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

Striae distensae are characterized by a thinning of connective tissue stroma to produce linear, atrophic-appearing skin. Excessive adrenocortical activity, genetic factors and inherited defects of connective tissues, etc. are important causative factors in the formation of striae distensae, but the basic aetiology is not known. Total RNA was extracted from skin biopsies of five patients with striae distensae. The expression of genes coding for types I and III procollagen, elastin, fibronectin and beta-actin were studied and compared with those of four sex- and age-matched healthy individuals. The percentages of types I and III procollagen mRNA were 9.9 +/- 2.9% (mean +/- s.d.) and 10.6 +/- 1.6%, respectively, of the corresponding controls. The value for fibronectin mRNA in striae distensae was 7.3 +/- 1.8% of the control. The steady-state ratio fibronectin/type I procollagen mRNAs was 0.12 +/- 0.01 in striae distensae and 0.18 +/- 0.01 in the control. These observations suggest that expression of collagens, elastin and fibronectin genes are apparently decreased, and that there is a marked alteration of fibroblast metabolism, in striae distensae.
Clin Exp Dermatol 1994 Jul
PMID:Decreased expression of collagen and fibronectin genes in striae distensae tissue. 795 66

We assessed the prevalence of nail abnormalities in 272 children with alopecia areata who were seen in our department during an eight-year period. Of these, 126 (46%; 50 girls, 76 boys) had nail abnormalities that were related to alopecia areata. Nail pitting was detected in 92 patients, including 37 with alopecia totalis or alopecia universalis. Three patients experienced an onychomadesis of all 20 nails during the acute onset of alopecia areata universalis. Thirty-two (11.7%) had nail thinning and severe nail plate surface abnormalities that were consistent with a diagnosis of trachyonychia.
Pediatr Dermatol 1994 Jun
PMID:Prevalence of nail abnormalities in children with alopecia areata. 804 48

Although nail abnormalities have been reported to occur in 1% to 10% of patients with lichen planus, in children with lichen planus they are rarely mentioned in the literature. An 11-year-old boy had a two-month history of nail dystrophy affecting all the fingernails and the great toenails. The nail plates showed longitudinal ridging and thinning as well as onycholysis and distal splitting. There were no cutaneous or mucous membrane abnormalities. A nail biopsy specimen showed hyperkeratosis, hypergranulosis, and acanthosis in the ventral portion of the proximal nail fold and in the nail matrix. A band-like lymphocytic infiltrate was present in the superficial dermis, and the basal layer showed vacuolar alterations. A diagnosis of lichen planus was made. Treatment was intramuscular triamcinolone 20 mg once a month for six months. Since 1969 only 13 proved pediatric cases of lichen planus limited to the nails have been reported, including two children with 20-nail dystrophy and four with idiopathic atrophy of the nails.
Pediatr Dermatol 1993 Mar
PMID:Lichen planus limited to the nails in childhood: case report and literature review. 849 65

Monilethrix is characterized by beaded or moniliform hair, which results from the periodic thinning of the hair shaft. The beaded hair thus produced is subject to excess weathering and premature fracturing at the internodes. Clinically, monilethrix presents with short, fragile, broken hair. The follicular abnormalities range from subtle perifollicular abnormalities range from subtle perifollicular erythema and hyperkeratosis to horny follicular papule formation. At the ultrastructural level, cytolysis and keratin tonofilament clumping (epidermolysis) are seen in the cortical cells of the bulb of the hair follicle. Microsatellite markers flanking the keratin gene clusters at 17q12-q21 and 12q11-q13 were used to perform linkage analysis in a monilethrix pedigree. This study demonstrates linkage of monilethrix in a pedigree to microsatellite DNA loci mapping to the region on chromosome 12 containing the type II keratin cluster. A major group of structural hair proteins, the basic type II trichocyte keratins, map within this epithelial cytokeratin gene cluster. This study implicates a mutation in a trichocyte keratin gene in the pathogenesis of a structural hair disorder.
J Invest Dermatol 1996 Apr
PMID:Linkage of monilethrix to the trichocyte and epithelial keratin gene cluster on 12q11-q13. 861 25

A case of proximal subungual onychomycosis due to Microsporum canis in a 36-year-old woman is presented. The onychomycosis involved the left thumb and the little fingernails, with thinning of the nail plate and crumbling of the nail plate surface. A milky-white discoloration of the proximal portion of the left thumbnail was also evident. A 2-mm longitudinal nail biopsy showed a large number of fungal elements in the whole length of the nail plate. Fungal hyphae were more numerous in the ventral nail plate and produced detachment of the superficial nail plate. The nail bed was not invaded by fungal elements and was devoid of inflammatory changes. Proximal subungual onychomycosis is uncommon in immunocompetent individuals but has frequently been described in patients with AIDS. In our patient, in whom the proximal subungual onychomycosis was due to M. canis, there were no clinical or biochemical signs of immunodeficiency. Oral treatment with terbinafine, 250 mg/daily for 2 months, produced clinical and mycological cure.
Br J Dermatol 1996 Jan
PMID:Proximal subungual onychomycosis due to Microsporum canis. 874 10

Fluticasone propionate (FP) 0.05% (CutivateTM) cream is a novel corticosteroid used for the treatment of corticosteroid-responsive dermatoses. To date there are no published data concerning its effect on cutaneous atrophy. This randomized, double-blind study of 40 volunteer subjects was performed to investigate the kinetics of skin thinning induced by topical 0.05% FP cream vs. placebo after once-daily application for 2-8 weeks. The results of this study showed no significant effect on the skin thickness of subjects after 8 weeks' treatment with 0.05% FP cream compared with placebo.
Clin Exp Dermatol 1996 May
PMID:The kinetics of skin thinning induced by topical fluticasone propionate 0.05% cream in volunteer subjects. 891 56

Seven children with Proteus syndrome (PS) are reported. The majority of clinical findings coincide with what is reported in the literature. New findings were blue sclerae, telecanthus, epiblepharon, endotropy, hemimegaly of the optic nerve, occipital dysmyelination and compression of the corpus callosum, craneosynostosis, decalcification and thinning of the cortical layer of long bones, and talipes equinus. The clinical findings, possible etiology, differential diagnosis, and treatment of PS are discussed.
Pediatr Dermatol
PMID:Proteus syndrome: new findings in seven patients. 905 Jul 55

Lichen planus pigmentosus (LPP) has thus far been described as a condition of unknown etiology which clinically differs from the classical lichen planus (LP) by exhibiting dark brown macules and/or papules mostly in exposed areas and flexural folds and a longer clinical course without pruritus or scalp, nail or mucosal involvement. Histopathologically, LPP shows the typical changes seen in LP, but with thinning of epidermis. We report a case of LPP that developed in a unilateral, zosteriform pattern on the left flank of a 49-year-old man. This case seems to lie in the middle of the spectrum between classical LP and ashy dermatosis, and, to the best of our knowledge, is the first report of LPP presenting in the zosteriform pattern.
J Dermatol 1997 Mar
PMID:Lichen planus pigmentosus presenting in zosteriform pattern. 911 19

Alpha-hydroxy acids (AHA) such as glycolic acid have recently been used extensively in cosmetic and dermatological formulas. In low concentration (2-5%) glycolic acid is believed to facilitate progressive weakening of cohesion of the intercellular material of the stratum corneum (SC), resulting in uniform exfoliation of its outermost layers (the stratum disjunctum). Since thinning of the SC as well as changes of intercellular lipids could theoretically compromise the barrier functions of the skin, we investigated the mode of AHA action on the SC to determine whether enhanced desquamation compromises the barrier structures of the SC and changes transepidermal water loss (TEWL) values. Electron microscopy of the epidermis biopsied from the volar forearm of human volunteers after 3 weeks of treatment with a 4% glycolic acid formulation twice daily was employed to evaluate 1) epidermal morphology and thickness of the SC, (2) the lamellar body and SC lipid bilayer organization, and (3) desquamative events based on degradation of desmosomes. TEWL values and SC hydration were recorded prior to and at the end of the study. Electron microscopy revealed no ultrastructural changes in the nucleated layers of the epidermis. The lamellar body (LB) secretory system in the stratum granulosum (SG), and intercellular lipid lamellae in the SC in both vehicle- and glycolic acid-treated samples were comparable to normal human SC. Within the SC, enhanced desmosomal breakdown, promoting loss of cohesion and desquamation, was restricted to the stratum disjunctum while desmosomes of the stratum compactum were unaffected. Treated areas displayed histologically, a more compact appearing SC. TEWL values remained unchanged in glycolic acid- and vehicle-treated skin. Our findings indicate that the barrier structures of the SC are not disrupted by glycolic acid formulations at the concentration used. One of the mechanism of action of AHA on the SC seemed to be a "targeted" desmosomal (corneosomal) action without compromising the barrier structures of the skin.
Arch Dermatol Res 1997 Jun
PMID:Mode of action of glycolic acid on human stratum corneum: ultrastructural and functional evaluation of the epidermal barrier. 924 19

The decline in skin thickness that occurs with aging interests many different groups. Among these are pharmaceutical, cosmeceutical, and cosmetic companies promoting antiaging or antiwrinkling products, geriatricians and rheumatologists treating elderly and steroid-dependent patients who are "outliving" their skin, cosmetic surgeons, and dermatologists. Dermatologists are frequently asked how to prevent or slow aging of the skin. The answer regarding "photoaging" of sun-exposed skin is obvious; the answer regarding aging of photoprotected skin is not. Although the bulk of epidemiologic literature about aging and thinning of photoprotected skin is from the 1970s, literature regarding risk factors for and treatment of aging and thinning of the bony skeleton is more recent. Because both skin and bone are composed of more than 70% type I collagen, it may be hypothesized that the pathophysiologic processes involved in chronological atrophy of both tissues may overlap, thereby providing a foundation for further investigation of the skin. A better understanding of skin and bone loss may motivate the "appearance-conscious" public to modify risk factors (e.g., begin exercising) or select hormonal therapies (e.g., postmenopausal hormone replacement) to reduce aging of the skin. These measures may provide additional benefits, such as decreasing the risk of osteoporosis.
J Am Acad Dermatol 1998 Feb
PMID:Risk factors for reduced skin thickness and bone density: possible clues regarding pathophysiology, prevention, and treatment. 948 82


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>