Chapter 1 reviewed the biology of human skin pigmentation, and it is now appropriate to consider the pathology of the melanin pigmentary system and, if possible, to clarify the mechanisms producing these abnormalities. Basically, disturbances in human pigmentation manifest clinically as either excessive pigmentation (hyperpigmentation) or deficient pigmentation (hypopigmentation). Any respectable textbook of dermatology will provide lists of the legion conditions which fall under the rubric of the hyperpigmentation and hypopigmentation disorders respectively. Most of these are rare and of no interest to the general reader. This chapter will discuss some selected examples of the hyperpigmentation disorders and the following chapter will consider certain conditions associated with hypopigmentation.

It must be emphasized at the outset that the diagnosis of hyperpigmentation may be difficult. The normal skin colour of a Caucasoid of Mediterranean origin, for example, may not differ in the intensity of its hue from the abnormal pigmentation of a fair-skinned Scandinavian patient. Furthermore, pigmentation of the oral mucosa (e.g. gums) is usually pathological in fair-skinned Caucasoids but not in the darker ethnic groups (see p. 76).

Hormonal and metabolic factors

Reference was made in Chapter 2 to hyperpigmentation caused by the sex hormones (oestrogens and progesterone) and particularly to the chloasma induced by pregnancy and oral contraceptive agents (see Fig. 2.2).

The classic pathological condition causing hyperpigmentation is Addison's disease. This disease, described by Addison in 1855, is due to a failure of the adrenal glands to produce sufficient quantities of the adrenal hormones (corticosteroids). A common cause (and probably the commonest in Third World countries) is tuberculosis of the adrenal glands. Addison's disease results in weakness, lassitude and low blood pressure.