Chronic infection is common as the thickened sebaceous fluid traps bacteria.Rhinophyma is characterised by hypertrophy of nasal skin, with hyperplasia and fibrosis of the sebaceous glands and connective tissue. The nasal tip and alae are preferentially affected by the hypertrophy, and the lower portion of the nose is predominantly affected. The underlying bony structure is not affected.The exact pathophysiological mechanism underlying the development of rosacea and rhinophyma is unknown, but a combination of neurovascular and immune disturbance is thought to be involved, causing inflammation, fibrosis, and vascularisation. Male predisposition
Even though females are more often affected by acne rosacea, they seldom go on to develop rhinophyma. It is thought that androgenic factors predispose men to develop rhynophyma. Diagnosis
Rhinophyma is diagnosed clinically based on presentation (erythema, telangiectasias, and nasal skin hypertrophy). Diagnosis is confirmed by histology. Treatment
Treatment consists of paring down the bulk of the tissue with a sharp instrument or carbon dioxide laser and allowing the area to re-epithelialise. Sometimes, the tissue is completely excised and the raw area skin-grafted. Epidemiology
Rhynophyma is most common in males of European heritage over the age of 50. Males are 5 to 30 times as likely to be affected as females, possibly due to androgenic factors. In the United States, people of predominantly Asian and African ancestry are only rarely affected by the condition. Society
Colloquial names for the condition include "whiskey nose", "gin blossom", and "potato nose".
Diagnosis
Diagnosis is based on the characteristic appearance of non-healing raised, scaling lesions that may ulcerate and become secondarily infected with organisms such as Staphylococcus aureus, in someone who has returned from an endemic area.In resource limited settings, fine-needle aspiration of the lesion  is confirmatory with identification of amastigote form of Leishmania. The gold standard for diagnosis is a PCR test. Treatment
American cutaneous and mucocutaneous leishmaniasis
The best treatment for American cutaneous and mucocutaneous leishmaniasis (ACML) is not known. Pentavalent antimonial drugs (sodium stibogluconate (SSG) and meglumine antimonate (Glucantime, MA)) have been used since the 1940s, but they are expensive, toxic, and painful. Treatments that work for one species of Leishmania may not work for another; therefore, it is recommended that the exact species be identified prior to initiating treatment. Unfortunately, leishmaniasis is an orphan disease in developed nations, and almost all the current treatment options are toxic with significant side effects.The best-studied treatments for ACML caused by two Leishmania species are listed below. However, one should note that most of the studies examining treatments of ACML were poorly designed. Therefore, no definitive treatment guidelines or recommendations are currently available, as large-scale and well-conducted studies are necessary to evaluate the long-term effects of current treatments. Leishmania braziliensis and Leishmania panamensis: There is good evidence that oral allopurinol plus intramuscular MA is superior to either medication alone. In addition, a 20-day course of intravenous MA was better than a 7-day course as well as a 3- or 7-day course of intravenous MA with paromomycin + 12% methylbenzethonium chloride.