Mild rosacea may not necessarily require treatment if the individual is not bothered by the condition. More resistant situations may require a combination approach, using several of the treatments at the same time. A combination approach may include prescription sulfa facial wash twice a day, applying an antibacterial cream morning and night, and taking an oral antibiotic for flares. A series of in-office laser, intense pulsed light, or photodynamic therapies may also be used in combination with the home regimen. It is advisable to seek a physician's care for the proper evaluation and treatment of rosacea.
Rosacea is a common, chronic cutaneous disorder with a prevalence of -10%, predominantly affecting women. The disease presents with a heterogeneous clinical picture characterized by transient flushing, persistent facial redness, telangiectasias, and, in more severe clinical forms, the presence of inflammatory papules and pustules in the central third of the face. Although its pathophysiology is complex and still remains unknown, factors that exacerbate the disease are well defined. They include genetic predisposition as well as external factors such as exposure to UV light, high temperature, and diet. Besides these well-known factors, recent studies suggest that drugs and vitamins could also be possible factors inducing rosacea-like dermatitis or aggravating pre-existing rosacea. Although these are less common possible triggering factors, the aim of this article is to present the current knowledge on the association between use of certain drugs or vitamins and rosacea.
Prednisolone is primarily eliminated by hepatic metabolism, to approximately 70 % by glucoronidation and to approximately 30 % by sulphatation. There is also conversion to 11ß,17ß-dihydroxyandrosta-1,4-dien-3-one and to 1,4-pregnadien-20-ol. The metabolites exhibit no hormonal activity and undergo primarily renal elimination. Negligible amounts of prednisone and prednisolone are found unchanged in the urine. The plasma elimination half-life of prednis(ol)one is approximately 3 hours. In patients with severe hepatic dysfunction the half-life may be prolonged and a dose reduction should be considered. The duration of the biological effects of prednis(ol)one exceeds the duration of the presence in the serum.