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01.Recent Advances In The Understanding And Treatment Of Hypothalamic Obesity In Humans (pp. 41-66)
02.Cutaneous Manifestations In Obese Patients (pp. 121-139)
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Recent Advances In The Understanding And Treatment Of Hypothalamic Obesity In Humans (pp. 41-66) $25.00
Authors:  Pinkney, Jonathan H.; Daousi, Christina; Macfarlane, Ian A. (1University of Liverpool , University Hospital Aintree)
Weight gain and obesity are common long term results of hypothalamic damage, and in the absence of well-established preventive or therapeutic strategies, patients and physicians face a difficult challenge. Despite insights into the neuroendocrine control of body weight gained from research on animals, and from humans with genetic obesity, progress in understanding and developing treatments for hypothalamic obesity in humans has been slow. Here we present a comprehensive review of the current state of this field. Most often, hypothalamic damage results from space-occupying lesions such as craniopharyngioma or infiltration by Acute Lymphoblastic Leukaemia. However, hypothalamic damage can also be aggravated by, or largely the result of otherwise successful treatment of these diseases with surgery, radiotherapy and chemotherapy. Obesity is also the major feature of several genetic syndromes that are associated with hypothalamic dysfunction, including the Prader Willi syndrome and mutations in the leptin and melanocortin systems. Following hypothalamic insults weight gain most often develops after damage to the medial hypothalamus, and this is mediated by a variety of mechanisms including hyperphagia, autonomic imbalance and hyperinsulinemia, low metabolic rate and defective thermoregulation. Pituitary insufficiency secondary to hypothalamic damage, or the direct result of damage to the pituitary itself, giving rise to deficiences of growth hormone, sex steroids and thyroid hormone can also contribute to weight gain and changes in body composition. Furthermore, damage to other structures in this region often leads to additional problems such as visual failure, somnolence and various other manifestations of brain injury, which may be associated with reduced physical activity and contribute further to weight gain. In contrast, individuals with bilateral damage to the lateral hypothalamus can present with anorexia and weight loss. In Prader Willi syndrome, the recent demonstration of increased plasma levels of ghrelin has given new impetus to research into the mechanisms responsible for hyperphagia. However, the predominant mechanisms of weight gain in the majority of individuals with hypothalamic obesity are difficult to resolve in clinical practice, and with the exception of GH replacement, few clinical trials have evaluated significant numbers of hypothalamic obese patients and so the roles of various behavioural, dietary, pharmacological and even bariatric surgical approaches are unresolved. Recent data suggest that somatostatin analogues stabilise weight, and may lead to modest weight loss in a subset of obese patients with craniopharyngioma and insulin hypersecretion. This is the first treatment that has shown potential to limit weight gain in human hypothalamic obesity. In summary, hypothalamic obesity in humans results from multiple mechanisms, the relative contributions of each varying from one individual to another, depending on the pattern of neuroendocrine dysfunction. It is hoped that treatments targeted at the predominant mechanisms will at last offer therapeutic progress in this field. 

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Recent Advances In The Understanding And Treatment Of Hypothalamic Obesity In Humans (pp. 41-66)