bromochloroacetic-acid has been researched along with Pruritus* in 8 studies
8 other study(ies) available for bromochloroacetic-acid and Pruritus
Article | Year |
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Keratin defects trigger the itch-inducing cytokine thymic stromal lymphopoietin through amphiregulin-epidermal growth factor receptor signaling.
Topics: Amphiregulin; Animals; Cytokines; ErbB Receptors; Humans; Keratins; Mice; Mice, Knockout; Pruritus; Signal Transduction; Thymic Stromal Lymphopoietin | 2019 |
[A rare tumor of the main biliary duct].
Topics: Abdominal Pain; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Common Bile Duct Neoplasms; Female; Humans; Jaundice, Obstructive; Keratins; Leukemia, Myeloid, Acute; Middle Aged; Peroxidase; Proto-Oncogene Proteins c-kit; Pruritus; Sarcoma, Myeloid; Vimentin | 2010 |
Clinical and immunohistochemical study of the effect of a cosmetic product in patients with asteatotic eczema.
Cutaneous xerosis is a common clinical condition associated with an altered barrier function of the stratum corneum. Xerotic skin appears dry, rough and slightly scaling. Patients complain of pruritus and stinging. Our aim was to investigate the clinical effects of a cosmetic ointment (Scherilan) in patients with circumscribed senile xerosis (also called asteatotic eczema). Moreover, variations in expression of epidermal proteins such as keratin (K)-5 and involucrin, detected by immunohistochemistry, were also evaluated before and after topical treatment. We enrolled 30 patients (11 males, 19 females) with asteatotic eczema. We examined dryness, roughness and desquamation and symptoms such as itching and dryness. A score of 0 to 3 was assigned to each of these parameters. A biopsy was performed in seven patients before and after a 21-day topical treatment. All skin specimens were then immunostained with antibodies to K5 and involucrin. At day 7 or 21 of treatment all signs of xerosis and pruritus were significantly reduced; furthermore, the reduction increased with the duration of therapy. Before treatment K5 was strongly expressed in stratum basale (SB) and stratum spinosum (SS), while involucrin was strongly expressed in stratum granulosum (SG) and the upper portion of SS. In contrast, after treatment immunostaining for K5 was restricted to SB and the lower part of SS, while involucrin showed intense staining in SG. We highlight the importance of treating cutaneous xerosis with an ointment such as this one, which probably induces an increase of lipid content of the SC intercellular matrix. Topics: Aged; Biopsy; Cell Proliferation; Cosmetics; Eczema; Epidermis; Female; Glycolates; Humans; Immunohistochemistry; Keratin-5; Keratins; Lipid Metabolism; Lipids; Male; Middle Aged; Ointments; Protein Precursors; Pruritus; Skin Diseases; Time Factors; Treatment Outcome; Vitamin E | 2005 |
Epidermal hyperproliferation and decreased skin barrier function in mice overexpressing stratum corneum chymotryptic enzyme.
Stratum corneum chymotryptic enzyme (SCCE; also known as kallikrein 7) is a serine protease that may have an important role in the skin desquamation process. We have recently described transgenic mice overexpressing human SCCE in suprabasal epidermal keratinocytes, leading to increased epidermal thickness, hyperkeratosis, dermal inflammation and signs of severe pruritus in older animals. In order to further evaluate the scce-transgenic mice as a potential disease model, we compared transgenic animals and wild-type littermates for patterns of epidermal keratin expression, in situ hybridization of scce-mRNA, scratching behaviour and measurements of transepidermal water loss (TEWL). In 3-day-old mice, despite readily detectable amounts of human scce-mRNA in the epidermis of transgenic animals, there were no histological differences in skin appearance, and no differences could be found in epidermal expression of the keratins 5, 6 and 10. In mice 7-8 weeks of age and older, there was strong suprabasal expression of keratins 5 and 6 in the epidermis of transgenic animals, suggesting that the thickened epidermis in these animals is the result of keratinocyte hyperproliferation. In transgenic animals 11 weeks of age and older there was an increased frequency of scratching, suggestive of pruritus, and also signs of a deteriorating skin barrier function, as reflected by an increased TEWL. There was no correlation between increased TEWL and increased frequency of scratching in individual animals, suggesting that the defect barrier function was not an effect of skin damage caused by scratching. Topics: Animals; Body Water; Epidermis; In Situ Hybridization; Kallikreins; Keratinocytes; Keratins; Mice; Mice, Transgenic; Pruritus; Serine Endopeptidases; Skin Physiological Phenomena | 2004 |
IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE/stat6 under specific pathogen-free conditions.
Atopic dermatitis (AD) is a pruritic inflammatory skin disease. Because IL-18 directly stimulates T cells and mast cells to release AD-associated molecules, Th2 cytokines, and histamine, we investigated the capacity of IL-18 to induce AD-like inflammatory skin disease by analyzing KIL-18Tg and KCASP1Tg, which skin-specifically overexpress IL-18 and caspase-1, respectively. They spontaneously developed relapsing dermatitis with mastocytosis and Th2 cytokine accumulation accompanied by systemic elevation of IgE and histamine. Stat6-deficient KCASP1Tg displayed undetectable levels of IgE but manifested the same degree of cutaneous changes, whereas IL-18-deficient KCASP1Tg evaded the dermatitis, suggesting that IL-18 causes the skin changes in the absence of IgE/stat6. KIL-18Tg and IL-1-deficient KCASP1Tg took longer to display the lesion than KCASP1Tg. Thus, AD-like inflammation is initiated by overrelease of IL-18 and accelerated by IL-1. Our present study might provide insight into understanding the pathogenesis of and establishing therapeutics for chronic inflammatory skin diseases including AD. Topics: Animals; Dermatitis, Atopic; Humans; Immunoglobulin E; Inflammation; Interleukin-18; Keratins; Mice; Mice, Transgenic; Promoter Regions, Genetic; Pruritus; Rabbits; Signal Transduction; Specific Pathogen-Free Organisms; STAT6 Transcription Factor; T-Lymphocytes; Th2 Cells; Trans-Activators | 2002 |
Lichen amyloidosus: a consequence of scratching.
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 | 1997 |
A particular subtype of ichthyosis congenita type III. Clinical, light, and electron microscopic features.
We report the case of a second patient with the extraordinary ultrastructural findings of vacuolated structures intermingled with membranes in the perinuclear part of the upper epidermal cells. Clinical, light microscopic, and electron microscopic features of this particular presentation of ichthyosis congenita type III have already been presented by K. M. Niemi and L. Kanerva in 1989. Although our patient has more or less the same light and electron microscopic findings, the clinical picture is more severe. The patient was born as a collodion baby. Later, he showed signs of generalized severe involvement with large scales, erythrodermia, and itching. Successful therapy with retinoids resulted in complete removal of the hyperkeratosis but left the striking reticulate skin pattern. Noting the heterogeneous clinical presentation, the specific electron microscopic findings are diagnostic. No biochemical data on this disease are known. Topics: Adult; Cell Nucleus; Cytoplasmic Granules; Dermatitis, Exfoliative; Dermatologic Agents; Epidermis; Humans; Hyalin; Ichthyosis; Keratins; Keratosis; Male; Microscopy, Electron; Mitochondria; Pruritus; Retinoids; Skin; Vacuoles | 1995 |
The cutaneous amyloidoses. I. Localized forms.
Topics: Adult; Aged; Amyloid; Amyloidosis; Collagen; Diagnosis, Differential; Female; Forearm; Humans; Keratins; Leg Dermatoses; Lichen Planus; Lipidoses; Male; Melanins; Middle Aged; Pruritus; Skin; Skin Diseases; Skin Neoplasms; Staining and Labeling | 1970 |