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Alopecia, hair loss abstracts ||
J Eur Acad Dermatol Venereol. 2002 Jul;16(4):361-6.
Scleroderma 'en coup de sabre' and progressive facial hemiatrophy. Is it possible to differentiate them?
Orozco-Covarrubias L, Guzman-Meza A, Ridaura-Sanz C, Carrasco Daza D, Sosa-de-Martinez C, Ruiz-Maldonado R.
The aim was to be able to evaluate the diagnosis of two diseases by a consensus of clinical opinion used in the Department of Dermatology of the National Institute of Paediatrics in Mexico City. To differentiate between scleroderma 'en coup de sabre' (SCS) and progressive facial hemiatrophy (PFH), colour slides of 13 patients diagnosed as SCS and nine as PFH were examined by two dermatologists and microscopic slides by two pathologists. In both cases, the slides were randomly presented and no clinical information was given. The clinical and histopathological findings were statistically compared with two-tailed tests and alpha = 0.05. Kappa coefficients were obtained to evaluate the concordance between dermatologists, pathologists, and in terms of the consensus diagnosis. The usefulness of photographic assessment is limited by the inability to palpate the consistency of lesions. The most important clinical feature that differentiated both conditions was cutaneous sclerosis present in eight of 13 patients with SCS and in none of the PFH patients (P < 0.005). Other clinical features more frequently found in SCS were cutaneous hyperpigmentation and alopecia. The more frequent clinical features in PFH were total hemifacial involvement and ocular changes. Statistically significant histopathological features were: connective tissue fibrosis present in all cases with SCS and two of nine patients with PFH (P < 0.0002); adnexal atrophy present in 11 of 13 patients with SCS, and in three of nine with PFH (P < 0.02), and mononuclear cell infiltrates in all patients with SCS cf. six with PFH (P < 0.05). Our results suggest that in most cases it is possible to differentiate SCS from PFH based on clinicopathological findings.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12224693&dopt=Abstract
Drug Ther (NY). 1972 Sep;7(9):46-8.
Desirable and undesirable cutaneous effects of oral contraceptives.
Krueger GG, Mcquarrie HG, Swinyer LJ.
PIP: A review of cutaneous reactions associated with oral contraceptives intended to help the practitioner is presented. The skin responses to gestagens depend upon the sensitivity of the patient, the nature of the gestagen, and the ratio of progestogen to estrogen. Reactions are classified according to their physiologic mechanisms: hormonal effects, immune response, altered porphyrin metabolism, and miscellaneous skin problems. Some of the reactions associated with pseudopregnancy include herpes gestationis, melasma, vaginal candidiasis, cholestatic jaundice, alopecia, and possibly hypertophic gingivitis, neurofibromatosis, and telangiectasia. Hormonal effects include acneform eruptions, diffuse hair loss, and decrease of sebum production. Adverse effects exerted via the immune system include: candidiasis, decreased delayed skin-test reactivity, increased viral infections, flare of lupus erthematosus, erythema nodosum, erythema multiforme, photodermatitis, and herpes gestationis. Altered porphyrin metabolism effects include induction of porphyria and of variegate porphyria. Beneficial effects of oral contraceptives include improvement of acne, lessening of premenstrual flaring of aphthous ulcers, and improvement of Fox-Fordyce disease with estrogenic preparations. There is an unclear association between seborrhea, epithelial inclusion cysts, and hidradenitis supporativa and contraceptive therapy.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12229528&dopt=Abstract
Mol Genet Metab. 2002 Dec;77(4):314-8.
A novel nonsense mutation in the ligand binding domain of the vitamin D receptor causes hereditary 1,25-dihydroxyvitamin D-resistant rickets.
Malloy PJ, Zhu W, Bouillon R, Feldman D.
Division of Endocrinology, Gerontology, and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford University Medical Center, Room S005, Stanford, CA 94305-5103, USA.
Hereditary 1,25-dihydroxyvitamin D resistant rickets (HVDRR) is a genetic disorder most often caused by mutations in the vitamin D receptor (VDR). In this report, we present our findings on a young girl who exhibited the typical clinical features of HVDRR with early onset rickets, hypocalcemia, secondary hyperparathyroidism, and elevated serum concentrations of alkaline phosphatase and 1,25-dihydroxyvitamin D [1,25(OH)(2)D(3)]. The patient also had total body alopecia. Fibroblasts from the patient were cultured for analysis of the VDR structure and function. In [3H]1,25(OH)(2)D(3) binding assays, no significant specific binding to the VDR was observed in cytosols from the patient's fibroblasts. The patient's fibroblast were also totally resistant to high doses of 1,25(OH)(2)D(3) as demonstrated by their failure to induce expression of the 24-hydroxylase gene, a marker of 1,25(OH)(2)D(3) activity. DNA sequence analysis of the VDR gene uncovered a unique C to T mutation in exon 8. The mutation changed the codon for glutamine to a premature stop codon at amino acid 317 (Q317X). Restriction enzyme analysis showed that the patient was homozygous for the mutation. Both parents were heterozygous for the mutant allele. In conclusion, we have identified a novel mutation in the VDR, Q317X, as the molecular defect in a patient with HVDRR. The Q317X mutation deletes 110 amino acids of the ligand-binding domain of the VDR and results in the loss of [3H]1,25(OH)(2)D(3) binding and target gene transactivation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12468277&dopt=Abstract
Seeing is believing. Learning by anecdotal observations is an old way of science.
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