References: Hair growth and hair loss
Ann Acad Med Singapore. 2001 Jul;30(4):409-13.
A retrospective study of incontinentia pigmenti seen at the National Skin Centre, Singapore over a 10-year period.
Chan YC, Giam YC.
National Skin Centre, 1 Mandalay Road, Singapore 308205.
INTRODUCTION: Incontinentia pigmenti is a rare X-linked dominant disease which affects the ectodermal tissues, usually lethal in males. MATERIALS AND METHODS: A retrospective analysis of clinical data obtained from the photographic documentation and casenotes of patients diagnosed to have incontinentia pigmenti at the National Skin Centre. The study covered the period from January 1990 to December 1999. RESULTS: Twenty-six patients were diagnosed to have incontinentia pigmenti of the Bloch-Sulzberger type; 23 (88.5%) were females and 3 (11.5%) were males. There were 20 Chinese, 3 Malay and 3 Indian patients. Most patients had cutaneous manifestations at birth or within the first week of life. Cutaneous features included vesicles, papules, verrucous plaques and splash-like hyperpigmentation along the lines of Blaschko. The cutaneous lesions were widespread in 21 (81%) and localised in 5 (19%) patients. In some cases, hypopigmented atrophic streaks (2 patients) or whorled scarring alopecia (4 patients) were seen. Extracutaneous manifestations, seen in 5 (19%) patients, included neurological, dental and ocular defects. One Malay girl had severe neurological involvement associated with ocular abnormalities. A positive family history was present in 6 (23%) patients. The 3 male patients were Chinese without any family history. CONCLUSIONS: Each stage of the disease comes with its own set of differential diagnosis, including infections e.g. herpes virus infection and other types of genodermatoses e.g. linear and whorled nevoid hypermelanosis. The phenomenon of whorled scarring alopecia, hitherto unreported in the literature, corresponded to the lines of Blaschko. In the 3 Chinese male patients, the disorder probably originated from a new mutation. X chromosome inactivation in females during early embryogenesis results in a mosaic population of cells and this explains the linear and patchy manifestations of incontinentia pigmenti.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11503550&dopt=Abstract
J Eur Acad Dermatol Venereol. 1999 Mar;12(2):123-5.
The risk of coronary heart disease in men with androgenetic alopecia.
Sasmaz S, Senol M, Ozcan A, Dogan G, Tuncer C, Akyol O, Sener S.
Department of Dermatology, Inonu University, Medical School, Turgut Ozal Medical Center, Malatya, Turkey.
BACKGROUND: The meaningful association of androgenetic alopecia and coronary heart disease has been well documented, but few studies have focused on the importance of lipid parameters, such as total cholesterol, triglycerides, high density lipoprotein-cholesterol, low density lipoprotein-cholesterol, lipoprotein (a), apolipoprotein A1 and apolipoprotein B in patients with androgenetic alopecia. OBJECTIVE: The aim of this study is to investigate the relation between androgenetic alopecia and coronary heart disease and to determine the significance of certain lipid parameters on this relationship. SUBJECTS: Forty-one men with vertex type androgenetic alopecia (study group) and 36 men, age-matched, with normal hair status (control group) were the subjects of this study. RESULTS: We found significant differences in serum lipoprotein (a) and triglyceride levels between the study and control groups (P < 0.05). Forty-seven percent of patients and 30% of controls had a lipoprotein (a) level more than 30 mg/dl higher than the level critical for atherosclerotic heart disease. CONCLUSION: Dermatologists should investigate lipid profile, especially lipoprotein (a), of patients with androgenetic alopecia and refer to a cardiologist if necessary.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10343940&dopt=Abstract
J Invest Dermatol. 2001 Aug;117(2):173-8.
A new strategy for modulating chemotherapy-induced alopecia, using PTH/PTHrP receptor agonist and antagonist.
Peters EM, Foitzik K, Paus R, Ray S, Holick MF.
Department of Medicine, Boston University Medical Center, MA 02118, USA.
Parathyroid hormone (PTH) related peptide (PTHrP) and the PTH/PTHrP receptor (PTH/PTHrP-R) show prominent cutaneous expression, where this signaling system may exert important paracrine and/or autocrine functions, such as in hair growth control. Chemotherapy-induced alopecia - one of the fundamental unsolved problems of clinical oncology - is driven in part by defined abnormalities in hair follicle cycling. We have therefore explored the therapeutic potential of a PTH/PTHrP-R agonist and two PTH/PTHrP-R antagonists in a mouse model of cyclophosphamide-induced alopecia. Intraperitoneal administration of the agonist PTH(1-34) or the antagonists PTH(7-34) and PTHrP(7-34) significantly altered the follicular response to cyclophosphamide in vivo. PTH(7-34) and PTHrP(7-34) shifted it towards a mild form of "dystrophic anagen", associated with a significant reduction in apoptotic (TUNEL+) hair bulb cells, thus mitigating the degree of follicle damage and retarding the onset of cyclophosphamide-induced alopecia. PTH(1-34), in contrast, forced hair follicles into "dystrophic catagen", associated with enhanced intrafollicular apoptosis. We had previously shown that an induced shift in the follicular damage-response towards "dystrophic catagen" mitigates cyclophosphamide-induced alopecia, whereas a shift towards "dystrophic catagen" initially enhanced the hair loss, yet subsequently promoted accelerated hair follicle recovery. Therefore, this study in an established animal model of chemotherapy-induced alopecia, which closely mimics human chemotherapy-induced alopecia, strongly encourages the exploration of PTH/PTHrP-R agonists and antagonists as novel therapeutic agents in chemotherapy-induced alopecia.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11511291&dopt=Abstract
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