Pigmentation, drug-induced

An increase in pigmentation of eyelid skin is also possible. This increased skin pigmentation can occur several months after latanoprost therapy is begun. Once the drug is discontinued, the drug-induced pigmentary changes usually subside. 

Drug-induced pigmentation on the skin, hair, nails, and mucous membranes is a result of melanin synthesis, increased lipofuscin synthesis, or post-inflammatory pigmentation. 

Post-inflammatory pigmentation can follow a variety of drug-induced inflammatory cutaneous reactions fixed eruptions are known to leave a residual pigmentation that can persist for months. 

The fact that cytochrome P-450 functions as terminal oxidase for these reactions is supported by both indirect and direct evidence (a) the drug-induced increase in the hydroxylase activity of liver microsomes is accompanied by a similar increase in microsomal cytochrome P-450 (25, 26), an indication that this pigment participates in the mixed-function oxidation of drugs (b) maximal reversal of the characteristic CO inhibition of mixed function oxidations is accomplished by illuminating the enzyme assay system with monochromatic light of 450 m/x wavelength, the absorption maximum of the CO compound of reduced cytochrome P-450 (P-450 -CO). 

Harber LC, Bickers DR (1989) Drug induced photosensitivity (phototoxic and photoallergic drug reactions). In Photosensitivity diseases principles of diagnosis and treatment, 2nd edn. Decker, Toronto, pp 160-202 Hare PJ (1951) A case of occupational iron pigmentation of the skin. Br J Dermatol 63 63-66... 

Since interferons are almost always used in combination with ribavirin in patients with hepatitis C infection, it can be difficult to know whether adverse events, if drug-induced, are due to one or the other. In many cases authors do not even discuss this problem, often attributing the supposed adverse effects to the interferon. In some cases withdrawal of one of the agents can provide evidence, and in other cases there may be other clues. For example, in cases of skin pigmentation at the site of injection of interferons, the adverse effect may be presumed to be due to interferon [26 ], a type II between-the-eyes adverse effect [27 ]. In one case hemolytic anemia was attributed to interferon rather than ribavirin because the patient had previously taken a course of interferon without adverse effects [28" ] presumably the inference was that the patient had been sensitized by the previous course. A systematic review of cases in which the drugs were used together and individually can also yield useful information, as in the case of pneumonitis in patients being treated with interferon and ribavirin, attributed to interferon [29" ]. Similarly, in cases of ocular myasthenia [30" ], pleural effusion [31 ], and cataract [32" ] the interferon was blamed because no previous cases were found in association with ribavirin alone. In cases in which the adverse event persists... 

Taurog A, Dorris ML, Doerge DR. Minocycline and the thyroid antithyroid effects of the drug, and the role of thyroid peroxidase in minocycline-induced black pigmentation of the gland. 

A variety of relatively uncommon dermatological side effects have been noted to be associated with antipsychotic agents. These include maculopapular rashes, urticaria, and erythema multiforme (Arana, 2000). Photosensitivity and skin pigmentation can also occur during treatment with these drugs. Although skin pigmentation has been most frequently reported with chlorpromazine, this can occur with thioridazine and trifluoperazine (Harth and Rapoport, 1996). In addition, treatment-induced alopecia has been reported for haloperidol, olanzapine, and risperidone (Mercke et ah, 2000). 

Clarithromycin has been associated with fixed dmg emp-tions and hypersensitivity reactions (41,42). In one case a clarithromycin-induced fixed drug eruption was reproduced by oral provocation, whereas patch tests on both unaffected and residual pigmented skin were negative (43). 

Eisen D, Hakim MD. Minocycline-induced pigmentation. Incidence, prevention and management. Drug Saf 1998 18(6) 431-40. 

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