New Vitiligo Cure
Related areas such as phytochemistry, biological activities of natural products, and quality control issues and methods relevant to botanical products. Dr. Soumayanath's research has focused on investigating traditional plant remedies used in the treatment of vitiligo, psoriasis, and diabetes, both in terms of defining their modes of action and as sources of potential new therapeutic agents for these diseases.
The oral absorption of clofazimine is estimated to be about 50 . It is a highly lipid-soluble drug that is distributed into lipoidal tissue and the reticuloendothelial system. Urinary excretion of unchanged drug and metabolites is negligible. Its half-life after repeated dosage is estimated to be about 70 days. Severe gastrointestinal intolerance to clofazimine is relatively common. Skin pigmentation, ichthyosis and dryness, rash, and pruritus also occur frequently.
The most common early signs of chronic arsenic poisoning are muscle weakness and aching, skin pigmentation (especially of the neck, eyelids, nipples, and axillae), hyperkeratosis, and edema. GI involvement is less prominent in long-term exposures. Other signs and symptoms that should arouse suspicion of arsenic poisoning include garlic odor of the breath and perspiration, excessive salivation and sweating, stomatitis, generalized itching, sore throat, coryza, lacrimation, numbness, burning or tingling of the extremities, dermatitis, vitiligo, and alopecia. Poisoning may begin insidiously with symptoms of weakness, languor, anorexia, occasional nausea and vomiting, and diarrhea or constipation. Subsequent symptoms may simulate acute coryza. Dermatitis and keratosis of the palms and soles are common features. Mee's lines are found characteristically in the fingernails (white transverse lines of deposited arsenic that usually appear 6 weeks after exposure). Desquamation and scaling of...
The incidence of skin cancer is strongly influenced by inherited genetic variation. At the population level, skin pigmentation is the most obvious factor modulating risk. Individuals with inherited deficiences in the repair of UV-damaged DNA are at even greater risk, prominently xeroderma pigmentosum patients. In a different fashion, PTCH1 in BCC, certainly, ESS1 in SCC, perhaps, and CDKN2A in melanoma, in rare cases, behave as classical 'gatekeeper' tumor suppressors predisposing to skin cancer.
Skin pigmentation in man is highly variable. It ranges from a complete lack due to mutations in tyrosinase ('albino') to very intense, e.g. in populations from equatorial Africa. In most humans, pigmentation is inducible in response to sun exposure. It is regulated by interaction of melanocytes with the neighboring keratinocytes and by the hormone aMSH (melanocyte stimulating hormone).
The effects of pharmaceutical photoinstability have been with us for many centuries. The ancient Egyptians may not have known why certain effects took place but they were wise enough to be able to see their positive effects and exploit them for the treatment of known maladies. Examples supporting this statement are the use of crude psoralens by ancient Egyptians to treat vitiligo, a fact well documented by Abdel M. Mofty14 of the University of Cairo in the 1940's and during more modern times the 1903 Nobel Prize in Medicine, given to, Niels R. Finsen for his finding that skin lesions of tuberculosis often resolved after exposure to ultraviolet light.14
IL-2 can be given by subcutaneous or intravenous injection or infusion. Its toxicity has limited its widespread use in patients. The vast majority of patients are affected by the grade I II toxicities commonly associated with other cytokines, including fever, nausea and vomiting, diarrhoea, fatigue, myalgia and arthralgia. Erythema at the site of injection is also common. The most severe toxicities occur at higher doses and are associated with a vascular leak syndrome, which is manifested by hypotension, tachycardia and oliguria, and can result in multiorgan damage (Table 10.4). This syndrome is thought to be mediated by nitric oxide produced in response to local secondary release of cytokines such as TNF, IL-1 and IFN-7. A number of TNF inhibitors have been evaluated in order to reduce this but with little benefit (Margolin et al., 1997). Autoimmune phenomena can occur following treatment with IL-2 (Gaspari, 1994). These include hypothyroidism, pemphigus, psoriasis and vitiligo....