Hyperpigmentation may be the sign o...

Hyperpigmentation may be the sign of a benign or relatively easily treated condition, or it may indicate the air of a life-threatening condition of that kind as melanoma. This two-part article readys a suggested approach to adult patients with increased pigmentation and reviews various underlying causes.

Melanocytes and Pigmentation

Melanocytes are derived embryonically from neural crown cells that migrate into the basal layer of the epidermis. In the skin, melanocytes continuously effect melanosomes--organelles that are transferred to keratinocytes. The melanosomes reverse tyrosine to melanin, giving skin its color. subject to the stimulus of hormones or irritation, the production of melanosomes increases, leading to hyperpigmentation. In reply to sun exposure or idiopathically in any disorders, hyperplasia of melanocytes be met withs and causes hyperpigmentation. (1)

The same melanocyte concentration is current in persons of all races who have normal skin. However, an races have larger melanosomes, giving their skin a darker color. (23)

Diagnostic Approach

A simple way to approach hyperpigmentation is to consider whether the increase in color is caused from an increase of melanin, an increase in melanocytes, or the deposition of another substance that adds color to the skin (Figure 1) fix uponed disorders and their characteristics are discussed in the following sections and summarized in Table 1; other disorders are discussed and summarized in part II of this article.

[FIGURE 1 OMITTED]

A directed history and physical examination present clues to the underlying cause of hyperpigmentation. The history should address the time of attack of the lesion, because near disorders (e.g., neurofibromatosis) are congenital, while others bring to maturity in childhood (e.g., ephelides) or during pregnancy (eg melasma). Systemic symptoms may indicate the carriage of hyperthyroidism, Addison's disease, or diabetes-related disorders. A review of medication use, fill up use, and exposure to plants and ultraviolet radiation can help determine whether hyperpigmentation is caused from a medication side effect or a phototoxic reaction.

The size and number of the lesions are useful in diagnosing neurofibromatosis, ephelides, and lentigines. The border, color, and character of a lesion help to distinguish melanoma from a benign lesion, while the distribution of skin changes assists in the diagnosis of melasma and acanthosis nigricans. Congenital Lesions: Cafe au Lait Macules

Cafe au lait (coffee with milk) macules can be congenital, or they may make known in childhood. These flat macules usually arise on the trunk and can have a sleek or irregular border (Figure 2) They range from 02 to 4 cm in diameter in infants if it be not that can reach 30 cm in diameter in adults. (3) The hyperpigmentation is caused according to increased melanin in melanocytes and basal keratinocytes. (4)

Cafe au lait macules may be a sign of neurofibromatosis. The diagnosis of this disease requires the air of at least two of seven criteria established at a National Institutes of Health (NIH) consensus disclosure conference (Table 2). (5) The appearance of six or more cafe au lait macules is single in kind of the diagnostic criteria; axillary or groin freckling is another (Figure 3) Hence, the nearness of axillary or groin freckling should quick a search for cafe au lait macules, and vice versa. If neurofibromatosis is suspected or confirmed, an ophthalmologist can discover optic gliomas and iris hamartomas, which are additional criteria for the diagnosis of neurofibromatosis. The American Academy of Dermatology has practice guidelines based in succession the NIH definition. (5) [Evidence flush C, consensus opinion]

Cafe au lait macules themselves require treatment simply if cosmesis is requested. Surgical or laser treatment from a cosmetic dermatologist may be considered upon an individual basis. From a practical standpoint, neurofibromas, which can take place throughout the body, pose more of a cosmetic and functional trouble (Figure 4).

Consultation with a geneticist may be provident because neurofibromatosis is an autosomal dominant condition, although spontaneous mutations cause 50 percent of cases. (6) one patients have cafe au lait macules without neurofibromatosis; their children are not at increased risk for the disease.

Diffuse Hyperpigmentation

Diffuse hyperpigmentation may have a systemic cause, similar as Addison's disease, hyperthyroidism, or hemochromatosis. It also may be met with because of a medication side effect

In Addison's disease, the adrenal glands fail to make adequate amounts of mineralocorticoids and glucocorticoids. When elevations of melanocyte-stimulating hormone and adrenocorticotropic hormone (also referr to as corticotropin) horizontals occur as the pituitary gland tries to stimulate the adrenal glands, melanin production increases, causing hyperpigmentation with a "muddy" appearance. (7) The hyperpigmentation is diffuse, on the contrary more pronounced in sun-exposed areas and in the perineum, axillae, areolae, palms, and ones (8) Patients with Addison's disease should be treated with mineralocorticoid and glucocorticoid replacement to shorten the drive for excess production of adrenocorticotropic hormone and melanocyte-stimulating hormone.