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PREFACE

Endocrinology of Aging in Diagrams and Images. Clinical Aspects.

The aged organism can express disease differently than younger adults; as a consequence, the endocrinologist, internist, family doctor, and all the other physicians who encounter elderly patients, should be aware that their symptoms and laboratory tests require special consideration. This is so both for interpreting clinical manifestations and deciding on therapeutic approach. Disregarding these differences may lead to significant medical errors with dire consequences.

Many of age-related changes in metabolism and body composition resemble those typically seen with a variety of disturbances in hormone balance. For example, there are decreases in lean body and muscle mass and in bone density, increases in percent body fat and insulin resistance, and reductions in resting metabolic rate, energy levels, and libido. These same phenomena are variably observed in young adult patients with deficiencies of growth hormone (GH), sex steroid hormones, and thyroid hormone as well as with cortisol excess. To complicate matters further, such changes may also occur in the setting of a variety of chronic diseases and over- or under-nutrition. Moreover, aging is associated with an increased incidence and prevalence of a host of illnesses, including endocrine disorders such as autoimmune hypo- and hyperthyroidism.

Conceptually, it is well understood that endocrine disorders fall into the category of pathophysiology, so that any signs or symptoms of glandular dysfunction are generally explainable by pathophysiological analysis. However, age must be taken into account. This is because physiological changes that occur as we get older alter the pathophysiology of the clinical picture. The central task of this monograph is to explain the characteristic pathological expressions of hormonal alterations with advancing age. The goal of the reader should be to learn and appreciate those changes.

The following chapters are traditionally divided according to specific endocrine systems and will provide the reader, in an orderly fashion, with the most up-to-date published information regarding what is known about how function of endocrine systems is altered during the aging process. It is also the intention of the authors to provide perspective as to how such changes may be both caused by, and the extent to, which they may be causal of, the pathophysiology of senescence.

At the beginning of this work we briefly explore the biological basis of human aging, noting that it is a process primarily based on wear, but modified by compensatory regulatory responses. This is where we and other living things differ from inert matter, which ages by wearing, without the regulatory compensation or repair. Take muscle tissue as an example. If this tissue were to age just by cell attrition, individual prostration would be very premature. This is because without deposition of collagen as a repairing and stabilizing element, the gradual disappearance of myocyte tissue would soon lead to disorganization of muscle components with loss of movement, so that, functional collapse would be very early. Thus, repair and stabilization by collagen deposits corresponds to one mechanism of aging regulation.

Another regulatory phenomenon in the aging process is the rise of LDL-cholesterol, for which demand increases with age, probably because cell membranes are subjected to the deleterious effects of free radicals that require cholesterol for stabilization. However, hypercholesterolemia may be atherogenic, as evidenced by inherited forms in the young. Hence, regulation itself may become pathogenic if it exceeds certain boundaries. Part of the physician’s role, as in this example, is to evaluate the data on natural history of a phenomenon with an analysis contrasting benefits for normal aging regulation with potential for damage (eg. of hypercholesterolemia) as a risk factor.

Thus, dyslipidemia is an example of the difficulty to distinguish normal from pathological, in a metabolic-endocrine clinical picture of an elderly patient. Other examples include, type 2 diabetes and osteoporosis, which are closely related to age, and therefore, with the aging process.

Endocrine activity moves to the beat of aging. We only need mention the classic finding that in men, testosterone production gradually declines with advancing age. Serum testosterone levels in the 5th decade may be reduced by 50% from those exhibited in young adults, reaching remarkably low levels in the elderly. Thus, there is obviously a real difficulty in differentiating hypogonadism in the older male from aging per se. Here again the endocrinological challenge is to discern physiology from pathology.

Endocrine disease can interfere with the aging process either accentuating wearing or decreasing regulatory mechanisms. For example, the typical restless hyperactivity of hyperthyroidism may manifest as exhaustion and inactivity in older patients (apathetic hyperthyroidism), leading to a clinical presentation similar to thyrotoxic myopathy. However, certain organs age almost exclusively by wearing. Osteoarthritis is a case where continued operation and overload of the joints are the main determinants of pathology. Hormonal influences are also involved in the process either protecting joints against degeneration or worsening evolution. Androgens, on one hand, and estrogens and thyroid hormones, on the other, influence the development of such events in one way or another. Osteoporosis is a comparable state. Therefore, we must carefully consider association of endocrine disease with osteoarthritic disorders, especially when hormone replacement therapy is needed.

Other relevant issues are discussed, including the questions whether elderly men and women with age-related reductions in sex hormones might or might not benefit from sex-appropriate hormone therapy, whether there is a “somatopause” and whether human GH treatment is harmful or beneficial in older patients with low levels of GH secretion, and the problems of subclinical hyper- and hypothyroidism in elderly patients as manifest by slightly low or high TSH levels. We believe that authors provide the relevant data pros and cons on these important issues in a rational and balanced fashion, but the sagacious clinician will understand that, while such decisions should be data-driven, they can only be made one patient at a time and in accord with best practice and good clinical judgment. 

Finally, we could not forget to discuss benign prostatic hypertrophy and prostate cancer in this work. Although those are not, strictly speaking, endocrine disorders, both show a clear endocrine interaction in the context of its close relationship with aging.


In summary, this monograph presents endocrinology in relation to the aging process, paying particular attention to manifestations of advanced age. The reader will appreciate differences between the approaches of traditional clinical endocrinology and those that take into account the changes of aging. Those different features must be increasingly considered as the patient transitions from young adult to elderly. Moreover, we will have achieved the goal to which we are committed if, henceforward, the reader includes age as an essential factor for diagnostic and endocrine management.

The selected electronic format is composed of chapters with comprehensive text as well as visual content that have been developed as diagrams and graphic images. The work is aimed to become a friendly and quick reference guide, suitable for the practical clinician treating elderly patients with endocrine diseases and also for medical educators and students.

            Guadalajara and Madrid (Spain)/Phoenix (USA). November 2015.

                                                                                              Emiliano Corpas. M.D.; Ph.D.

                                                                                              S. Mitchell Harman. M.D.; Ph.D.

                                                                                              Antonio Ruiz-Torres. M.D.; Ph.D.



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