Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

'Ageing is a multistep, multifaceted, time-dependent phenomenon characterized by the decreased ability of a system to respond to exogenous and endogenous stress from either physical, chemical or biologic agents'. Cutaneous ageing provides a visible model of the interaction between endogenous (intrinsic) factors and exogenous (extrinsic) factors. In skin, the principal extrinsic-factor is ultraviolet light (UV) which is responsible for the constellation of changes termed photoageing. In recent years, much interest has been directed towards defining the ageing processes in skin and excellent comprehensive reviews have been compiled. This review aims to highlight several areas of developing knowledge, and focuses on the potential importance of environmental changes as they influence skin ageing and carcinogenesis. Repeated reference to the effects of UV on the skin are inevitable in any review of skin ageing and this is scarcely surprising as the skin contains many cells as well as subcellular and extracellular chromophores which are capable of absorbing energy within the UV spectrum. Cellular chromophores include among others keratinocytes, melanocytes, Langerhans cells, dermal fibroblasts and mast cells. Subcellular chromophores include keratin, melanin, collagen, elastin and a number of proteins, lipids and steroids (such as vitamin D). Urocanic acid, a photoisomerization product of the amino-acid histidine, may provide some limited photoprotection and some believe it to be important in UV induced immunosuppression. Understanding events at the molecular and biochemical level has unfortunately not been paralleled by clinical advances and the common, troublesome skin-problems of old age such as cancer, xerosis and pruritus remain a major cause of morbidity and yet are poorly explained.
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PMID:Aspects of cutaneous ageing. 179 84

We report the case of a 20-year old male patient without significant familial or personal history who presented with a disseminated papular eruption on the abdomen, flanks and buttocks. The eruption was continual and proceeded by outbreaks, but it was not influenced by seasons. Physical examination of the skin, mucosae and skin appendages was otherwise normal. Histological examination showed all the criteria of perforating folliculitis as described by Mehregan and Coskey. On the basis of our case we would put perforating folliculitis back among the perforating dermatoses. The concept of this curious phenomenon is briefly reviewed; perforating folliculitis is part of the third group of the so-called primary forms. The clinical features are suggestive of the disease, with its small pigmented papules centred around a keratotic plug, forming a permanent disseminated eruption. Histology shows a granuloma facing a lateral perforation of the hair follicle, a pseudo-epitheliomatous epithelial hyperplasia and the presence of hair and keratin debris in the perforation. Various keratolytic treatments have been applied without success; retinoids have not been tried. The main diagnostic and nosological problem is Kyrle's disease. In view of clinical and histological data, many authors regard Kyrle's disease as a major form of perforating folliculitis. Pruritus, ascribed to an underlying illness in Kyrle's disease, is thought to increase the importance of the lesions. The specificity of perforating folliculitis is discussed, but it seems that side by side with secondary forms occurring in recognized diseases, there may be primary forms of perforating folliculitis. Dyskeratosis might be a cause of the perforation.
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PMID:[Perforating folliculitis]. 224 Oct 24

Kyrle's disease is a chronic, genetically determined, hyperkeratotic disorder occurring in the middle forties. We report fourteen cases of this disorder in a population of 1.5 million over a period of 15 years. We observed a female/male ratio of 6:1. Straw-colored keratotic plugs and flat scale show a marked predisposition for the calf, the tibial region, and the posterior part of the thigh. They vary in size from 1 to 4 mm, and there is occasional plaque formation. No koebnerization or pruritus was noted, and no statistically significant association with hepatic, renal, or diabetic disorders could be demonstrated. Microscopic features showed a consistent pattern of keratotic plug formation, with the plug sitting in an invaginated atrophic epidermis, and underlying dermal histiocyte and lymphocyte aggregation. All lesions contained orthokeratosis and parakeratosis, with some sections showing abnormal keratinization. Sodium dodecylsulfate gel electrophoresis did not demonstrate the presence of abnormal keratin bands.
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PMID:Kyrle's disease. 380 80

We report our experience in Singapore with the use of the new oral Retinoid-etretinate (Tigason RO 10-9359) in 23 patients suffering from various congenital disorders of keratinisation. In this study the drug was administered to 8 patients with Darier's disease, 7 patients with congenital ichthyosis, 4 patients with palmar plantar keratoderma, 2 patients with systematised epidermal naevus and 2 patients with progressive symmetrical erythrokeratoderma. The best results were obtained in patients with ichthyosis where complete clearance was possible. All patients with Darier's except one showed significant improvement. Palmar plantar keratoderma except for one patient gave only fair to minimal improvement. Etretinate was useful in systematised epidermal naevus and progressive symmetrical erythrokeratoderma. Pruritus and cheilitis were the commonest side effect. In two patients (both with Darier's disease) treatment was stopped because of side effects. The side effects were dose related. The histology showed a reduction of the keratin layer but remnants of the original features of the pathology were still present.
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PMID:Oral retinoid (Tigason R etretinate) therapy in congenital disorders of keratinisation. 622 85

Efficacy and tolerance of an alcoholic solution containing 0.64 mg betamethasone-dipropionate plus 20 mg salicylic acid (Diprosalic Solution) were compared with an alcoholic solution containing 0,64 mg betamethasone-dipropionate in a 3 week double blind study in 100 patients with psoriasis and other steroid-responsive dermatoses of dry nature, comprising scalp and other hairy and non-hairy areas of the body. This double blind study was followed by a 3 week open study in another 100 patients with similar diagnosis, using Diprosalic Solution only. Although the therapeutic results of the double blind study showed no significant differences between both treatment groups, distinct advantages of the drug containing salicylic acid could be clearly demonstrated, such as: 1. More rapid onset of action, 2. rapid clearing of scaling, pruritus and inflammation, 3. these advantages are in compliance with the fact that topically applied salicylic acid softens keratin, loosens cornified epithelium and desquamates the epidermis, making the underlying layers more accessible to the antiinflammatory steroid.
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PMID:[Therapy of erythrosquamous dermatoses. Betamethasone dipropionate plus salicylic acid in comparison with betamethasone dipropionate solution]. 622 42

In current textbooks of dermatology, lichen amyloidosus is said to be a papular, intensely pruritic type of amyloidosis of unknown aetiology. When this concept was developed, there was no way of discriminating between the different types of amyloid. It is now known that amyloid in lichen amyloidosus is not derived from immunoglobulins or serum proteins, as it is in systemic amyloidoses, but from keratin peptides of necrotic keratinocytes. Even several years ago, chronic scratching was invoked as a possible cause of damage to keratinocytes in lichen amyloidosus. In support of this hypothesis, four cases are presented. Apart from amyloid in the papillary layer, all biopsy specimens revealed histopathological signs of chronic scratching (epithelial hyperplasia with hypergranulosis and compact orthokeratosis, coarse collagen in vertical streaks in the stratum papillare), such as are also found in prurigo nodularis and lichen simplex chronicus. Lichen amyloidosus is considered to be a variant of these conditions. Just as in prurigo nodularis and lichen simplex chronicus, pruritus seems to be the cause and not a symptom of the papular skin lesions. Consequently, treatment of lichen amyloidosus should not be directed at removing amyloid, but at improving the pruritus.
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PMID:[Lichen amyloidosus--disease entity or the effect of scratching]. 775 42

A 46-year-old woman with the Dowling-Meara variant of epidermolysis bullosa simplex (DM-EBS) presented with worsening recurrent, pruritic, circinate crops of clear and haemorrhagic herpetiform blisters affecting her trunk and limbs. Electron microscopy showed tonofilament aggregation and an intra-epidermal level of blister formation confirming a diagnosis of DM-EBS rather than an acquired immunobullous disorder. Antihistamines failed to control the intense pruritus, but dapsone (up to 150 mg daily) was beneficial. Mutations of basal cell keratin genes (K14 and K5) are thought to be of aetiopathological significance in this form of epidermolysis bullosa, but the underlying cellular mechanisms responsible for the clinical deterioration and severe itching in this adult patient are not yet clear.
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PMID:Epidermolysis bullosa simplex Dowling-Meara: troublesome blistering and pruritus in an adult patient. 843 22

Disseminated superficial porokeratosis (DSP) is a rare cause of secondary cutaneous amyloidosis. An 83-year-old male patient showed an increase in both size and number of DSP lesions after contracting pulmonary tuberculosis. The DSP lesions of the patient consisted of numerous annular eruptions on both sun-exposed and sun-protected areas, which occurred over a period of 20 years. Multiple skin biopsies were taken from normal or lesional/sun-exposed or sun-protected skin samples. Histopathologic examination included routine H&E stains, Congo red stains, thioflavin-T stains and anticytokeratin antibodies (AE1, AE3). And the results were as follows; 1) Positive staining with Congo red and thioflavin-T indicated an amyloid nature for the deposits, 2) confinement of the amyloid deposition just below the lesional epidermis (while sparing the neighboring uninvolved or distant normal skin) indicated some role of the lesional epidermis, and 3) positive staining with AE3 further indicated an epidermal origin-type II epithelial keratin-of the amyloid. We present a case of DSP with a local amyloid deposit, characterized by association of positive familial background, severe pruritus and pulmonary tuberculosis.
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PMID:Secondary cutaneous amyloidosis in disseminated superficial porokeratosis: a case report. 1098 3

P, a 20-year-old laborer displayed initial symptoms of the disease in question when he was 10 years old. Initially he had an asymptomatic progressive loss of hair on the scalp. A couple of years later he had mild to moderate pruritus, and the appearance of slate-blue eruptions on the scalp and elsewhere on the body. This resulted in a complete loss of hair on the vault of the scalp, which led him to seek specialist opinion. Skin surface examination revealed the presence of grayish-blue acuminate follicular papules, disposed singly and in groups (plaques). The pilo-sebaceous orifices were conspicuously obliterated and filled by keratin plugs. Perifollicular erythema was a predominant feature on the scalp. The lesions were present over the scalp, around the neck, chest, back, axillae, groin and legs. Shiny atrophied scalp skin depicting scarring alopecia mimicking male-type baldness was a salient feature. In addition, it was studded with conspicuous acuminate papules in its center (Fig. 1a). The known nonhairy (glabrous) skin had classic lichen planus lesions (Fig. 1b). Hemotoxylin-eosin stained microsections prepared from typical lichen planus (LP) lesions over the abdomen and those of lichen planopilaris (LPP) of the scalp were simultaneously studied. The former revealed changes in the epidermis comprising of hyperkeratosis, increase in thickness of stratum granulosum, hydropic degeneration of the basal cell layer and band-like lympho-histiocytic infiltrate pressing against and invading the epidermis, while the latter revealed uniform atrophy of the epidermis and vacuolization of basal cells. The hair follicles were dilated and were filled with keratin plugs. In addition to fibrosis of the dermis, pigment laden microphages and lympho-histiocytic infiltrate was prominent. The follicles and the sebaceous glands were absent. However, arrectores pilorum and sweat glands were preserved (Fig. 2a,b).
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PMID:Lichen planopilaris. 1170 23

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.
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PMID:Epidermal hyperproliferation and decreased skin barrier function in mice overexpressing stratum corneum chymotryptic enzyme. 1504 Apr 72


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