Biomedical subjects
Publications and source records attributed to S Kossard.
A 52-year-old woman who developed a pale sclerotic second left toe with loss of the nail plate is described. Biopsy showed changes of lichen sclerosus. There were no other skin or genital lesions present.
A 54-year-old woman had a 3 year history of a recurrent bilateral axillary rash during the summer months. Both axillae showed hyperkeratotic, fissured and cobblestone plaques. Skin biopsy showed the histology previously defined as axillary granular parakeratosis. This finding may indeed represent an unusual contact reaction to anti-perspirants interfering with epidermal keratinization.
In this two-part series we review the acquired scalp alopecias. A broad spectrum of diseases result in alopecia. In this first part we provide a framework for the assessment and diagnosis of scalp hair loss, and begin covering the individual conditions. The non-scarring alopecias covered include effluvium, androgenetic alopecia, alopecia areata, trichotillomania, and loose anagen syndrome. The scarring alopecias cause permanent pilosebaceous follicle loss; the lymphocyte-associated scarring alopecia described encompasses lichen planopilaris, discoid lupus erythematosus, pseudopelade, and follicular mucinosis. Part II will cover the neutrophil-associated and infiltrative processes causing scarring alopecia followed by the medical management of alopecia. There is particular reference to newly described conditions and progress in the understanding of older conditions. More recently characterized conditions include the loose anagen syndrome, chronic telogen effluvium, and the frontal fibrosing variant of lichen planopilaris.
We report a 70-year-old woman who over a 7-year period developed a widespread violaceous, reticulate and striate eruption with a keratotic component in a clinical pattern previously described as keratosis lichenoides chronica. Multiple biopsies showed a lichenoid reaction centred over the acrosyringium and eccrine ducts entering the epidermis. The acrosyringeal ducts were surrounded by an epidermis that was associated with saw-tooth acanthosis. The ducts displayed hypergranulosis and keratin plugs that extended into the stratum corneum. In the upper dermis the eccrine ducts showed squamous metaplasia with liquefaction of degeneration of their basal cells as well as apoptotic keratinocytes. The subepidermal acrosyringial zone and the eccrine ducts were associated with lymphocytic inflammation and fibrosis. These histopathological findings may represent the counterpart of lichen planopilaris targeting the eccrine ducts. The clinical features defining keratosis lichenoides chronica probably represents a heterogeneous group of conditions including this distinctive subset of lichen planus which we have termed lichen planoporitis.
BACKGROUND: Lichen planopilaris usually produces multifocal areas of scarring alopecia. Recently, a condition in postmenopausal women characterized by progressive frontal hairline recession associated with scarring has been described. OBJECTIVE: Our purpose was to study the clinical and histopathologic features and results of treatment in a group of women with the frontal variant of lichen planopilaris and to compare the immunohistochemical profile of scalp biopsy specimens from this subset with that found in the multifocal variant of lichen planopilaris. METHOD: The clinical data as well as the histopathologic findings in 16 women with frontal fibrosing alopecia were collated. The immunohistochemical profile of six scalp biopsy specimens from the frontal hairline were compared with six specimens from women with multifocal lichen planopilaris. RESULTS: In addition to the progressive frontal fibrosing alopecia in all 16 women, total loss or a marked decrease of the eyebrows was observed in 13. No evidence of lichen planus was observed at other sites. In one patient multifocal areas of lichen planopilaris developed in the scalp. The frontal fibrosing alopecia was slowly progressive but has stabilized in five patients. Biopsy specimens from the frontal hairline showed histologic changes identical to lichen planopilaris. Immunophenotyping failed to reveal any significant differences between the frontal and multifocal variants. No effective treatments emerged although oral steroids and antimalarials may temporarily slow the course. Hormone replacement therapy did not appear to influence the course of the alopecia. CONCLUSION: Progressive frontal fibrosing alopecia is a clinically distinct variant of lichen planopilaris that affects in particular elderly women and frequently involves the eyebrows. The basis for this lichenoid tissue reaction targeting frontal scalp follicles and eyebrows is unknown.
One hundred and thirty-one small cell melanomas were reviewed with respect to clinical data submitted with each specimen and the histological pattern of each tumour. Of the small cell melanomas, 80% developed in individuals over the age of 50 years. There was a 2:1 male predominance with 58% of the tumours in men occurring on the back. All but one melanoma showed a lentiginous intraepidermal pattern. The dermal component was characterized by cords and nests of hyperchromatic melanocytes associated with interstitial fibrosis. Small cell melanomas may be recognized as thin lesions and are commonly located in chronic sun-damaged skin of elderly individuals. They may represent a special naevoid variant of lentigo maligna melanoma.
A 79-year-old man presented with a pigmented nodule on the right ear which, on epiluminescence microscopy, demonstrated a diffuse grey-blue colour. Skin biopsy revealed an irregularly acanthotic epidermis with lobular clusters of atypical keratinocytes that projected into the dermis in the pattern of an invasive squamous cell carcinoma. Numerous dendritic melanocytes were present throughout the lesion. Although the close relationship between the highly dendritic intra-epidermal melanocytes and the atypical keratinocytes raised the issue of whether this tumour represented a malignant melanoacanthoma, the authors considered the lesion to be better classified as an unusual variant of pigmented squamous cell carcinoma.
Liver disease is now a well recognized association with lichen planus. Recent reports suggest that the hepatitis viruses may play a central role in this association. The present report describes a case of a lichenoid reaction to hepatitis B vaccination, which has only been rarely documented previously. A 16-year-old male developed a widespread pruritic erythematous eruption 5 weeks after receiving his second dose of hepatitis B vaccine. The eruption evolved to produce strikingly blue macules before spontaneously disappearing. A skin biopsy showed an intense lichenoid reaction. The hepatitis B surface antigen component of the vaccine is probably responsible for this reaction as well as for other rare immunologically mediated reactions to hepatitis B vaccination. These reactions may provide insight into the pathogenesis of the cutaneous features of natural hepatitis B infection.
The authors describe a 30-year-old woman who over 2 years had a persistent papulopustular follicular eruption on the face. Skin biopsy showed eosinophilic folliculitis and there was a rapid response to indomethacin.
Blue nevus is a benign pigmented lesion of dermal melanocytes with a number of histologic and clinical variants, of which the major types are the common blue nevus, cellular blue nevus and combined nevus. This study describes 9 cases of hypopigmented blue nevus (HBN), a variant of common blue nevus in which there is minimal identifiable melanin pigment. We also discuss the usefulness of the immunoperoxidase stain HMB-45 in relation to the diagnosis of HBN and the lesions with which it may be histologically confused, namely common intradermal nevus, dermatofibroma, neurofibroma, dermal scar and desmoplastic malignant melanoma. The HMB-45 stain was found to be uniformly positive in all 9 cases of HBN, in contrast to the other dermal lesions which have been reported as either negative or showing only focal positivity. The physical distribution and age range of the patients in this study was similar to the age and sites for common BN, supporting the relationship between the 2 lesions. The occurrence of HBN in predominantly young adults indicates that this lesion is not a phenomenon due to ageing or degenerative change, and should be regarded as a variant of common blue nevus.
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Cutaneous reactions to vitamin K1 (phytomenadione) are uncommon. They can present as acute eczematous reactions or late reactions that resemble localized scleroderma after vitamin K1 injections. A case is reported here of a patient who developed bilateral sclerodermoid plaques in a cowboy's holster pattern, which persisted for more than 10 years after subcutaneous vitamin K1 injections. Positive intradermal test with vitamin K1 that persisted as an erythematous indurated plaque at the test site for more than 5 months confirmed marked cutaneous hypersensitivity to vitamin K1 in this patient. Serial biopsies of the erythematous plaque at the test site showed transition from spongiotic eczematous features initially to inflammatory morphoea-like histology over a 5 month period. Possible pathogenic mechanisms for phytomenadione-induced pseudoscleroderma are discussed.
The following case report is of a 49 year old man who presented with a 20 year history of small asymptomatic flesh coloured firm papules which were concentrated on his face, neck and upper trunk. The diagnosis of multiple fibrofolliculomas of the familial type was reached.
A 73 year old woman developed prurigo papules which were complicated by blisters. Skin biopsy and immunofluorescence revealed bullous pemphigoid. The diagnosis of pemphigoid nodularis was made.
A comparative immunohistochemical study was performed on skin biopsies from 10 patients with lichen planus and 10 patients with discoid lupus erythematosus (DLE). A panel of antibodies against T lymphocytes (UCHL-1, OPD-4, CD8, CD43), B lymphocytes (L-26), granulocytes (Leu-M1), activation markers (Ki-1, LN-3), macrophages, fibroblasts and dendritic cells (FXIIIa, S-100, Mac-387, KP-1, vimentin), endothelial cells (CD34), and epithelial cells (epithelial membrane antigen) was employed using a peroxidase-anti-peroxidase technique. The recently released CD8 antiserum required microwave antigen retrieval of formalin-fixed, paraffin-embedded tissue to label lymphocytes. The results showed many similarities in the lymphocyte subsets and macrophages between lichen planus and discoid lupus erythematosus. The most important differences between the two conditions were statistically significant increases in the number of S-100+ cells in the epidermis and dermis, FXIIIa+ cells in the dermis and CD34+ vessels within the inflammatory infiltrate in lichen planus.
The author reports a 75-year-old man who developed a blue-black macule, which on biopsy showed sheets of deeply pigmented melanophages. This represents an example of tumoral melanosis that may be the result of complete regression of a melanoma.
The capacity of micro-organisms and infestations to induce flare or mimic a wide variety of dermatological disorders has long been appreciated. The development of new techniques such as in situ hybridization and the polymerase chain reaction has permitted a re-examination of old concepts such as the tuberculids and bacterids. In addition new discoveries have highlighted the biological potential of micro-organisms to stimulate or depress the immune system through potent biological active products and has led to new insights in the mechanisms through which organisms may produce skin changes. Histological simulants of dermatological disease may also be induced by micro-organisms and these may need to be distinguished by clinical correlation.
Merkel cell carcinoma of the skin usually has a trabecular, intermediate-cell or small-cell pattern of differentiation. We report the case of a 66-year-old man who developed a progressive multinodular plaque that showed a prominent desmoplastic component on preliminary biopsy. Immunohistochemical and ultrastructural studies and the final surgical specimen confirmed that the tumor was a Merkel cell carcinoma. The presence of desmoplasia may mask the diagnosis of Merkel cell carcinoma.