Catálogo de publicaciones - libros

Melatonin (N-acetyl-5-methoxytriptamine) is the best-known among the indoles produced by the pineal gland (also called the epiphysis) according to a circadian rhythm. The pineal gland is the regulator of photic and nonphotic effects of the sun; indeed, it is the anatomical structure that coordinates the body’s functions with the most important environmental rhythm, that is the light/dark rhythm. This fact may help us in understanding the history of the pineal gland: ancient myths and philosophic systems all over the world assigned a significant role to this gland, with respect to the health of the body and the spirit. Indeed, Cartesius (Reneé Descartes) described the pineal gland as the site of the soul. The Greek name given by Vesalius to the pineal gland, epiphysis (επι = above; φυσισ = nature), implies that it is the counterpart of the hypophysis (υπο = below φυσισ = nature), whereas effectively the physiological activity of the pineal gland counterbalances that of the hypothalamic-pituitary-adrenal (HPA) axis.

The mechanism of loss of weight (cachexia), appetite (anorexia), and strength (asthenia) of most patients with advanced, incurable cancer encompasses a complex combination of paraneoplastic primary anorexia-cachexia syndromes (ACS). In addition, there are often secondary ACS due to other complications of advanced cancer, such as severe symptoms, disrupted function of the gastrointestinal tract, and reduced physical ability [ 1 ].

The management of cancer in the older person is an increasingly common problem, as 60% of all neoplasms occur in individuals age 65 and older [ 1 ]. Aging is associated with a progressive decline in life-expectancy, functional reserve, and social resources, and an increased prevalence of comorbidity [ 2 ]. This process is highly individualised and poorly reflected in chronologic age. The diversity of the older population affects both clinical practice and clinical research, and underlies the main challenges of geriatric oncology. These include the formulation of individual treatment plans and of research protocols.

The anorexia/cachexia syndrome is one of the most common causes of death among patients with cancer and is present in 80% at death [ 1 ]. The term ‘cachexia’ derives from the Greek kakòs , which means ‘bad’, and hexis, meaning ‘condition’. The characteristic clinical picture of anorexia, tissue wasting, loss of body weight accompanied by a decrease in muscle mass and adipose tissue, and poor performance status that often precedes death has been named cancer-related anorexia/cachexia (CAC) [ 2 ] [ 5 ]. Since the 1980s, the previous concepts explaining CAC were replaced by a more complex insight, which stresses the interaction between metabolically active molecules produced by the tumour itself and the host immune response. One of the main features of the cachectic syndrome is anorexia, which may be so significant that spontaneous nutrition is totally inhibited. The pathogenesis of anorexia is most certainly multifactorial but not yet well understood.

Patients with cancer often suffer from progressive involuntary weight loss, which is called cancer wasting. Clinical features of this syndrome include anorexia, early satiety, depletion of lean and fat body mass, muscle weakness, fatigue and impaired immune function. It occurs in 30–90% of cancer patients depending on location, stage, type, grade, spread and anticancer treatment [ 1 ]. Patients with cancer of lung, pancreas, head-and-neck area and upper gastrointestinal tract often suffer from wasting [ 2 ] [ 5 ].

Involuntary weight loss and its end-stage manifestation, the anorexia and cachexia syndrome, is a frequent complication of cancer. The incidence of weight loss varies both with the primary site of the malignancy and its stage. At presentation, 15–48% of cancer patients report weight loss, while more than 80% of those with advanced disease note involuntary weight loss [ 1 ]. A weight loss of as little as 5% from premorbid weight predicts a poor prognosis, particularly among patients with lymphoma, lung, breast or gastrointestinal malignancies. Weight loss of less than 5% adversely impacts survival, with the greatest effect seen in those patients with good performance status [ 1 ]. Involuntary weight loss adversely affects quality of life as well [ 2 ] [ 4 ].

The focus of palliative care is illness-oriented, with the main aim being to relieve suffering. In contrast, the disease-oriented approach aims to improve the natural course of a disease and the length of life. Caring for nutritional issues of patients with advancing, progressive and terminal illness improves when the nutritional interventions focus on the effects of the illness on patients and relatives, and do not target curative or diseaseoriented endpoints (such as weight, oral intake). This brief chapter highlights the concept of palliative care, issues of palliative nutritional endpoints and decision making, the potential importance of treatment of symptoms and syndromes such as constipation as causes for secondary anorexia/ cachexia, issues of palliative symptom and syndrome management, and terminal care.

Cancer cachexia is a major symptom burden for patients with cancer.Cachexia occurs in up to one half of all patients diagnosed with cancer [ 1 ] and is more frequent in patients with lung and upper-gastrointestinal cancer.Cancer cachexia results from the interaction of the host and the tumour. However, the nature of this interaction is incompletely understood [ 2 ] [ 5 ], including the dynamics of the host response (activation of the systemic inflammatory response, metabolic, immune and neuroendocrine changes) and those tumour characteristics or tumour-derived products that influence expression of the syndrome (e.g. proteolysis-inducing factor [PIF]). The relative importance of individual mediators and pathways in different patients or tumour types is unclear, as is the reason why individuals with apparently similar tumours should show considerable variation in their tendency to develop cachexia.As ability to discriminate the relative importance in vivo of different mediators improves, so too should the ability to develop appropriately targeted therapy.

Cancer cachexia is a multifactorial, multifaceted problem for which there is no uniform pathophysiological or clinical definition [ 1 ]. It is generally accepted as a complex syndrome with several cardinal features, including anorexia, early satiety, severe weight loss, muscle wasting, ischaemia, anaemia and oedema [ 2 ]. The essential characteristic that distinguishes cachexia from simple starvation is that the features of cachexia cannot be readily reversed by nutritional support alone [ 3 ].

A large fraction of patients with advanced cancer develop cachexia [ 1 ], a wasting syndrome characterised by anorexia, asthenia, and profound losses of adipose tissue and skeletal muscle mass. The association of cachexia syndrome with poor prognosis, loss of functional status and poor quality of life has motivated researchers to develop therapeutic strategies for this problem [ 2 ].