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Bruce R. Smoller (editor) - Clinical and Pathological Aspects of Skin Diseases in Endocrine, Metabolic, Nutritional and Deposition Disease

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Book:
Clinical and Pathological Aspects of Skin Diseases in Endocrine, Metabolic, Nutritional and Deposition Disease
Author:
Bruce R Smoller editor / Franco Rongioletti editor
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Springer
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2010
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Clinical and Pathological Aspects of Skin Diseases in Endocrine, Metabolic, Nutritional and Deposition Disease: summary, description and annotation

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It is a pleasure to introduce this new book, Clinical and Pathological Aspects of Skin Diseases in Endocrine, Metabolic, Nutritional, and Deposition Disease, edited by two of my friends and respected colleagues, Franco Rongioletti and Bruce R. Smoller. In fact, I was very ent- siastic when I learned that they were preparing this work. Although endocrine, metabolic, w, and deposition diseases are regularly included in general textbooks of dermatology and d- matopathology, one gains the general impression that these topics receive little emphasis and are mainly included for completeness. The prospect of having all of this information in one volume, lovingly described and detailed by experts in the feld, should be of great interest not only to dermatologists, pathologists, and dermatopathologists but also to internists and en- crinologists, who may well gain a different perspective on these disorders. As a derma- pathologist, I am also pleased that this project has been organized and undertaken by two distinguished authorities in cutaneous pathology. This assures a close integration of histo- thology and other laboratory techniques with the clinical aspects of these disorders, which will make it possible perhaps for the frst time to view these conditions in a truly comprehensive way. So I invite you, the reader, to open this volume and dig in; be prepared for an eye-catching, intellectually stimulating, and ultimately rewarding experience! Charlottesville, VA James W. Patterson v w Foreword II Dermatopathology is a bridge between Dermatology and Pathology.

Bruce R. Smoller (editor): author's other books

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Part 1
Cutaneous Endocrine Disease

Bruce R. Smoller and Franco Rongioletti (eds.) Clinical and Pathological Aspects of Skin Diseases in Endocrine, Metabolic, Nutritional and Deposition Disease 10.1007/978-1-60761-181-3_1 Springer New York 2010

1. Adrenal Disease

Kenneth B. Calder 1 and Bruce R. Smoller

(1)

Department of Pathology and Cell Biology, University of South Florida, 12901 Bruce B. Downs Blvd, 11, Tampa, FL 33612, USA

Kenneth B. Calder

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Key Points

The clinical signs and symptoms of Cushing syndrome and adrenal insufficiency include a constellation of findings that can involve most major organ systems of the body, including the skin.
There are no specific clinical manifestations of Cushing syndrome or adrenal insufficiency which are pathognomonic for these conditions, thus making the diagnosis a challenge.
Cutaneous manifestations of hypercortisolism include: facial redness (plethora), epidermal atrophy, acne, purpura, hirsutism, and striae distensae.
Hyperpigmentation is a feature of adrenocorticotropic hormone (ACTH)-dependent Cushing disease, while it is not a feature of Cushing syndrome due to primary adrenal hypercortisolism.
The most common skin manifestation of Addison disease is hyperpigmentation, presenting as scattered hyperpigmented macules, diffuse homogenous hyperpigmentation, or hyperpigmentation of the palmar creases and flexural areas.
Pheochromocytomas can rarely present with Addison-like hyperpigmentation or Cushing disease-like hyperpigmentation because of an increase in ectopic ACTH production.

Keywords

Cushing syndrome Addison disease Pheochromocytoma

1.1 Introduction

As a major part of the neuroendocrine system, the hypothalamicpituitaryadrenal axis is responsible for numerous physiologic responses including adaptation to stress, glucose metabolism, blood pressure control, sexuality, mood and emotion, and immune response [].

The outer most layer of adrenal cortex, the zona glomerulosa, is responsible for the production of aldosterone which regulates blood pressure via renal sodium and potassium excretion/absorption. The secretion of aldosterone is influenced by angiotensin II, potassium concentrations, and to a lesser extent ACTH. In the second layer of the adrenal cortex, the zona fasciculata, ACTH stimulates the production of androgens, androstenedione, and dehydroepiandrosterone (DHEA) [].

1.2 Clinical and Pathological Aspects of Skin Manifestations

1.2.1 Cushing Syndrome

Cushing syndrome is the eponym used to describe the clinical findings and symptoms related to overexposure to glucocorticoids. Currently, the most common cause of Cushing syndrome is due to exogenous or iatrogenic hypercorticism [].

Patients with the loss of diurnal variation of ACTH and cortisol secretion have sustained increased levels of cortisol and present with the following symptoms: weight gain, psychological disturbances, decreased libido, hyperglycemia, hypertension, and a constellation of skin findings.

The clinical cutaneous manifestations of hypercortisolism include facial redness ( plethora ), epidermal atrophy , acne (Fig. ].

Fig. 1.1

Acne and central obesity in Cushing syndrome

Fig. 1.2

Hirsutism in Cushing syndrome

Fig. 1.3

Striae distensae in Cushing syndrome

Fig. 1.4

Central obesity with striae in Cushing syndrome

Fig. 1.5

Supraclavicular pad in Cushing syndrome

Fig. 1.6

Moon face in Cushing syndrome

In patients with hypercorticism, the patients skin can appear atrophic, paper-thin, and translucent. Histologically, there is thinning of the epidermis, loss of the normal rete dermoepidermal junction pattern, and loss of the ground substance between collagen and elastin in the dermis resulting in a disorganized appearance of the dermal fibers [].

Fig. 1.7

Histopathology of atrophic skin in Cushing's syndrome (HE stain)

With the loss of dermal support and decreased elasticity, ecchymoses or purpura from minor trauma are more common in areas like the arms and legs. The plethoric appearance of skin is related to dilatation of weakened vessel walls in an already thin epidermis. Cutis marmorata and purplish mottling of the lower extremities (Fig. ].

Fig. 1.8

Purplish mottling of the limbs

Hyperpigmentation is not a feature of Cushing syndrome due to primary adrenal hypercortisolism because the elevated levels of glucocorticoids inhibit the secretion of ACTH and MSH.

Other common skin findings associated with elevated glucocorticoids include hypertrichosis , hirsutism , and acne . The acne lesions associated with hypercorticism are typically uniform in appearance, and unlike acne vulgaris, comedones and cysts are rare. In general, acne and hirsutism tend to be more pronounced in cases of Cushing syndrome due to increased production of adrenal androgens which can also cause male-pattern baldness and clitoral hypertrophy. In Cushing disease, the features of increased androgen production are usually more mild and limited to hypertrichosis of the cheeks and upper lips with lanugo-like hair [].

Other skin manifestations with important clinical implications include the increased risk for infection and delayed wound healing . The immunosuppressive effects of excess glucocorticoids make patients more susceptible to cutaneous staphylococcal, candidal, and dermatophyte infections. The classic hyper- or hypopigmented scaly macules of tinea versicolor can be seen over the chest and upper back, along with infections by such organisms as Trichophyton rubrum resulting in onychomycosis, tinea pedis, and/or tinea corporis [].

1.2.2 Addison Disease

Addison disease is defined as primary adrenal gland insufficiency, which can be divided into three general categories: adrenal dysgenesis, impaired steroidogenesis, and adrenal destruction. In Addison disease, the ability of the adrenal cortex to produce glucocorticoids (cortisol) and mineralocorticoids (aldosterone) is compromised, resulting in increased levels of pituitary ACTH. In secondary adrenal insufficiency due to decreased pituitary ACTH production, glucocorticoid synthesis is impaired but mineralocorticoid production is not affected. Therefore, primary adrenal insufficiency is characterized by mineralocorticoid deficiency and hyperpigmentation, not characteristic of secondary adrenal insufficiency [].

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