pilo-sebaceous orifices were conspicuously obliterated and filled by keratin plugs. Perifollicular erythema was a predominant feature on the scalp. The lesions were present over the scalp, around the neck, chest, back, axillae, groin and legs. Shiny atrophied scalp skin depicting scarring alopecia mimicking male-type baldness was a salient feature. In addition, it was studded with conspicuous acuminate papules in its center (Fig. 1a). The known nonhairy (glabrous) skin had classic lichen planus lesions (Fig. 1b). Hemotoxylin-eosin stained microsections prepared from typical lichen planus (LP) lesions over the abdomen and those of lichen planopilaris (LPP) of the scalp were simultaneously studied. The former revealed changes in the epidermis comprising of hyperkeratosis, increase in thickness of stratum granulosum, hydropic degeneration of the basal cell layer and band-like lympho-histiocytic infiltrate pressing against and invading the epidermis, while the latter revealed uniform atrophy of the epidermis and vacuolization of basal cells. The hair follicles were dilated and were filled with keratin plugs. In addition to fibrosis of the dermis, pigment laden microphages and lympho-histiocytic infiltrate was prominent. The follicles and the sebaceous glands were absent. However, arrectores pilorum and sweat glands were preserved (Fig. 2a,b).     

Solitary plexiform neurofibroma is not pathognomonic of von Recklinghausen's neurofibromatosis: a report of a case

A 42-year-old Caucasian man presented with a 1.8-cm nodule in the proximal thigh (Fig. 1) that had been slowly enlarging for approximately 5 years. The patient had no family history of neurofibromatosis. Physical examination revealed none of the other stigmata of this neurocutaneous disorder. D.A.F. performed an elliptical excision as an out-patient procedure. Grossly, the lesion was homogeneously opalescent and gelatinous. The tissue was fixed in 10% formalin and embedded in paraffin. Routine hematoxylin and eosin stained sections were prepared. The most notable feature on low power magnification was a large, circumscribed, lobular proliferation of spindle cells in a loose fibrillar background that distorted much of the dermis and subcutaneous fat (Fig. 2). On high power magnification, a population of cells with ovoid and S-shaped nuclei admixed within densely packed eosinophilic collagenous material was seen at the center of the lobule (Fig. 3A). A small amount of mucin was also present. Within this cellular area, a dense population of S-shaped spindle cells with eosinophilic cytoplasm was arranged in a parallel array forming microfascicles. At the periphery of this cellular component, a similar population of cells was arranged against a loose fibrillar background of abundant mucin (confirmed by colloidal iron stain) and scattered mast cells (Fig. 4). Lining the lobule was a compressed rim of thin, delicate collagen bundles and perineurial cells. Pleomorphic nuclei and mitotic figures were not observed. The surrounding dermis and subcutaneous tissue were unremarkable. Thickened collagen bundles at the center of the lobule could be seen with a frichrome stain. An S-100 protein immunoperoxidase stain highlighted scattered Schwann cells within the lobule (Fig. 3B), and nerve bundles adjacent to the neurofibroma served as infernal positive controls.     

Inflammatory cells in skin lesions of scabies

Cell infiltrates of biopsy specimens from nodular or papulovesicular skin lesions of seven patients with scabies were characterized by α-naphthyl acetate esterase (ANAE) staining and immunoperoxidase labelling. T lymphocytes were the dominant cells in the dermal inflammatory infiltrates of both nodular and papulovesicular lesions. Their mean proportion in the deeper dermal infiltrates was 64% and in the papillary infiltrates 42%. However, they were few in number around the burrows in the epidermis. In contrast, macrophages were frequent in the epidermis and papillary dermis, where they accounted for 47% and 25% respectively of all mononuclear cells. Immunoperoxidase staining revealed immunoglobulin-positivc plasma cells (from 1% to 10%, of all mononuclear cells) only in the dermal infiltrates of nodular lesions. IgE-positive plasma cells were encountered in all four specimens. These results emphasize the importance of macrophages in scabies infestation and suggest that a local IgE-mediated antibody response may occur in nodular lesions of scabies.     

Immunohistochemical localization of interleukin-6-like immunoreactivity to peripheral nerve-like structures in normal and inflamed human skin

Interleukin-6-like (IL-6-like) immunoreactivity was sought in inflamed and normal human skin using the same immunohistochemical technique as for detection of neuropeptides. Such immunoreactivity was found in dermal and in a few intraepidermal nerve-like fibres in biopsy specimens from inflamed skin from patients with positive epicutaneous patchtest reactions to nickel sulphate, and in skin specimens from patients with atopic dermatitis and prurigo nodularis. However, IL-6-like immunoreactivity was also found in nerve-like fibres in specimens from nonlesional skin. In skin from patients with positive epicutaneous patch-test reactions there was a statistically significantly (P<0.01) higher number of IL-6-positive nerve fibres in the epidermis than in normal skin, in contrast to the papillary dermis, in which no difference was found. Moreover, there were clusters of nerve-like fibres with IL-6-like immunoreactivity in the dermis of prurigo nodularis lesions. In these nerve-like fibres, the colocalization of the immunoreactivities for IL-6 and calcitonin gene-related peptide was indicated. Localization of immunoreactivity to nerve-like structures surrounding the eccrine sweat glands indicates that IL-6 is present in autonomic as well as in sensory nerve fibres.     

Poikiloderma of Civatte: a histopathological and ultrastructural study

BACKGROUND: Poikiloderma of the face and neck (Civatte) has not been studied in depth for decades, especially as far as the histopathology is concerned. MATERIAL AND METHODS: We studied 50 consecutive patients with poikiloderma of Civatte (PC). Their evaluation included: history, physical examination, lesional skin biopsy and histological examination of sections stained with hematoxylin-eosin, PAS, Fontana-Masson, acid orcein Giemsa for elastic fibers and toluidine blue for mast cells. In 10 randomly selected subjects, a second skin biopsy was performed and specimens were examined under the electron microscope. RESULTS: There were 34 females (68%) and 16 males. The mean age at diagnosis was 47.8 years for females and 61.7 years for males. Histological examination revealed an atrophic (62%), flattened (84%) epidermis with hyperkeratosis (92%) and occasional follicular plugging (34%). In some cases, mild hydropic degeneration of the basal cell layer was evident (46%). Melanin was irregularly distributed in the lower epidermis (94%), and melanophages were often present in the dermis (92%). The most prominent and constant feature (100%) was solar elastosis of the papillary dermis. The blood vessels were almost invariably dilated (96%) with a mild perivascular lymphohistiocytic infiltrate (78%), sometimes with plasmacytes (56%). At the ultrastructural level, the epidermis showed only minor changes. The dermoepidermal junction was intact. The most constant findings were swelling and disruption of the collagen fibers as well as focal degeneration of the collagen bundles. Occasionally, several vacuolar spaces were found just under the basal lamina. Melanin-laden macrophages scattered in the dermis were also detected. CONCLUSIONS: PC shows distinct histological and ultrastructural features, supporting the theory that it represents a separate entity. The histology of PC is characteristic but not pathognomonic. On this basis, the differential diagnosis from Riehl's melanosis, poikiloderma atrophicans et vasculare and other acquired poikilodermas can be made. Ultrastructural findings were consistent with the histological findings. Changes of the dermal connective tissue (solar elastosis) predominated, providing morphological evidence for the role of ultraviolet radiation in the pathogenesis of PC.