References: Hair growth and hair loss
attbi.com
Latanoprost, a selective FP prostanoid receptor agonist used in the treatment of glaucoma, has a hypertrichotic side effect. Using the macaque model of androgenetic alopecia, we examined the effect of latanoprost on hair growth. Eight monkeys were divided into 2 groups; one group received a daily topical application of 50 microg/ml of latanoprost for 5 months; a control group had a daily application of vehicle. For an additional 3 months, 2 monkeys from each group were given 500 microg/ml latanoprost, while the remaining monkeys continued with the previous treatment. Hair growth was evaluated by monthly photographs and phototricho-graphic analysis. Fifty microg/ml of latanoprost caused minimal hair growth. Latanoprost at 500 microg/ml induced moderate to marked hair regrowth with 5-10% conversion of vellus hairs to intermediary or terminal hairs. The vehicle group showed no effect. Further evaluation of latanoprost as an agent for treatment of human androgenetic alopecia is indicated.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12013211&dopt=Abstract
J Formos Med Assoc. 2002 Mar;101(3):223-6.
High-dose steroid pulse therapy for the treatment of severe alopecia areata.
Tsai YM, Chen W, Hsu ML, Lin TK.
Department of Dermatology, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan, Taiwan.
Growing evidence shows alopecia areata (AA) to be a T cell-mediated organ-specific autoimmune disease. This study aimed to evaluate the efficacy of high-dose steroid pulse therapy in Taiwanese patients with severe widespread AA exceeding 40% of the scalp. A total of 17 Taiwanese patients with severe AA lasting less than 2 years were treated once monthly at the outpatient clinic for six sessions. Children younger than 12 years of age received oral prednisolone (5 mg/kg) in three divided doses, while for adults, 500 mg methylprednisolone was infused intravenously over 2 hours. Patients with multifocal AA exhibited the most favorable response, with more than 75% hair regrowth (9/11). Relapse occurred in two patients at 4 and 8 months after the last treatment, respectively. One patient with ophiatic AA showed a transient response, but subsequently lost hair even upon continuation of therapy. Two patients of four with alopecia totalis had full hair regrowth but one lost hair again 6 months later. In the only patient with alopecia universalis, less than 10% hair regrowth occurred. No major side effects were observed. In summary, 11 of 17 patients (64.7%) had more than 75% hair regrowth after steroid pulse therapy. Our results indicated that steroid pulse therapy, given at 5-10 mg/kg once monthly for an average of 6 months, is effective and well tolerated in Taiwanese patients with severe multifocal AA lasting less than 2 years.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12051021&dopt=Abstract
umich.edu
Deafness, with loss of sensory (hair) cells, results in progressive pathophysiological changes ending in the degeneration of most auditory nerve neurons. It is now possible to consider these events in the broader context of anti-apoptotic survival factors in the peripheral and central nervous system. One consequence of deafferentation of a neuron is the loss of neurotrophins that can lead to a change in oxidative state (formation of free radicals), changes in intracellular Ca(2+), and an up-regulation of apoptotic genes. Interventions that can modify availability of neurotrophins, [Ca(2+)](I), and/or free radical formation or their destructive effects, may preserve the auditory nerve. Some interventions (neurotrophins) may also lead to a regrowth of neurites. Studies in this area are of basic value and also of immediate clinical interest for the application of the cochlear prosthesis to the severe and profoundly deaf, since the benefits of this prosthesis are directly dependent on auditory nerve survival and the proximity of stimulating electrode to neuron. We, and others, have found that auditory nerve degeneration can be prevented by chronic electrical stimulation. We have demonstrated in vivo that this effect can be blocked by tetrodotoxin, thus indicating that propagated action potentials are a necessary condition, and by verapamil (Ca(2+) channel blocker), supporting in vitro studies by others, indicating that L-type Ca(2+) channels are necessary for stimulation-induced rescue of the deafferented auditory nerve. The intensities of electrical stimulation required for rescue are at levels sufficient to express the intermediate-early gene c-fos which can initiate transcription of anti-apoptotic genes and pathways, and up-regulate expression of neurotrophins that may act in an autocrine manner to protect the nerve from death. We, and others, have found that chronic local delivery (osmotic pump and microcannulation of the inner ear fluid spaces) of individual neurotrophins and cocktails of factors can also enhance survival of the deafferented nerve, and some can also initiate a regrowth of degenerated peripheral processes of the nerve into the region of the destroyed sensory epitheliae. Recently, we have shown that this rescue can occur with delayed intervention, after degeneration of some neurons has begun, more closely mimicking the human clinical situation. Finally, we have shown that interventions with antioxidants may also be effective in preventing pathophysiological changes of the auditory nerve following deafness. These studies in the auditory periphery support the 'neurotrophic factor hypothesis' as proposed as a general mechanism underlying neurodegenerative and age-related pathology of the central nervous system. Additional animal studies can yield a rational scientific basis to justify human trials, with a goal to maintain auditory cell survival and initiate and direct fiber growth to the next generation of prosthesis. Intimate contact between electrode and a dense population of auditory neurons should greatly enhance the benefits of these devices for the profoundly deaf. Copyright 2002 S. Karger AG, Basel
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12053141&dopt=Abstract
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