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S S Roper

Publications and source records attributed to S S Roper.

3 recordsLinked to original sources
PubMed1985

Cutaneous histiocytosis syndromes.

Cutaneous histiocytosis may take two principal forms. It is either a benign proliferative process or a relentless, progressive process with a poor prognosis. In histiocytic medullary reticulosis, histiocytes demonstrate nuclear atypia and the outcome is uniformly fatal. Benign cephalic histiocytosis X causes lesions similar to those of histiocytosis X, but Langerhans' cells are absent. In congenital self-healing histiocytosis X, the Letterer-Siwe-like cutaneous infiltrate contains Langerhans' cells, but the lesions heal spontaneously without treatment. The nodular cutaneous lesions of juvenile xanthogranuloma appear in infancy and resolve without treatment; however, the higher percentage (10%) of associated ocular lesions may lead to glaucoma and blindness. In histiocytosis X, the cutaneous lesions show a marked proliferation of Langerhans' cells, with prognosis dependent on the patient's age and the extent of organ dysfunction. Patients who survive the acute form of the disease may develop diabetes insipidus, growth retardation, pulmonary fibrosis, and biliary cirrhosis. A subtle immunologic defect has been identified in patients with histiocytosis X, yet the pathogenesis of the disease is still speculative. Familial disease occurring in early infancy should be differentiated from complete or partial immunodeficiency syndromes. Guidelines for evaluating patients with cutaneous histiocytosis are reviewed.

Adult↗
PubMed1985

An animal model for altering the irritability threshold of normal skin.

Theory behind conditioned hyperirritability (autoeczematization) predicts the lowering of the irritation threshold in the presence of a pre-existing dermatitis. We have attempted to develop an animal model that parallels the syndrome seen in man. Groups of 10 guinea pigs were shaved and depilated; irritation thresholds to benzalkonium chloride and trichloroacetic acid were determined using 1 cm diameter open patches. Reactions were scored 24 h later on the basis of erythema and induration. Animals having as little as 1.56 cm2 of skin acutely inflamed with a known irritant had lowered irritation thresholds to the same irritant on normal skin at remote sites (p less than 0.01). Mild irritation of a much larger surface area produced the same effect (p less than 0.01). More extensive, severe dermatitis did not lower the irritation threshold further. Acute dermatitis induced by a contact allergen (DNCB) lowered the irritation threshold of normal skin to the same level as that obtained with irritants (p less than 0.01). Induction of chronic cutaneous ulcers 3-4 cm in diameter lowered the irritation threshold of normal skin to the same point defined by the acute studies (p less than 0.01). These results indicate that an acute irritant or contact dermatitis, as well as chronic skin ulceration, may alter the reactivity of unaffected normal skin to exhibit a heightened response to irritation. This model appears to differ from that seen in humans, in that a more extensive or chronic dermatitis did not further heighten the susceptibility to irritation.

Animals↗