Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired ichthyosis is an important clinical finding; internal malignancy, systemic disease and medication are recognised associations. We present a 70-year-old lady with acquired ichthyosis and leiomyosarcoma, one of the less frequently associated malignancies. An additional unusual finding was generalised thinning and loss of pigment affecting her hair. Scalp biopsy showed histological evidence of ichthyosis. Following resection of the tumour the ichthyosis resolved and there was regrowth of darker hair.
J Eur Acad Dermatol Venereol 1998 Mar
PMID:Acquired ichthyosis, alopecia and loss of hair pigment associated with leiomyosarcoma. 955 15

The objective was to test the hypothesis that there is a correlation between thinning of the skin and bone in patients on chronic oral glucocorticoids (GCs). This was a one-time cross-sectional analysis performed in an academic referral center. The study group consisted of 14 patients on GCs for a variety of disorders, including dermatomyositis, pemphigus vulgaris, pyoderma gangrenosum, and urticarial vasculitis. Skin thickness was compared with that of 24 sex- and age-matched controls. The main outcome measures were the bone density of the lumbar spine (L2-L4) and the skin thickness. The skin thickness (mm, mean +/- SEM) in GC-treated (n = 7) vs unmedicated age-matched Caucasian women (n = 20) was 0.84 +/- 0.04 vs 1.02 +/- 0.04 (t = 3.07, P < 0.01) in the upper arm, 1.13 +/- 0.09 vs 1.49 +/- 0.05 (t = 3.65, P < 0.002) in the dorsal forearm, and 0.96 +/- 0.07 vs 1.17 +/- 0.02 (t = 2.92, P < 0.01) in the ventral forearm. L2-L4 bone densities averaged 106 +/- 2% in the GC-treated female patients relative to the age and sex-matched controls. There was no correlation between skin thickness and bone density. In GC-treated (n = 4) vs unmedicated Caucasian men matched for age (n = 4), skin thickness was 1.09 +/- 0.4 vs 1.33 +/- 0.05 (t = 3.51, P < 0.02) in the upper arm, but was not significantly different at the two forearm sites. No correlation between skin thickness and bone density was observed. The level of type I procollagen mRNA in skin from three GC-treated patients was 45% of the value in three age-matched controls. In conclusion, GCs cause statistically significant thinning of skin independently of the effects on bone.
Arch Dermatol Res 1998 Jul
PMID:Lack of correlation of skin thickness with bone density in patients receiving chronic glucocorticoid. 974 94

The term peripheral ulcerative keratitis represents a spectrum of inflammatory diseases, characterized by cellular infiltration, corneal thinning, and ulceration. Neutrophilic dermatoses are rarely associated with peripheral ulcerative keratitis. To date, peripheral ulcerative keratitis has only been reported in patients with pyoderma gangrenosum. Separate episodes of pyoderma gangrenosum, Sweet's syndrome, and pustular vasculitis developed in a 60-year-old patient with rheumatoid arthritis over an 8-year period. Over the past 2 years, 3 episodes of peripheral ulcerative keratitis occurred. Cyclosporine (4 mg/kg/d) treatment was started on confirmation of pyoderma gangrenosum. Over the ensuing 2 years, it became evident that the activity of her ocular and skin diseases, as well as her arthritis, paralleled the administration or cessation of cyclosporine therapy. Dermatologists should be aware of the association of Sweet's syndrome, pyoderma gangrenosum, and pustular vasculitis with peripheral ulcerative keratitis. This rare ocular manifestation and the serious sequelae when left untreated make recognition crucial. Cyclosporine proved to be a very effective treatment for all of our patient's diseases.
J Am Acad Dermatol 1999 Feb
PMID:Peripheral ulcerative keratitis--an extracutaneous neutrophilic disorder: report of a patient with rheumatoid arthritis, pustular vasculitis, pyoderma gangrenosum, and Sweet's syndrome with an excellent response to cyclosporine therapy. 1002 62

Wrinkles are a major topic in dermocosmetology; the purpose of this work has been to go deeper into the knowledge of cutaneous damage underlying these modifications of skin surface. Up to now, the number of published works about the histological structure of wrinkles is not very large. Therefore to complete the findings, we studied 46 subjects of both sexes, between 57 and 98-year-old, enabling us to obtain 157 skin biopsies of wrinkles (face) and sun-protected areas (abdomen). We used different histological techniques involving histochemistry, immunohistochemistry, electron microscopy and quantification by image analysis in addition to classic standard techniques. This study has allowed us to confirm published structural modifications of wrinkles, but also to display many other original alterations. The increased thinning of the epidermis atrophied with age is confirmed by the study of desmoplakins outlining the cellular contours of keratinocytes. Such a thinning is accompanied by a decrease in several markers of epidermal differentiation at the bottom of the wrinkles: filaggrin, keratohyalin granules and transglutaminase I, disturbing desquamation and the capacity of the horny layer to retain water. The dermoepidermal junction is modified by a decrease of collagen IV and VII, which, combined with fewer and fewer oxytalan fibres under wrinkles, weakens this interface. The deposition of abnormal elastotic tissue in the dermis, with an interruption of these deposits under wrinkles and an atrophy of dermal collagen more pronounced under wrinkles, boosts the magnitude and depth of wrinkles. The composition of the other dermal constituents is also altered with, more particularly, a marked decrease of chondroitin sulphates in the papillary dermis under wrinkles, combined with an asymmetrical variation of glycosaminoglycans on both edges of wrinkles. The atrophy of the hypodermis, also more marked under wrinkles, with a thickening of fibrous lines, also makes the depth of wrinkles more pronounced. Wrinkle formation appears at the same time as numerous modifications in different cutaneous structures, which may be mutually amplified. Such a study by pointing out altered elements in skin physiology, makes the development of specific treatments possible in order to mitigate this unwelcome cutaneous deterioration.
Br J Dermatol 1999 Jun
PMID:A histological study of human wrinkle structures: comparison between sun-exposed areas of the face, with or without wrinkles, and sun-protected areas. 1035 68

The peripheral corneal melting syndrome (PCMS) is a rare disease consisting of marginal corneal thinning that can progress to perforation. The PCMS carries a grave prognosis and it is of vital importance that dermatologists are aware that this may be responsible for a painful red eye in a patient with psoriasis. We highlight the features of the PCMS developing in an elderly woman with long-standing psoriasis to increase awareness of its significance, and hypothesize that an association may exist between the two conditions. Only one previous report has been published in which the authors speculate on the possible association of this syndrome with psoriasis. That few other cases have been described is either a consequence of under-reporting by both ophthalmologists and dermatologists unaware of a link or because the relationship between the syndrome and psoriasis is genuinely coincidental.
Br J Dermatol 1999 Aug
PMID:The peripheral corneal melting syndrome and psoriasis: coincidence or association? 1046 14

It is well established that the efficacy of corticosteroids under occlusion with hydrocolloids (HCD) is superior compared to monotherapy with topical corticosteroids. However, following treatment with more potent corticosteroids, increased side effects and a more pronounced rebound might be expected. In the present clinical study, the efficacy of relapse after and the safety characteristics of two treatment modalities were compared: clobetasol-17-propionate lotion under an HCD dressing once weekly versus clobetasol-17-propionate ointment without an HCD twice daily. Clinical assessments were recorded and skin biopsies were taken before therapy, at clearance and 6 weeks after clearance. A panel of monoclonal antibodies to characterize epidermal proliferation, differentiation and inflammation were selected. In addition, clinical and histological assessments for skin atrophy were made. Both therapies had a major therapeutic effect, which was reflected in the clinical and immunohistochemical parameters. The only difference between the two therapies was a faster remission induction time in patients treated with corticosteroids combined with HCD. Six weeks after discontinuation of treatment, similar clinical and histological signs of relapse were observed for both therapies. Clinically, there were no signs of skin atrophy but histologically, epidermal thinning occurred to the same extent with both therapies but proved to be reversible within 6 weeks of discontinuation of treatment. From this study it can be concluded that the combination of HCD and corticosteroids is able to induce relatively fast remission compared to corticosteroid monotherapy but relapse and safety characteristics are comparable to the unoccluded corticosteroid therapy.
Arch Dermatol Res
PMID:Clobetasol-17 propionate lotion under hydrocolloid dressing (Duoderm ET) once weekly versus unoccluded clobetasol-17-propionate ointment twice daily in psoriasis: an immunohistochemical study on remission and relapse. 1048 7

Several lines of evidence suggest that sensory nerves ending at the skin have profound influences on their target, the epidermis. To test the hypothesis, we examined the consequences of denervation on the paw skin of rats by eliminating its innervation. We investigated temporal changes of nerve degeneration, keratinocyte proliferation and differentiation, gene expression, and epidermal thickness. Nerve terminals in the epidermis began to degenerate within 24 h after denervation. All epidermal nerves were completely degenerated by 2 d. During the interval of nerve degeneration, there was a significant reduction of bromodeoxyuridine incorporation from 24 h of nerve injury (39 +/- 7% of the control side, p 0.01). By 2 d, there was a further reduction of bromodeoxyuridine labeling (11 +/- 8%, p < 0. 0001). The incorporation of bromodeoxyuridine remained depressed when the skin was denervated (35 +/- 11%, p < 0.01). Four days after eliminating skin innervation, the denervated epidermis became thinner than the control epidermis (70 +/- 8% of the control, p < 0. 01). Epidermal thinning was associated with a significant decrease in expression of glyceraldehyde-3-phosphate dehydrogenase and beta-actin transcripts (33 +/- 8% of the control epidermis from postoperative day 4, p < 0.001). Other aspects of keratinocyte differentiation, including the patterns of keratin expression, and programmed cell death, were unaltered by skin denervation. These data indicate that skin denervation is sufficient to influence keratinocyte proliferation and therefore epidermal thickness.
J Invest Dermatol 1999 Oct
PMID:Modulation of keratinocyte proliferation by skin innervation. 1050 44

We report 6 adolescent females apparently affected by diffuse partial woolly hair. The patients complained of thinning and curling of some hair of the scalp. Examination revealed two distinct hair populations. The first hair population was straight, normally pigmented and of normal length, thus considered "normal" hair. The second hair population was wavy, curly, thinner and apparently slightly shorter, thus considered abnormal. Direct examination of the abnormal hair population under a light microscope revealed a curled pattern of the hair shaft, and single torsions. With light microscopy the clinically normal hair had no abnormalities. Under scanning electron microscopy (SEM) the abnormal hair had curly and flattened hair shafts of 30-60 mum in diameter, oval shaped sections, canalicular formations, single torsions and cuticular weathering. With SEM, clinically "normal" hair had a diameter between 60-80 mum, with no major relevant abnormalities except for weathering. These results are suggestive of a new variant of acquired kinking (curling) of hair simulating diffuse partial woolly hair. The absence of clinical alterations in the proximal area of the affected hair and the spontaneous improvement with time, suggests that this variant may result from environmental exposure (weathering, cosmetic procedures) in predisposed individuals.
Eur J Dermatol
PMID:Acquired partial curly hair. 1052 33

We described a case of Werner's syndrome associated with osteosarcoma. A 37-year-old Japanese man was diagnosed as having Werner's syndrome by the presence of juvenile cataracts, skin sclerosis and hyperpigmentation of the feet, high-pitched voice, characteristic bird-like appearance of the face with beak-shaped nose, thinning of the entire skin and hyperkeratoses on soles, hyperlipemia, hyperuricemia, diabetes melitus, and the mutated responsible gene (WRN). He had a 3-month history of a tumor on his left forearm. Histologically, the tumor included four histological patterns; a malignant fibrous histiocytoma-like, a desmoid-like, a dermatofibrosarcoma protuberans-like, and a chondrosarcoma-like pattern. Tumoral osteoid formation was also found in the tumor. Therefore, the tumor was diagnosed as osteosarcoma.
J Dermatol 1999 Oct
PMID:A case of Werner's syndrome associated with osteosarcoma. 1055 36

Monilethrix is an autosomal dominant hair disorder characterized by a beaded appearance of the hair due to periodic thinning of the shaft. The phenotype shows variable penetrance and results in hair fragility and patchy dystrophic alopecia. Mutations of the helix-encoding region in two hair-specific keratins (hHb1 and hHb6) have been identified. We have now investigated two unrelated monilethrix patients and identified two different novel heterozygous point mutations of the same codon in exon 7 of the hHb6 gene. Dystrophic hair samples obtained from both patients showed the typical beaded appearance by scanning electron microscopy. Both mutations affected the first base of codon 402 (glutamic acid). In patient A, a G to C transition occurred causing a glutamine substitution (GAG to CAG: E402Q) whereas in patient B, the transition was G to A yielding a lysine substitution (GAG to AAG: E402K). The sequence of the 1A helical regions of hHb1 and hHb6 as well as the 2B helical region of hHb1, were normal. Unaffected relatives did not have the hHb6 mutation and this codon was found to be highly conserved showing no alteration in the normal population (100 alleles examined). Both mutations disrupted a Taq I restriction site and restriction fragment length polymorphism analysis showed that a diagnostic 361 bp fragment could confirm the mutation. Thus, two new point mutations of the hair-specific keratin gene hHb6 have been identified in this genetic disease.
J Invest Dermatol 1999 Dec
PMID:Two different mutations in the same codon of a type II hair keratin (hHb6) in patients with monilethrix. 1059 61


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