Punctate and linear angiectases. Anderson-Fabry disease (angiokeratoma corporis diffusum).
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Adult↗
Biomedical subjects
J Bhawan
Publications and source records attributed to J Bhawan.
In vivo and in vitro SPRR1 gene expression in normal and malignant keratinocytes.
The small proline-rich protein 1 (SPRR1) gene encodes a precursor of the keratinocyte cornified envelope. To understand SPRR1 regulation we investigated its expression and modulation in keratinocytes in vivo and in vitro. SPRR1 was strongly expressed in suprabasal layers of the epidermis in newborn skin but only weakly expressed in adult skin. Both in vivo and in vitro, SPRR1 was not expressed in undifferentiated cells of basal or squamous carcinomas. However, within the same tumors and in premalignant lesions of squamous cell origin, cells with histologic evidence of differentiation showed a relative increase in SPRR1 transcript level. Within 24 h physiologic doses of uv irradiation induced SPRR1 mRNA in vivo. To investigate the possibility that SPRR1 expression is regulated by uv-induced cytokines, keratinocytes were stimulated with interleukin-1 (IL-1) and interleukin-3 (IL-3). Both significantly induced SPRR1 mRNA, while TGF-beta, known to lower IL-1 receptor in keratinocytes, down-regulated it. Moreover, proximity to inflammatory cells in vivo was associated with SPRR1 induction in anaplastic tumor cells. Our data suggest that SPRR1 is induced early in differentiation of normal keratinocytes but is not expressed in anaplastic cells of keratinocyte origin. Further, its regulation in skin appears to be modulated at least in part through cytokine release.
Adult↗
Isolated dyskeratotic acanthoma. A variant of isolated epidermolytic acanthoma.
Disorders affecting the maturation of the epidermis are regarded as incidental findings in normal skin and otherwise unrelated benign lesions. These include epidermolytic hyperkeratosis, focal acantholytic dyskeratosis, and pagetoid dyskeratosis. The former two entities also occur as primary pathologic lesions. We report a hyperkeratotic lesion with a specific histologic pattern consisting of dyskeratotic cells throughout the epidermis and a parakeratotic horn, with large, rounded cells at all levels of the stratum corneum. Because we believe it to be a variant of the solitary, acquired lesions characterized by abnormal epidermal maturation, such as epidermolytic acanthomas, we suggest the term "dyskeratotic acanthoma" for this lesion.
Aged↗
Photoaging versus intrinsic aging: a morphologic assessment of facial skin.
Histologic studies have become increasingly important in recognizing morphologic differences in photoaged versus intrinsically aged skin. Earlier histologic studies have attempted to evaluate these changes by examining anatomical sites which are not comparable, such as face and buttocks. As part of a multicenter study, we have quantitatively examined a panel of 16 histologic features in baseline facial skin biopsies from 158 women with moderate to severe photodamage. When compared to the postauricular area (photo protected), biopsies of the crow's feet area (photo exposed) had a twofold increase in melanocytes and a statistically significant increase in melanocytic atypia (p < .0001) and epidermal melanin (p < .0001). Other epidermal changes included reduced epidermal thickness (p < .01), more compact stratum corneum (p < .0001) and increased granular layer thickness (p < .0001) in the crow's feet skin. There was increased solar elastosis (p < .0001), dermal elastic tissue (p < .0001), melanophages (p < .0001), perivascular inflammation (p < .05) and perifollicular fibrosis (p < .01) but no change in the number of mast cells or dermal mucin in the photo exposed skin. Our data document quantitative differences in photoaged versus intrinsically aged facial skin and provides the groundwork for future studies to evaluate the efficacy of new treatments for photoaged skin.
Aged↗
Massive papillary dermal fatty infiltration in a patient with psoriasis.
A 36-year-old Caucasian man presented with chronic, slightly erythematous, scaly plaques of 6 years duration. Some improvement was noticed after treatment with topical steroids. Differential clinical diagnoses included psoriasis and eczema. A biopsy revealed psoriasiform changes with "fatty vacuoles" replacing the papillary dermis. The histogenesis of these findings is unknown. Even though small foci of fatty vacuolization have been observed in association with heavy inflammatory infiltrates in skin, this is the first reported case of massive fatty infiltrates in a non-neoplastic disorder of the skin associated with only sparse inflammatory infiltrate.
Adipocytes↗
Keratinocyte degeneration in human facial skin: documentation of new ultrastructural markers for photodamage and their improvement during topical tretinoin therapy.
We examined epidermal impairment in photodamaged Caucasian skin by light and electron microscopy and observed two types of degeneration of the basal and suprabasal keratinocytes. The first was an electron-lucent degeneration predominantly seen in the periphery of the cells. The marked lucent degeneration occurred in 14% of the basal and suprabasal keratinocytes, predominantly in cells immediately adjacent to melanocytes. In skin specimens with a large number of such damaged keratinocytes, bleb-like keratinocytic protrusions or electron-lucent intercellular structures were also seen. Many vacuolar structures were observed just under the dermoepidermal junction, occupying 9% of the junction length. These structures were produced by herniation of the degenerative portion of the basal and suprabasal keratinocytes, and appeared to be phagocytized by dermal macrophages. The vacuolar alterations in the basal layer and dermoepidermal junction previously reported at the light microscopic level probably represent these intercellular lucent structures, bleb-like protrusions and vacuole-like structures at the electron microscopic level. The second type, dark-staining keratinocytes, probably representing an extensive degenerative process, constituted 4% of the basal and suprabasal keratinocytes. After 12 months of topical tretinoin treatment, dramatic improvement of both degenerative processes of the keratinocytes was noted.
Administration, Cutaneous↗
Effect of beta-carotene supplementation on the human sunburn reaction.
Beta-carotene, a quencher of excited species such as singlet oxygen and free radicals, has been reported to protect against cutaneous photodamage, including sunburn acutely and photocarcinogenesis chronically. The present double blind placebo-controlled study examines the effect of beta-carotene supplementation on the human sunburn response and specifically on the induction of sunburn cells at the time of peak reaction intensity (24 h) after a single solar simulated light exposure 3 times the individually determined minimal erythema dose (MED). Administered orally either as a single 120 mg dose to dietarily restricted subjects or for 23 d as a daily 90 mg supplement to subjects on standard diets, beta-carotene increased plasma and skin levels of beta-carotene compared to both pretreatment levels and placebo-treated controls, but provided no clinically or histologically detectable protection against a 3 MED sunburn reaction. Thus, these data suggest that oral beta-carotene supplementation is unlikely to modify the severity of cutaneous photodamage in normal individuals to a clinically meaningful degree.
Aged↗
Ultrastructural effects of topical tretinoin on dermo-epidermal junction and papillary dermis in photodamaged skin. A controlled study.
We examined the effects of daily topical application of 0.05% tretinoin cream on photodamaged Caucasian facial skin by electron microscopy. Specimens obtained pretreatment, after 6 and 12 months of tretinoin therapy (20 patients), and after 6 months of vehicle treatment (5 patients) were compared in a blinded fashion, with special attention to the dermoepidermal junction and papillary dermis. Baseline specimens disclosed various degrees of damage including reduplication of basal lamina, smudging and sparsity of collagen fibers, and nodular arrangement of degenerated microfibrils in the papillary dermis. No significant changes were observed at 6 months in the papillary dermis of either tretinoin-treated or vehicle-treated patients. After 12 months of tretinoin treatment, however, disorganized collagen fibers, which were conspicuous in 11 patients at baseline, were replaced by new well-organized collagen fibers in a wavy pattern in 6 patients. In addition, the amount of nodularly degenerated microfibrillar material decreased in 15 of 18 patients with this finding at baseline. In contrast, no significant change was noted in the number of anchoring fibrils per unit length of the lamina densa. These observations provide further evidence that topical treatment with 0.05% tretinoin produces papillary dermal reconstruction, for which more than 6 months of application were required.
Administration, Topical↗
Histologic evaluation of chronic human wounds treated with hydrocolloid and nonhydrocolloid dressings.
BACKGROUND: Studies of acute surgical wounds in pigs have shown granulomatous tissue reactions induced by hydrocolloid dressings. OBJECTIVE: We examined biopsy specimens from chronic wounds in humans treated with hydrocolloid or nonhydrocolloid dressings to determine whether such reactions occurred. METHODS: A blinded retrospective analysis of 22 chronic ulcer biopsy specimens from 22 patients was performed by two dermatopathologists independently. RESULTS: No differences were seen between hydrocolloid-treated and non-hydrocolloid-treated wounds. Granulation tissue was seen in all specimens. No cavities, eosinophilic inclusions, polarizable material, or multinucleated giant cells were identified. CONCLUSION: There are no significant histologic differences between hydrocolloid-treated and non-hydrocolloid-treated wounds in humans.
Biopsy↗
Plexiform granular cell tumor. A report of two cases.
A previously undescribed variant of granular cell tumor with an interesting plexiform pattern was found in the lower leg of a 10-year-old girl and on the back of a 12-year-old girl. Clinically, the patients presented with intradermal plaques that were accompanied by variable degrees of pain or tenderness. Histopathologic examination revealed granular cell tumors with various sized fascicles, particularly around nerve bundles, in a plexiform pattern. Cytoplasmic granules were PAS positive. Immunohistochemical studies showed tumor cells to be strongly positive with S-100 protein and weakly positive with alpha-1-antichymotrypsin and vimentin. These findings offer further support for a neural origin for granular cell tumors.
Back↗
Ultraviolet irradiation induces c-fos but not c-Ha-ras proto-oncogene expression in human epidermis.
The link between sun exposure and skin cancer is well established, but the mechanism of photocarcinogenesis is still incompletely understood. In vitro experimentation has shown that induction of the c-fos proto-oncogene occurs in cultured human keratinocytes after ultraviolet exposure, and c-Ha-ras mutations are commonly present in human skin neoplasms removed from chronically sun-exposed sites. In the present study, the effect of UV irradiation on the expression of these two proto-oncogenes was examined. The sun-protected volar forearm of six subjects was exposed to a standardized erythemogenic dose of solar-simulated light, and punch biopsies were obtained after 1 h and 24 h from the irradiated area and a nearby shielded area. Expression of c-fos, determined by in situ hybridization of histologic cross-sections, was detected in the basal and lower epidermal layers in all biopsies. However, at 1 h there was a marked increase that returned to baseline by 24 h. c-Ha-ras mRNA could not be detected by riboprobe hybridization in any of the biopsy specimens. Our data demonstrate transient induction of c-fos but not c-Ha-ras expression, at least at the timepoints studied, following a modest UV exposure in normal skin. This phenomenon may lead to the subsequent constitutive over-expression and super-inducibility of c-fos observed in cultured keratinocytes derived from photodamaged skin and may facilitate the development of skin cancer.
Aged↗
Epidermal differentiation enhances CRABP II expression in human skin.
The cellular retinoic acid-binding proteins (CRABP I and II) are thought to mediate the effects of retinoic acid on target cells. We have used riboprobes complementary to CRABP I and II mRNAs to study the expression of these messages in normal and abnormal human skin. CRABP II was expressed predominantly in the suprabasal layers of the epidermis, with stronger expression in newborn than in sun-protected adult skin. Interestingly, the epidermis adjacent to or overlying squamous cell or basal cell carcinomas also showed strong expression, whereas the tumor cells were negative, with the exception of more differentiated cells surrounding the "keratin pearls" within squamous cell carcinomas. CRABP II mRNA was also found in the more differentiated cells of the hair follicles, in the outer root sheath. CRABP I message was undetectable in the epidermis or in the dermis of normal skin but was detected in the cells of the papillary dermis surrounding basal and squamous cell carcinomas. These data suggest that increased levels of CRABP II mRNA accompany keratinocyte differentiation in vivo.
Adult↗
Giant folliculosebaceous cystic hamartoma.
We report a case of a giant cystic cutaneous adnexal hamartoma which showed fibrofollicular units embedded in the stroma with aberrant fat tissue. There were many sebaceous lobules in the fibrofollicular units, and its histologic features were consistent with conventional folliculosebaceous cystic hamartoma. Given the unique clinical history and appearance, this lesion is considered to be a congenital variant.
Adult↗
Three modes of melanosome transfers in Caucasian facial skin: hypothesis based on an ultrastructural study.
The transfer mechanism of melanosome from the melanocyte into the keratinocyte was investigated in mildly photodamaged Caucasian facial skin by electron microscopy. Three ways of transfer are suggested by our observations. The first mechanism probably occurs through the following process: 1) protrusion and insertion of the thick dendrite of the melanocyte into the basal keratinocyte, 2) formation of sac-dendrite complex in the subnuclear region, 3) digestion and segregation of the enclosed dendrite, 4) formation of the cistern in the paranuclear region, and 5) pinching-off of the melanosomes in single or aggregated form from the tip of the cistern. The second mechanism probably takes place through a membrane fusion between the melanocyte and the keratinocyte. Such a membrane fusion possibly forms a passage way for release of the melanosome from the former cell to the latter. The third mechanism is considered to include exocytosis of the single melanosome from the melanocyte followed by the endocytosis through the formation of coated-pit in the keratinocyte.
Adult↗
Evaluation of the photoprotective effect of oral vitamin E supplementation.
BACKGROUND AND DESIGN: Solar-induced cutaneous damage is mediated partly via oxidative pathways. Some evidence exists for a photoprotective role of antioxidants. In a double-blind, placebo-controlled study, we examined the effect of a long-term, orally administered antioxidant against UV-induced epidermal damage. Healthy human subjects supplemented their usual diet daily with either 400 IU of oral vitamin E (alpha-tocopherol acetate) or placebo over a 6-month period. Minimal erythema dose and histologic response to threefold minimal erythema dose exposure were determined at baseline, 1 month, and 6 months. RESULTS: The minimal erythema dose did not vary substantially at the three time points within each treatment group or in the vitamin E-supplemented group vs the placebo group. The number of sunburn cells produced by a threefold minimal erythema dose exposure was also not significantly different between the two groups. Of note, however, vitamin E levels in plasma increased only modestly and in skin biopsy specimens were unchanged following 1 month and 6 months of supplementation. CONCLUSIONS: No clinical or histologic difference in the response to UVB could be detected between the placebo and vitamin E-supplemented groups. In this small study, daily ingestion of 400 IU of oral alpha-tocopherol daily does not provide meaningful photoprotection.
Administration, Oral↗
Computerized video image analysis in dermatopathology.
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Computer Systems↗
A unique case of apocrine carcinoma on the male pubic skin: histopathologic and ultrastructural observations.
We report a case of cutaneous adenocarcinoma on the pubic region of a 56-year-old male. The exophytic tumor showed solid, ductal, and glandular patterns with decapitation secretion and mucinous carcinoma-like nests. Despite the exophytic nature of the lesion, an invasive growth pattern into the deep dermis and subcutaneous fat was seen. An additional characteristic of this tumor was the presence of Paget's phenomenon. From these findings, we conclude that this tumor is an apocrine adenocarcinoma having an unusual clinical appearance and unique histopathological features which have some similarities to apocrine carcinoma of the breast and some to syringocystadenoma papilliferum and nipple adenomatosis.
Adenocarcinoma↗
Cytoskeletal events underlying dendrite formation by cultured pigment cells.
In contrast to neurite outgrowth, pigment cell dendrite formation is relatively unstudied. Keratinocyte-conditioned medium (KCM) induces a striking dendricity in human melanocytes and B16 melanoma cells that is detectable within 30 min, maximal in 24-48 hr, and quantifiable by computerized image analysis. Cytochalasin B (CB), known to disrupt actin microfilaments, completely blocks dendrite formation if added to cultures before or with KCM. This effect is rapidly reversible, and dendrites appear within 1 hr after refeeding with KCM alone. In contrast, CB treatment fails to disrupt existing dendrites previously induced by KCM. Agents known to cause microtubule disassembly (colchicine, nocodazole, or vinblastine) do not inhibit dendrite formation if added before or with KCM. In contrast, these agents disrupt established dendrites. Inhibition of protein synthesis with cycloheximide or actinomycin D completely blocks dendrite formation, but if cultures are provided fresh KCM lacking protein synthesis inhibitors, dendrites reappear within 24 hr. Actin microfilaments visualized with a monoclonal antibody or rhodamine-phalloidin are poorly organized in untreated cells, but form numerous fibers localized along dendrites in KCM-treated cells. Microtubules visualized with a monoclonal anti-tubulin antibody are localized in the center of dendrites. These cytoskeletal changes occur without altering beta actin or beta tubulin mRNA levels. Taken together, these data implicate actin microfilaments in dendrite outgrowth, but not in maintenance, and conversely microtubules in dendrite maintenance but not in formation. These keratinocyte-induced changes involving beta actin and beta tubulin polymerization appear to require both new protein synthesis and post-translational regulation. The observed similarities between melanocytes and other neural crest-derived cells suggest that cutaneous pigment cells might serve as an alternative model for studies of neurite outgrowth.
Actins↗