Vitiligo is a spontaneous irregular depigmentation of skin which can occur at any stage in life with a worldwide prevalence ranging from 0.5% to 4%. Conservative therapies include photochemotherapy, phototherapy with UVB radiation, systemic steroids and pseudocatalase. Modern options include treatment with topical immunomodulators (tacrolimus, pimecrolimus), analogues of vitamin D3, laser and surgery. The face and neck respond best, while the acral areas are least responsive. No single therapy for vitiligo can be regarded as the most effective as the success of each treatment modality depends on the type and location of vitiligo.
    Melanocytes may still be present in long-standing (>25 years) depigmented skin of patients with vitiligo. L-phenylalanine uptake and turnover in the pigment forming melanocytes is vital for initiation of melanogenesis. Phenylalanine hydroxylase activities increase linearly with inherited skin color yielding eightfold more activities in black skin compared to white skin. 
   Camacho and Mazuecos performed an uncontrolled retrospective survey of a group of 193 patients (171 participants after screening) with evolving vitiligo who were treated with oral (50 or 100 mg/kg daily) and topical (10% gel) phenylalanine plus sun exposure . When the study closed, 100% repigmentation was achieved in 122 patients on the face, 35 on the trunk, and 33 on the limbs. Patients who were treated during the months of high solar radiation (and therefore also used the topical phenylalanine) achieved greater repigmentation. No side effects were reported.

   Peroxides are responsible for the destruction of melanocytes (pigment cells). Patients with vitiligo cannot efficiently remove hydrogen peroxide (H2O2) due to low catalase, glutathione peroxidase, and thioredoxin reductase levels. Patients with vitiligo also have problems maintaining calcium balance in their skin. Pseudocatalase cream is an externally applied UVB-activated product containing calcium chloride, manganese chloride, and sodium bicarbonate, which functions like catalase by removing peroxides from vitiligo affected skin and inhibits the progression of pigment loss. 
   On the National Vitiligo Foundation website (http://nvfi.org/pages/medprof/update_on_therapies.pdf), Dennis P. West, Ph.D., Professor of Dermatology at Northwestern University in Chicago, IL, reported that a specific compounded prescription containing pseudocatalase, calcium chloride, manganese chloride, sodium bicarbonate, and distilled water in a vanishing cream base could be applied externally to inhibit the progression of pigment loss. Pseudocatalase cream is usually applied twice daily to the entire skin surface. Light treatments or sun exposure are usually used to restore pigment. Dr West notes that patients usually begin to see control of pigment loss in 2-4 months. The duration of treatment is indefinite, or as determined by a physician, and there are no known systemic side effects.
   The use of pseudocatalase cream can lead to recovery of the oxidative damage in the epidermis and remarkable repigmentation in this disorder. Melanocytes can recover their functionality in vivo and in vitro upon the removal of hydrogen peroxide. Thirty-three patients with the depigmentation disorder vitiligo were successfully treated with a new topical application of pseudocatalase, calcium and short-term UVB light exposure. First repigmentation occurred in the majority of cases after 2-4 months. Complete repigmentation on the face and dorsum of the hands appeared in 90% of the group. In all patients, active depigmentation was arrested. None of them developed new lesions during treatment. No recurrence of the disease was observed during a 2-year follow-up.

  

Skin Pharmacol Appl Skin Physiol 1999 May-Jun;12(3):132-8
J Pathol 2000 Aug;191(4):407-16
J Investig Dermatol Symp Proc 1999 Sep;4(1):91-6

  

   The androgen hypothesis originated with the Nobel-winning work of Charles Huggins, who, together with coauthor Clarence Hodges, reported in 1941 that castration caused prostate cancer (PCa) regression in men with metastatic disease, and that testosterone (T) administration caused PCa progression, "prostate cancer is androgen-dependent, and that testosterone 'enhanced the rate of growth' of prostate cancer. Forty years later, Fowler et al. found that 87% of men with metastatic prostate cancer who received exogenous testosterone suffered exacerbation, leading to the oft-repeated suggestion that TRT in men with prostate cancer was akin to 'pouring gasoline on a fire.' 2
   "This historical concern that has led to hesitation in TRT administration for men without prostate cancer appears unfounded... Several longitudinal studies have shown no influence of serum testosterone levels on the risk of developing prostate cancer...2
   "The androgen hypothesis was proposed and accepted before knowledge of hormone receptors, PSA, and prior to reliable measures of T. Anecdotal observations in small numbers of men with metastatic PCa were generalized beyond reason, findings were oversimplified, and contrary evidence was ignored. Huggins and Hodges, for example, based their conclusions that T activated PCa on the erratic and now-abandoned blood test, acid phosphatase, in only two men treated with T injections for no more than 18 days, one of whom was already castrated...2
   "Indeed, the evidence against the androgen hypothesis was always obvious to anyone who wished to see: PCa occurs as men age and T declines; PCa never occurs in young men during the peak T years." 2
    Observations in humans, animals, and PCa cell lines have led to the Saturation Model, ie, that "androgens have a finite, limited ability to stimulate prostate tissue, malignant or benign. This refinement is simple yet profound. Yes, prostate tissue requires androgens for optimal growth. However, it can only use a relatively small amount, beyond which additional androgen is merely excess. The saturation point is well below physiologic concentrations, which explains why manipulation of serum T into or out of the castrate range produces large changes in prostate biology, whereas normal prostate and PCa appear completely indifferent to variations in serum T from the near-physiologic to supraphysiologic range."2
   Muller et al. of Department of Surgery, Duke University School of Medicine found that "baseline serum testosterone and DHT levels were unrelated to PCa detection or grade. Our findings of the lowest testosterone levels being associated with the lowest PCa risk with no further changes with higher testosterone support a saturation model but must be confirmed in future studies..." After the exclusion criteria were applied, their study consisted of 149,354 men with prostate cancer.3