bromochloroacetic-acid and Neurodermatitis

Lichen amyloidosus (LA) is generally said to be a pruritic type of amyloidosis of unknown cause. Histopathologically, it is characterized by epidermal changes of lichen simplex chronicus and by deposits of amyloid in the papillary dermis that are derived from keratin peptides of necrotic keratinocytes. Chronic scratching is responsible for the development of lichen simplex chronicus and may lead to necrosis of individual keratinocytes.. Our purpose was to evaluate whether chronic scratching may also be responsible for the formation of amyloid in LA.. We studied patients with LA in regard to histopathologic findings, onset of pruritus, associated diseases, and response to treatment.. In most cases, pruritus had preceded the skin lesions. Eight of nine patients suffered from diseases other than LA that may be associated with pruritus. Histopathologically, amyloid was confined to areas that also showed signs of lichen simplex chronicus. Systemic treatment with sedating antihistamines and intense local treatment with corticosteroids were found to be effective.. LA is considered to be a variant of lichen simplex chronicus in which scratching leads to necrosis of keratinocytes and eventually to the formation of amyloid in the papillary dermis. Because chronic scratching seems to be the cause and not the result of the deposits of amyloid, treatment should be directed at the amelioration of pruritus.

Topics: Administration, Cutaneous; Adrenal Cortex Hormones; Aged; Amyloid; Amyloidosis; Antipruritics; Chronic Disease; Collagen; Disease; Female; Histamine H1 Antagonists; Humans; Keratinocytes; Keratins; Keratosis; Leg Dermatoses; Male; Middle Aged; Necrosis; Neurodermatitis; Pruritus; Remission Induction; Skin; Skin Diseases

Electron microscopic analyses of lichen simplex chronicus Vidal (LSC) are reported. The submicroscopic organization is described. The frequent occurrence of collagen fibres directly juxtaposed to and contiguous with the lamina basalis seems to be a distinguishing feature of the LSC. Discontinuations in the lamina basalis are rarely indicated. A ubiquitous fragmentation and a certain paucity of tonofilamentous structure are present in cells preceding parakeratosis. There is an indubitable paucity of tonofilament-keratohyalin association. Mitochondria, endoplasmic reticulum and ribosomes are abundant. Odland bodies of type II are completely dominant. Parakeratosis and observed submicroscopically deficient or incomplete orthokeratosis are related to the numbers of defective Odland bodies. The keratinization of some acanthotic disorders is discussed.

Topics: Adult; Collagen; Epidermis; Humans; Keratins; Male; Middle Aged; Neurodermatitis; Syndrome

The rate and pattern of epidermal lipogenesis from [14C] glucose were measured in fifteen patients with psoriasis and three with lichen simplex, compared with twenty controls. In 'uninvolved' epidermis from psoriatic subjects the mean lipogenic rate was slightly raised, although the increase was not statistically significant. There was a positive correlation between overall lipogenic rate and the percentage of isotope appearing in free sterol, while the relative proportions of the other lipid classes were unchanged. By contrast, in control epidermis sterol percentage was negatively correlated with lipogenic rate. In psoriatic lesions total epidermal lipogenesis (per unit surface area) was raised compared with matched control 'uninvolved' epidermis. Also raised were percentage labelling of free sterol and of combined (free sterol and monoesters), and the free sterol: monoester ratio was increased. Similar findings were obtained with lesions of lichen simplex, suggesting that disturbed sterol metabolism may be a common feature in conditions of abnormal keratinization.

Topics: Adolescent; Adult; Aged; Esters; Female; Glucose; Humans; Keratins; Lipids; Male; Middle Aged; Neurodermatitis; Psoriasis; Skin; Sterols; Syndrome

Topics: Adolescent; Child; Drug Therapy; Geriatrics; Griseofulvin; Keratins; Leg Ulcer; Neurodermatitis; Pharmacology; Psoriasis; Tinea