Artikel over middelen plus en de beschrijvingen ervan

[WannaKnowMore]

Deze artikel heb ik gekopierd en geplakt van een internationale bodybuilding forum, en bodybuildings die erfelijk kaal worden versnellen het akaal worden door meer hormonen te gebruiken en dat zet weer om in DHT en de meeste accepteren het ook niet om kaal te worden, daarom heeft een bodybuidling die met veel DHT in zijn lichaam rondloopt en erfelijke aanleg heeft om kaal te worden dit ertikel geschreven.

enjoy

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Balding and Steroid Use
By: Nan Man

The bain of using steroids can be the side effects one of the most feared is the risk of going bald with the use of steroids after all we want is to have that great physique and not look worse with a bald scalp right.

First of all a little background info on me I am 29 years old have been training on and off since I was 15 and have been using various anabolic since I was 17 my father is went bald before he was 30 and my uncles on my side had the same problems.

I started losing my hair slowly as I upped the doses and then went into a great deal of research to try and find a solution to this problem which I am sure bothers everyone as much as it does me.

I have used basically every hair loss medicine under the sun and have formed these conclusions on them.

Before I go any further let me state I am not doctor and all these findings are my personal opinion on this subject but I do/have taken steroids and suffer from hair loss.

My first point would be to say that contrary to what all other gurus etc are saying is that propecia makes hair loss worse with steroid users.

The main new hair loss drug is Propecia also known as Proscar both of them having the active ingredient Finasteride.

Finasteride works by inhibiting an enzyme with in the body called Alpha 5 reductase this enzyme is responsible for converting the naturally present testosterone in to dihydrotestosterone (DHT) the main culprit in hair loss.

All steroids testosterone included attach themselves to the androgen receptor, which is located at different sites within the body.

The problem with propecia and all the other products which inhibit alpha 5 reductase is that they only really work on testosterone and not with any other compounds.

Now this is perfect for guys who don't juice or take any roids but us Steroid users take various different compounds, which complicate the matter.

For example using deca with propecia stops the body converting nandrolone into dihydronandrolone (DHN)

DHN unlike Dht is acutally less androgenic than nandrolone and less likely to cause hair loss than nandrolone itself.

[WannaKnowMore]

Also with drugs like d-bol and primobolan these do not go through alpha 5 reductase conversion process at all making Propecia and Azelaic acid (another commonly used compound in hair loss meds which works by inhibiting alpha 5 reductase) and any other compounds which inhibit alpha 5 reductase to not have any effect on the hair loss factor on these kinds of drugs.

Also the use of finasteride has left many people complaining of side effects of reduced sex drive and a hard time timing getting erections (!).

Basically this gets to my point that Alpha 5 reductase inhibitors are useless in steroid users unless they plan on using testosterone alone in any cycles.

I would recommend to any steroid users that they get off the propecia and not to use any alpha 5 reductase inhibitors (azealic acid is another commonly used one).

Ok so far we have established that alpha 5 reductase inhibitors are not great for combating hair loss in steroid users, In an ideal world we would have a Topical drug which would have local and not internal actions and would work by blocking the androgen receptor site therefore blocking all androgens which come it’s way and not just just DHT as is required in normal non steroid using public.

This leave us asking what to use needing an androgen receptor blocker which is topical and therefore does not have the internal side effects that propecia has here we come to spirolactone and flutamide both topical androgen receptor blockers.

1)Spirolactone

It’s been firmly established that alopecia. androgenetica, more commonly known as male pattern baldness or just pattern baldness, is initiated by dihydrotestosterone (DHT) attaching to the receptor sites on the hair follicles [1.2.3.4.]. Genetically, only the follicles on the top of the head are encoded with the receptor sites[5.6.24.], which explains why hair along the side of the head and in the back of the head is not lost with age. The attached DHT on the receptor site is perceived as a foreign body and the immune system begins to destroy the hair follicle, shortening the growth phase and causing the hair shaft to become progressively finer in texture[6]. In extreme cases, only a vellus hair remains. The good news is that the follicles have the inherent capacity to mature to their former size.

Encouraged with the success of finasteride to reduce the amount of DHT in the scalp of patients with male pattern baldness (MPB), doctors and scientific researchers took another look at existing medications that are known to act as anti-androgens.

However, there have to be stringent criteria for an anti-androgen that can be used to combat or even reverse pattern alopecia. The ideal anti-androgen should have the following properties: (1) It has to have potent anti-androgen activity; (2) It should selectively prevent or successfully compete with DHT without changing testosterone levels; (3) It should be effective topically, so it can be conveniently applied with minoxidil solutions and (4) Even though it’s easily absorbed into the skin, it should not have any systemic effects.

That’s a tall order. Surprisingly enough, there is such a medication: spironolactone. And it’s not a new medication [7.8.]. For over thirty years spironolactone has been used as an antihypertensive and a diuretic. More recently, it has been used to treat hirsutism in women [9.10.]. Using spironolactone to treat hirsutism may sound contradictory, but body hair (e.g.chest, face, axilla, pubis, etc.) is promoted by testosterone and sincespironolactone is a potent anti-androgen, it’s successfully used to eliminate unwanted hair on the body[11].

On the top of the head, where the hair is adversely affected by DHT, spironolactone has just the opposite effect [7.12.13.15.25.]. Spironolactone exhibits anti-androgenic effects in both males and females [14.15.]. Taken orally, it is such a potent anti-androgen that, although it is an effective anti-hypertensive drug, it is rarely used to treat men with hypertension because of its feminizing properties, including painful gynecomastia [16.17.].

However, applied topically, spironolactone does not have any systemic side effects [12.18.19.20.]. Clinical evaluations of topical applications of spironolactone concluded that "as far as the topical use is concerned spironolactone seems to be highly effective with absence of systemic effects"[19]. Physicians have been treating patients for MPB for well over twelve years and there have not been any reports of systemic side effects.

Among its other properties as an anti-androgen, spironolactone is a potent competitive inhibitor of DHT at its receptor sites[21]. Therefore, spironolactone effectively prevents DHT from attaching to the receptor sites on the hair follicles[22]. As a result, the follicles no longer atrophy and can mature again to their normal size. And it does so without decreasing the circulating levels of DHT in the body. By comparison, finasteride inhibits the formation of DHT, causing troublesome side effects in many patients.

Multiple studies in various medical centers document that spironolactone is effective when applied topically[22]. In studying the anti-androgenic effects of topical spironolactone at the Department of Dermatology at New York University School of Medicine, researchers established that spironolactone concentrations of 0.01% to 5% produced a dose responsive decrease[23]. Making a 2% solution the ideal scenario.

Still, there are some minor drawbacks with the use of topical spironolactone. The spironolactone has an inherent disagreeable odor and spironolactone is not particularly stable in solution form. When spironolactone is combined in the same bottle containing minoxidil, however, the resulting solution becomes extremely malodorous. So the solutions cannot be stored together in the same container.

Bibliography

1. Hamilton JB: Male hormone stimulation is prerequisite and an incitant in common baldness. Am J Anat 71:451-480, 1942

2. Rattner H: Ordinary baldness. Arch Dermatol Syph 44:201-213, 1941

3. Rook A, Dawber R: Diseases of the Hair and Scalp. Oxford, Blackwell Scientific Publications, 1982

4. Baden HP: Diseases of the Hair and Nails. Chicago, Year Book Medical Publishers, 1987

5. Lattanand A, Johnson WC: Male pattern alopecia: A histopathologic and histochemical study. J Cutan Pathol 2:58-70, 1975

6. Blauer M, Vaalasti A, Pauli SL, Ylikomi T, Joensuu T, Tuohimaa P: Location of androgen receptor in human skin. J Invest Dermatol 97:264-268, 1991

7. Menard RH, Stripp B, Gillette JR: Spironolactone and testicular cytochrome P-450: Decreased testosterone formation in several species and changes in hepatic drug metabolism. Endocrinology 1974;94:1628-1636

8. Menard RH, Martin HF, Stripp B, et al: Spironolactone and cytochrome P-450: Impairment of steroid hydroxylation in the adrenal cortex. Life Sci 1975;15:1639-1648

9. Schapiro G and Evron S. A novel use of Spironolactone:treatment of hirsutism. J Clin Endocrinol Metab. 1988;51:429-432

10. Cumming D, Yang J, Rebar R, Yen S.: Treatment of hirsutism with Spironolactone. JAMA. 1982;247:1295-8.

11. Boiselle A, Tremblay RR: Clinical usefulness of spironolactone in the treatment of acne and hirsutism, abstracted. Clin Res 1978;26:840A

12. Yamamoto A, Ito M. Topical spironolactone reduces sebum secretion rates in young adults. J Dermatol, 1996 Apr,23:4,243-6

13. Berardesca E, Gabba P, Ucci G, Borroni G, Rabbiosi G: Topical spironolactone inhibits dihydrotestosterone receptors in human sebaceous glands: an autoradiographic study in subjects with acne vulgaris. Int J TissueReact 10:115-119, 1988

14. Burke BM, Cunliffe WJ: Oral spironolactone therapy for female patients with acne, hirsutism or androgenetic alopecia. Br J Dermatol 112:124-125, 1985

15. Stripp B, Taylor AA, Bartter FC, et al: Effect of spironolactone on sex hormones in man. J Clin Endocrinol Metabol 1975;41:777-781

16. Mann NM: Gynecomastia during therapy with spironolactone. JAMA 190:160-162,1963

17. Rose LI, Underwood RH, Newmark SR, Kisch ES, Williams GH: Pathophysiology of spironolactone-induced gynecomastia. Ann Int Med 87:398-403, 1977

18. Corval P, Michaued A, Menard J, et al: Antiandrogenic effect of spironolactones: Mechanism of action. Endocrinology 1975;97:52-8

19. Messina M, Manieri C, Musso MC, Pastorino R.: Oral and topical spironolactone therapies in skin androgenization. Panminerva Med, 1990 Apr-Jun,32:2,49-55

20. Wendt A, Hasan SH, Heinz I, Tauber U: Systemic effects of local antiandrogen therapy. Arch Dermatol Res 273:171,1982

21. Price VH: Testosterone metabolism in the skin: A review of its function in androgenetic alopecia, acne vulgaris, and idiopathic hirsutism includingrecent studies with antiandrogens. Arch Dermatol 1975;111:1496-1502

22. Stoughton RB: Penetration of drugs through the skin. Dermatologica 152 (suppl): 27-36, 1976

23. Matias JR, Malloy V, Orentreich N: Synergistic antiandrogenic effects of topical combinations of 5 alpha reductase and androgen receptor inhibitors in the hamster sebaceous glands. J Invest Dermatol 91:429-433, 1988

24. Takayasu S, Wakimoto H, Itami S, Sano S: Activity of testosterone 5 alpha-reductase in various tissues of human skin. J Invest Dermatol 74:187-191,1980

25. Sawaya ME, Hoenig LS, Hsia SL: Increased androgen binding capacity in sebaceous glands in scalp of male pattern baldness. J Invest Dermatol 92:91-95, 1988, Martin HF, Stripp B, et al: SpiroH

[WannaKnowMore]

2) Flutamide

Flutamide is stronger than spirolactone and has been used as an oral prostate cancer medecine for quite some time.

Flutamide is one of the strongest androgen receptor blockers available and can be used topically with great effect.

Flutamide is available under many brand names in oral form and unlike spirolactone can be mixed in a minoxidil solution for topical use.

It is recommended that pestle and mortar into a fine powder crush 10 tablets of flutamide up and dissolved into a minoxidil solution of 60 mls and used twice a day. Flutamide comes in 250 mg tablets which commonly retail at around $2 a pill.

Flutamide research

ntov A, Serafimovich S, Gilhar A Ben-Gurion University of the Negev, The Institutes for Applied Research, PO Box 653, Beer-Sheva, Israel. [Medline record in process] The purpose of this study was to test the ability of topical formulations of finasteride and flutamide to re-enlarge hair follicles in male-pattern baldness. This was evaluated by an experimental model of human scalp skin graft transplanted onto SCID mice. A comparison was made between formulations containing finasteride and flutamide, and a vehicle formulation in terms of the mean hairs per graft, length, diameter of the shafts, and structures of the growth stages of the hair. Flutamide and finasteride had a significantly higher effect (P<0.05) than the placebo in all the tested parameters, but flutamide demonstrated more hair per graft and longer hair shafts than finasteride (P<0.05). The number of hairs per graft for flutamide and finasteride groups were 1.22+/-0. 47 and 0.88+/-0.95 hairs/0.5 mm2 graft, respectively, versus 0. 35+/-0.6 hairs/graft for vehicle-treated graft. Similarly, hair lengths for flutamide and finasteride were 5.82+/-0.50 and 4.50+/-0. 32 mm, respectively, versus 2.83+/-0.18 mm for the vehicle-treated grafts. An in vitro diffusion study of flutamide gel using hairless mouse skin demonstrated the beneficial effect of the vehicle composition in comparison with a hydroalcoholic solution or a gel containing no penetration enhancer. It is therefore suggested that this topical composition containing flutamide or finasteride may effectively result in regression of male-pattern baldness

Study showing flutamide is the strongest androgen receptor blocker

Clin Endocrinol Metab 1984 Jul; 59(1):51-55 The use of human skin fibroblasts to obtain potency estimates of drug binding to androgen receptors. Eli C, Edelson SKAlthough several drugs with antiandrogenic properties have been used to treat such conditions as prostatic carcinoma, precocious puberty, acne, and hirsutism, their relative strengths in human tissues are not known. Most of the compounds that are effective clinically in opposing androgen action interact with the androgen receptor in various assay systems. To determine in human cells the relative potencies of these agents as well as others with androgenic properties, we measured the abilities of various compounds to compete with [3H]dihydrotestosterone [(3H]DHT) for androgen-binding sites in dispersed human genital skin fibroblasts at 22 degrees C. The concentrations of unlabeled DHT, methyltrienolone (a synthetic non- metabolizeable androgen), and testosterone required for 50% inhibition of [3HJDRT binding were similar, approximately 1 riM [0.87+1-0.12 (+1- SE), 1.18+1-0.18, and 1.01 +A 0.20 riM, respectively]. The relative binding activities, defined by the ratio of the concentration of methyltrienolone to he concentration of competitor required for 50% displacement of [311]DHT, were as follows: flutamide greater than ~956 (a synthetic antiandrogen) greater than megestrol acetate greater than cyproterone acetate greater than estradiol greater than spironolactone much greater than testolactone greater than cimetidine. Danazol, an androgen agonist that causes hirsutism, was nearly as effective as spironolactone in its ability to compete for the fibroblast androgen receptor, 50% inhibition of fibroblast [3H]DRT binding was achieved by 1.76+1-0.31 nM spironolactone and 2.85+1-0.50 tiM danazol. Two other compounds that induce hirsutism, diphenylhydantoin and diazoxide, did not displace [3H]DHT. We conclude that 1) of the compounds tested, flutamide, which is rapidly metabolized in vivo to a much less potent competitor, is the most potent antiandrogen in its ability to interact in vitro with human skin fibroblast androgen receptors; 2) estradiol is a relatively potent androgen receptor binder; and 3) this receptor asay, combined with metabolic clearance and pharmacokinetic considerations, should be useflil in selecting drugs for androgen and antiandrogen therapy.

The other point of the of androgen receptor blockers is that they will block the androgen receptor site regardless of the androgen being d-bol primo winny or dht so will work better for all types of steriods and not just testosterone.

This concludes the use of anti androgens and using hormonal mechanisms and their use in hair loss.

Also there has been a lot of discusion about the shampoo Nizoral and it’s use in hair loss so far it has been shown to have some small effect and may be of use to use as an additive to the other drugs mentioned.

Research on Nizoral

Authors Pierard-Franchimont C. De Doncker P. Cauwenbergh G. Pierard GE. Institution Department of Dermatopathology, University of Liege, Belgium. Title Ketoconazole shampoo: effect of long-term use in androgenic alopecia. Source Dermatology. 196(4):474-7, 1998. Abstract BACKGROUND: The pathogenesis of androgenic alopecia is not fully understood. A microbial-driven inflammatory reaction abutting on the hair follicles might participate in the hair status anomaly. OBJECTIVE: The aim of our study was to determine if ketoconazole (KCZ) which is active against the scalp microflora and shows some intrinsic anti-inflammatory activity might improve alopecia. METHOD: The effect of 2% KCZ shampoo was compared to that of an unmedicated shampoo used in combination with or without 2% minoxidil therapy. RESULTS: Hair density and size and proportion of anagen follicles were improved almost similarly by both KCZ and minoxidil regimens. The sebum casual level appeared to be decreased by KCZ. CONCLUSION: Comparative data suggest that there may be a significant action of KCZ upon the course of androgenic alopecia and that Malassezia spp. may play a role in the inflammatory reaction. The clinical significance of the results awaits further controlled study in a larger group of subjects.

Immunosuppresants the future in Hair loss???

This just about covers the hormonal mechanisms and their regard to androgenic alopecia.

The androgens seem to cause the hair loss by causing the body to see the hair follicles as a foreign body and make the immune system attack them.

This effect has been thoroughly covered in the use of the immunosuppresant drug cyclcosporin which is used in organ transplants to stop the body rejecting the organs.

One of the most common side effects of cyclosporin is hypertrichosis and in studies cyclosporin has had an 80% sucess rate in reversing alopecia. Unfortunately cyclosorin only worked orally and not topically the reason for this is the high molecular weight of cyclosporin and therefore the lack of topical absorption.

Using cyclosproin orally is definitely not recommended as it has many acute side effects.

There is another drug with in the class of topical immunospersants which works much better topically due to it’s much lower molecular weight this drug is called Tacrolimus (also known as FK506).

[WannaKnowMore]

Tacrolimus (FK506) the best current treatment for hair loss and regrowth

Tacrolimus is the current best drug for hair loss in my opinion unfortunately it is not commonly available in topical form though the drug company Fujisawa has an NDA awaiting for tacrolimus for it’s use in atopic dermatitis (eczema).

Currently the only place which carries tacrolimus is www.communitydrug where it is priced at $130 for 30 mls this price will significantly drop when the official form of the drug from the manufacturer Fujisawa is FDA approved later this year.

Tacrolimus for me personally has regrown so much of the hair I have lost over the past few years making my hair loss become hardly noticeable.

In the studies it has been used at only once or twice a week I myself have opted to use it 1ml every other day.

This is the first drug which works in a way completely aside from hormonal manipulation or through the potassium k channel openers (minoxidil is a drug of this class) and is the best current way to treat hair loss.

There is much research on tacrolimus as presented here

Title Hair growth-stimulating effects of cyclosporin A and FK506, potent immunosuppressants. Author Yamamoto S; Kato R Address Department of Pharmacology, School of Medicine, Keio University, Tokyo, Japan. Source J Dermatol Sci, 7 Suppl:1994 Jul, S47-54 Abstract Cyclosporin A (CsA), a cyclic endecapeptide, is a T cell-specific immunosuppressant and is successfully used in the field of organ transplantation. Another T cell-specific immunosuppressant, FK506, a more recently discovered macrolide antibiotic, is effective against graft rejection at much lower doses than CsA. Although totally different in structure, both compounds inhibit T cell activation by interfering with the production of interleukin-2 (IL-2) by inhibiting IL-2 gene expression, probably through the inhibition of calcineurin, a Ca2+/calmodulin-dependent phosphatase. Clinical studies have revealed that FK506 induces a variety of side effects in common with CsA. One of the most common side effects of CsA is hypertrichosis. The hair growth stimulating effect of CsA is observed not only in normal but also in pathological conditions of hair growth, i.e. in patients with alopecia areata and also in some patients with male-pattern alopecia. Although hypertrichosis is induced by both topical and oral administration of CsA, there has been no report showing that FK506 induces hypertrichosis. Recently we have found that topical application of FK506 to skins of mice, rats and hamsters markedly stimulates hair growth. This hair growth stimulating effect of FK506 is observed when applied topically but not by oral administration, even with a dose which causes marked immunosuppression. The hair growth stimulating effect of FK506 in normal animals may apparently be unrelated to its immunosuppressive effect. In vitro studies revealed that FK506 directly stimulates hair follicles. Mechanisms of hair growth stimulating effects of FK506 and CsA remain to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)

Title Effects of cyclosporin A on hair. Author Lutz G Address Department of Dermatology, Rheinische Friedrich-Wilhelms-UniversitÂat, Bonn, FRG. Source Skin Pharmacol, 1994, 7:1-2, 101-4 Abstract Cyclosporin A (CSA) is an immunosuppressive agent that has provided new approaches in transplantation medicine and in the treatment of autoimmune diseases. One of the most common dermatological side effects of oral CSA is dose-dependent hypertrichosis. This stimulating effect on hair growth encouraged a number of investigators to use CSA not only in the treatment of alopecia areata (AA), but also in male pattern alopecia (MPA). While oral application proved successful, the beneficial effect of topical application was very limited in both AA and MPA. Language of Publication

Title Hair growth modulation by topical immunophilin ligands: induction of anagen, inhibition of massive catagen development, and relative protection from chemotherapy-induced alopecia. Author Maurer M; Handjiski B; Paus R Address Department of Dermatology, Charité Hospital, Humboldt-Universität zu Berlin, Germany. Source Am J Pathol, 150(4):1433-41 1997 Apr Abstract Selected immunophilin ligands (IPLs) are not only potent immunosuppressants but also modulate hair growth. Their considerable side effects, however, justify at best topical applications of these drugs for the management of clinical hair growth disorders. Therefore, we have explored hair growth manipulation by topical cyclosporin A (CsA) and FK 506 in previously established murine models that mimic premature hair follicle regression (catagen) or chemotherapy-induced alopecia, two major pathomechanisms underlying human hair loss. We confirm that topical CsA and FK 506 induce active hair growth (anagen) in the back skin of C57BL/6 mice with all follicles in the resting stage (telogen) and show that both IPLs also inhibit massive, dexamethasone-induced, premature catagen development in these mice. Furthermore, we demonstrate that CsA and FK 506 provide relative protection from alopecia and follicle dystrophy induced by cyclophosphamide, possibly by favoring the dystrophic anagen pathway of follicle response to chemical damage. Although it remains to be established whether these IPLs exert the same effects on human hair follicles, our study provides proof of the principle that topical IPLs can act as potent manipulators of clinically relevant hair-cycling pathomechanisms. This strongly encourages one to explore the use of topical IPLs in the management of human hair growth disorders.

The effects of immunosuppressive peptidyl-prolyl cis-trans isomerase (PPIase) inhibitors, cyclosporin A, FK506, ascomycin and rapamycin, on hair growth initiation (anagen hair induction) in mouse were studied by topical application on the dorsal skin surface during the telogen phase of the hair cycle. Single applications of cyclosporin A and FK506 (10 to 100 nmol in 5 microliters of ethanol) induced new hair growth in 12 days within the restricted area where the compounds were applied. On the other hand, ascomycin and rapamycin did not initiate new anagen hairs even at higher doses (1 mumol in 5 to 10 microliters of ethanol). The effects of simultaneous application of the immunosuppressants were also tested by a single topical application. Ascomycin did not inhibit the anagen hair induction by cyclosporin A, but inhibited hair induction by FK506. Rapamycin inhibited new hair growth induced by cyclosporin A and FK506. These results suggest that the inhibition of PPIase is not required for the initiation of a new hair cycle in mice, and that anagen hair induction caused by cyclosporin A and FK506 is not a result of immunosuppression. The present results also indicate that a single application of an adequate quantity of cyclosporin A and FK506 is sufficient to initiate new hair growth

Fujisawa Contact: Maribeth Landwehr Communications (847) 317-8988

FUJISAWA HEALTHCARE, INC. SUBMITS NDA FOR MUCH ANTICIPATED DERMATOLOGY PRODUCT Deerfield, Ill., September 9, 1999 -- Fujisawa Healthcare, Inc. (Fujisawa) announced today that a New Drug Application (NDA) has been submitted to the U.S. Food and Drug Administration (FDA) for a new topical dermatology product. The submission seeks approval for the use of tacrolimus ointment in the treatment of atopic dermatitis.

Atopic dermatitis, commonly known as eczema, is a chronic skin disorder characterized by inflammation, itching, and scaling. It is estimated by the National Institutes of Health that more than 15 million people in the U.S. have symptoms of atopic dermatitis, with a significant presence in the pediatric population.

Tacrolimus ointment Phase III clinical trials were completed in March 1999. More than 1,000 patients suffering from atopic dermatitis participated in the study. Participants were treated at more than 40 clinical sites in the U.S. and ranged in age from two to 79. Of these patients, one-third were children under the age of 15. In approximately one-fifth of the patients, this condition involved or covered more than 75 percent of their bodies.

Topical tacrolimus is the first new therapy to specifically treat atopic dermatitis in over 40 years. "Sufferers of atopic dermatitis have been looking for a new form of relief for many years. Our tacrolimus ointment may provide an important additional treatment option for these patients and their families," said Ira Lawrence, M.D, vice president, research and development.

"We are confident in the data included in this NDA and are hopeful that the FDA will reach a favorable conclusion at the end of their review. Fujisawa's worldwide corporate mission is to contribute to healthier, more prosperous lives for people around the world by exploring the frontiers of human health and disease. We feel tacrolimus ointment will assist in the fulfillment of that mission," stated Noboru Maeda, chairman and chief executive officer, Fujisawa Healthcare, Inc.

Tacrolimus ointment will be manufactured for distribution in Fujisawa's Grand Island, N.Y. facility. Production has already begun for use in Japan, where tacrolimus ointment recently was approved for the treatment of atopic dermatitis under the brand name ProtopicÒ . Protopic is expected to be launched in Japan later this year.

The bottom line

As a steriod user you will not fall into the same class as the non steriod using public by the use of these medecines you shpuld be able to take steriods as you want and avoid the very agonising effect of hair loss caused by Steriod use.

Spirolactone costs $20 for a 60 ml bottle and is avaliable from www.minoxidil.com

[kevin]

Schop! Interessante thread, vooral Tacrolimus. Tiuri, sinds jij het inflammation gedoe goed doorgespit hebt, wat denk je van Tacrolimus?

[Tiuri]

Kevinme!!
Inderdaad zeer interessante thread. Even een eerste reactie op het fluridil-verhaal. Ik vraag me af wie Wannaknowmore precies citeert (misschien kan ie daar na al die tijd nog licht over doen schijnen?), maar het is een beetje een raar persoon. Diegene wilde blijkbaar zo graag dat flutamide goed zou werken, dat ie zelf in de onderzoekstekst heeft lopen pielen :):

Study showing flutamide is the strongest androgen receptor blocker:
We conclude that 1) of the compounds tested, flutamide, which is rapidly metabolized in vivo to a much less potent competitor, is the most potent antiandrogen in its ability to interact in vitro with human skin fibroblast androgen receptors;Waar hier "flutamide" staat, staat in de originele onderzoekstekst (zoals te vinden op PubMed (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6725525&query_hl=18)) "spirononactone"! :D :D :D

Dan straks een reactie op de rest.

[Tiuri]

Schop! Interessante thread, vooral Tacrolimus. Tiuri, sinds jij het inflammation gedoe goed doorgespit hebt, wat denk je van Tacrolimus?Inderdaad ZEER interessant.

Maar ik ga deze thread nu sluiten, puur om te voorkomen dat er waardevolle informatie verspreid op het forum terecht komt.

Discussies over cyclosporine graag voeren in:
Cyclosporine tegen AGA (http://www.haarweb.nl/forum/showthread.php?t=3465)

Discussies over tacrolimus graag voeren in:
Pimecrolimus (Elidel) en Tacrolimus (Protopic) (http://www.haarweb.nl/forum/showthread.php?t=6111)