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Biomedical subjects

A R Rhodes

Publications and source records attributed to A R Rhodes.

At least 19 recordsLinked to original sources
PubMed1992

Mid-dermal elastolysis with inflammation.

A 71-year-old white woman had finely wrinkled, erythematous patches of skin that met the clinical and histologic criteria for mid-dermal elastolysis. In addition to the loss of mid-dermal elastin described in previous cases, histopathologic examination revealed a superficial and deep perivascular inflammatory infiltrate of lymphocytes and plasma cells and interstitial collections of multinucleated giant cells containing phagocytized elastin. These results support a previously postulated inflammatory pathogenesis for mid-dermal elastolysis.

Aged↗
PubMed1991

Sun-induced freckles in children and young adults. A correlation of clinical and histopathologic features.

Sun-induced freckles are a risk factor for epidermal and melanocytic neoplasia. Whereas sun-induced freckles in children and older adults may be clinically indistinguishable, and sun-induced freckles in older adults usually consist of increased numbers of intraepidermal melanocytes, the histology of sun-induced freckles in children remains unsettled. Using L-3,4 dihydroxyphenylalanine (DOPA)-paraffin sections, the authors examined six sun-induced freckles and adjacent nonpigmented skin (ANP) in as many white male subjects, ages 10 to 23 years. Melanocyte frequency was expressed as the ratio of DOPA-reactive melanocytes to total epidermal basal unit cells. For each case, melanocyte frequencies in freckles were significantly greater than in ANP. Cellular atypia of melanocytes was noticed in four of six freckles. Reactivity of melanocytes for HMB-45 was noticed in two freckles studied, compared with no reactivity in three specimens of ANP studied. The authors conclude the sun-induced freckles in the young may consist of a hyperplasia of melanocytes (i.e., similar to solar lentigines in the elderly), sometimes with cellular atypia, and that these findings may be relevant to melanocytic neoplasia.

Adolescent↗
PubMed1990

Dysplastic melanocytic nevi and cutaneous melanoma: markers of increased melanoma risk for affected persons and blood relatives.

Dysplastic melanocytic nevi are potential precursors of cutaneous melanoma and markers of increased risk. This article presents representative case histories that illustrate the usefulness of careful follow-up of persons who have dysplastic melanocytic nevi or cutaneous melanoma, as well as examination of their blood relatives for the same lesions. Identification and periodic examination of such high-risk persons may result in the detection of melanoma in a curable phase. Our observations suggest that (1) dysplastic melanocytic nevi may aggregate in families of persons who have dysplastic melanocytic nevi or melanoma, even in the absence of a family history of dysplastic melanocytic nevi or melanoma and (2) formal genetic and natural history studies of persons who have dysplastic melanocytic nevi outside the familial melanoma setting are warranted.

Adolescent↗
PubMed1990

Genital lentiginosis: a clinical and histopathologic study.

We studied the clinical and histopathologic characteristics of melanotic macules of the penis and vulva. The 10 lesions studied were relatively large (up to 2 cm), multifocal, irregular in outline, and had variegated pigmentation. Most were regarded as clinically atypical in appearance. Histologic examination of the lesions showed basal layer hyperpigmentation, slight melanocytic hyperplasia, epithelial hyperplasia, and stromal melanophages. No cytologic atypia of melanocytes was detectable. Information is insufficient at present to predict the natural history of genital lentiginosis or its relation to mucocutaneous melanoma.

Adult↗
PubMed1990

Cutaneous melanoma and bilateral retinoblastoma.

We report the case of an otherwise healthy 37-year-old man who had had bilateral enucleation during early childhood for bilateral retinoblastomas, in addition to two cutaneous melanomas (the first appearing at age 27 years). He also had dysplastic melanocytic nevi and a history of cutaneous melanoma in his mother. Retinoblastoma may aggregate in families and is associated with DNA abnormalities of chromosome 13. Recent reports have emphasized the appearance of second malignancies in retinoblastoma survivors. The second malignancies include osteosarcoma, soft tissue sarcoma, and cutaneous melanoma. Cutaneous melanoma also may aggregate in families, usually in the setting of dysplastic melanocytic nevi. The features of this case and of similar reported cases suggest that there may be a greater than expected association between retinoblastoma and cutaneous melanoma.

Adult↗
PubMed1990

Combined immunodeficiency associated with xeroderma pigmentosum.

We report a 15-month-old boy with xeroderma pigmentosum, a history of repeated infections, and immune deficiency who developed a fatal pneumonia with parainfluenza type 1. Immunologic evaluation revealed a severe combined immunodeficiency with hypoglobulinemia, C3 deficiency, anergic response to skin testing, and an abnormal lymphocytic response to mitogens. We suggest that patients with xeroderma pigmentosum be evaluated carefully for immune deficiencies, should repeated infections occur.

Agammaglobulinemia↗
PubMed1990

Origin of cutaneous melanoma in a congenital dysplastic nevus spilus.

Cutaneous melanoma developed in contiguity with a congenital nevus spilus on the leg of a 79-year-old white woman. The unique features of the nevus spilus in this case were its relatively large size (diameter, 8 cm), irregular gross appearance, lifelong stability until the recent appearance of a tumor nodule, and the presence of intraepidermal melanocytic dysplasia appearing as multifocal elements within darkly pigmented speckles distributed throughout a lightly pigmented background of lentigo simplex. Based on this observation, we suggest that the presence of intraepidermal melanocytic dysplasia in nevus spilus may be a predisposing factor for the development of melanoma. The malignant potential of "dysplastic" nevus spilus requires further study.

Aged↗
PubMed1989

Dysplastic melanocytic nevi: a reproducible histologic definition emphasizing cellular morphology.

Histologic criteria commonly used to diagnose dysplastic melanocytic nevi (DMN) have not been correlated adequately with biology nor subjected to rigorous reproducibility studies. To address these failings, we developed histologic definitions emphasizing cellular morphology based on the appearance of typical melanocytes in sun-protected buttock skin, fully-evolved atypia in the vertical component of metastasizing primary cutaneous melanomas, and slight and moderate degrees of atypia defined within these limits in selected varieties of DMN. Reproducibility of our histologic definitions were tested by using two pathologists working independently to assess single routine tissue sections of 19 melanocytic lesions on two occasions at least 6 mo apart. Lesions included five previously diagnosed primary invasive cutaneous melanomas, seven lesions selected for gross morphologic features characteristic of DMN, and four solar lentigines and three common acquired nevomelanocytic nevi preselected for typical appearance and stable growth history. For the primary pathologist using the grading scheme, agreement rates between first and second readings were 84% for final diagnosis and 79% for the highest degree of cellular atypia; for the secondary pathologist, agreement rates for first and second readings for both parameters were 84%. Agreement rates comparing second readings of final diagnosis and highest degree of cellular atypia by the two pathologists were 89% and 79%, respectively. Most of the architectural and host response features commonly associated with DMN were less reproducible. In conclusion, we demonstrated very good reproducibility of histologic definitions used to differentiate the intraepidermal component of DMN from that of melanoma and benign melanocytic and nevomelanocytic hyperplasias, based on a biologic correlation emphasizing cellular morphology. Reproducible histologic definitions are a requisite first step in defining a clinical-pathologic correlation for DMN.

Adolescent↗
PubMed1988

Melanosomal alterations in dysplastic melanocytic nevi. A quantitative, ultrastructural investigation.

Abnormal-looking melanosomes are observed commonly in both intraepidermal melanocytes of cutaneous melanoma and dysplastic melanocytic nevi (DMN). This was investigated by using transmission electron microscopic examination to determine the percentage of abnormal melanosomes among 8267 melanosomes assessed in at least five solitary intraepidermal basal unit melanocytes from each of five specimens of DMN, superficial spreading melanoma (SSM), common acquired nevomelanocytic nevi (NMN), and normal skin (NS) adjacent to DMN. The percentage of abnormal melanosomes in DMN (mean + SD, 44 + 23%) was seven times greater than that in NMN (6 + 7%) and 22 times greater than that in NS (2 + 5% [P less than 0.001, both comparisons]), but only 80% that in SSM (57 + 19% [P less than 0.02]). Melanocyte area, nuclear area, and the ratio of nuclear area to cytoplasmic area did not account for the observed differences. Melanosomal alterations may be a useful marker of atypicality in melanocytic tumors.

Adult↗
PubMed1987

Risk factors for cutaneous melanoma. A practical method of recognizing predisposed individuals.

Cutaneous melanoma is rapidly becoming a potentially curable cancer if it is detected and properly treated in an early phase of development. Unlike other cancers, which are usually hidden from detection until they are relatively large or metastatic disease has occurred, cutaneous melanoma is readily detectable simply by examining the skin. Information is now available that will be useful in selecting individuals at greatest risk. The most important melanoma risk factors (in decreasing order of importance) for a given individual are as follows: a persistently changed or changing mole, adulthood, irregular varieties of pigmented lesions (including dysplastic moles and lentigo maligna), a congenital mole, Caucasian race, a previous cutaneous melanoma, a family history of cutaneous melanoma, immunosuppression, sun sensitivity, and excessive sun exposure. Selective screening and appropriate treatment of individuals who have these risk factors may reduce the morbidity and mortality of cutaneous melanoma.

Adult↗
PubMed1986

Disseminated intravascular coagulation and purpura fulminans in a patient with Candida sepsis. Biopsy of purpura fulminans as an aid to diagnosis of systemic Candida infection.

Disseminated intravascular coagulation and purpura fulminans developed in association with septicemia and meningitis due to Candida tropicalis in an 18-year-old female immunosuppressed renal allograft recipient. Although systemic Candida infection was initially suspected, blood cultures showed no growth of this organism until after its identification in the dermis of a skin biopsy specimen obtained from the site of purpura fulminans. This case illustrates the association between Candida sepsis and purpura fulminans, and demonstrates the usefulness of skin biopsy of purpura fulminans in the early diagnosis of Candida sepsis.

Adolescent↗
PubMed1986

Melanocytic precursors of cutaneous melanoma. Estimated risks and guidelines for management.

There are several recognizable melanocytic precursors of cutaneous melanoma. These precursors include lentigo maligna, dysplastic melanocytic nevi, congenital nevi (of any size), and darkly pigmented lesions of acral surfaces and mucous membranes. Lentigo maligna is an uncommon melanocytic dysplasia, present in 3 per 1000 individuals over the age of 50 years and accounting for 4 percent of all cutaneous melanomas. Dysplastic melanocytic nevi are present in 2 per cent of white adults, and may account for at least a fifth of cases of cutaneous melanoma. Congenital nevomelanocytic nevi are present in 1 per cent of newborns; the vast majority of congenital nevi are smaller than 3 to 4 cm in diameter, while very large congenital nevi are present in 1 in 20,000 to 1 in 500,000 newborns. Very large congenital nevi account for less than 0.1 percent of cutaneous melanomas, whereas small varieties of congenital nevi may account for 15 percent of cutaneous melanomas. If individuals with lentigo maligna live long enough, possibly a third to a half are said to develop melanoma. This figure may be biased high. Persons with dysplastic melanocytic nevi in the familial melanoma setting have an estimated lifetime risk of developing melanoma approaching 100 per cent. Persons with dysplastic melanocytic nevi in other settings may have a lifetime melanoma risk of 18 per cent. Persons with congenital nevi of any size may have a lifetime melanoma risk of at least 5 per cent. Early recognition of these precursor melanocytic tumors, particularly in high-risk individuals (i.e., those with a personal or family history of melanoma), and careful photographic follow-up or prophylactic excision of these lesions may be the most effective means of reducing the morbidity and mortality of cutaneous melanoma. The impact of routine screening and excision of presumed melanoma precursors is unknown. Clinical judgment is required to balance the theoretical risk of melanoma associated with a given precursor and the known risks of surgery and anesthesia for a given individual. It must be kept in mind that the vast majority of acquired melanocytic nevi in adults are harmless. Probably even the majority of dysplastic nevi and small congenital nevi will remain unchanged throughout life. The simple recognition of the existence of melanoma precursors will heighten suspicion for these lesions and raise awareness of the earliest signs of malignant change.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Congenital arrector pili hamartoma. A case report and review of the spectrum of Becker's melanosis and pilar smooth-muscle hamartoma.

Congenital pigmented arrector pili hamartomas are unique malformations of epidermis and pilar apparatus usually appearing as localized, lightly pigmented, hairy plaques. Characteristic microscopic features include smooth-muscle proliferation similar to irregularly disposed arrectores pilorum, and slight elongation of epidermal rete with hypermelanosis of the basal unit. An otherwise normally developed child who had this hamartoma at birth is described in an attempt to clarify the relationship between pilar smooth-muscle hamartomas and Becker's melanosis. We propose that these two entities belong at different poles of the same developmental spectrum of hamartomatous change.

Diagnosis, Differential↗