First, the skin may respond as a target organ, with different hormones having effects on specific areas of the skin. The target areas include all elements of the skin, including the epidermis, melanocytes, pilosebaceous units, dermal elements, adipose tissue, the cutaneous immune system, and endothelial cells. For example, growth hormone deficiency results in decreased amounts of dermal elastin, decreased thyroid hormone levels lead to pilosebaceous atrophy, and excessive glucocorticoid levels result in epidermal and dermal atrophy. Second, hormonal excesses or deficiencies may effect various metabolic functions that may indirectly influence the structure and function of the skin. Pinnal erythema may be associated with increase blood flow in hyperthyroid cats, xanthomas with dyslipoproteinemias, and calcinosis cutis with hyperadrenocorticism or hypervitaminosis D. Immunologic effects of hormonal disturbances are also responsible for many cutaneous lesions.
Secondary infections are common in patients with decreased thyroid function or hyperadrenocorticism.
The large relative size of the skin and the temperature gradient between the skin and body core are two factors responsible for this relationship. Histologic examination may help to identify the etiologic agent or mechanism of disease. Cutaneous lesions include erythema, alopecia, crusting, nodules, scaling, and excoriations resulting from pruritus. Interference with ingestive, digestive, absorptive or transport mechanisms of nutrients can result in skin disease. Many toxins are readily absorbed through the skin and may induce systemic disease from this route of exposure.