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      Anorexia–cachexia syndrome-like hypothalamic neuroendocrine dysfunction in a patient with a papillary craniopharyngioma

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          Abstract

          The craniopharyngiomas are solid cystic suprasellar tumors that can present extension to adjacent structures, conditioning pituitary and hypothalamic dysfunction. Within hypothalamic neuroendocrine dysfunction, we can find obesity, behavioral changes, disturbed circadian rhythm and sleep irregularities, imbalances in the regulation of body temperature, thirst, heart rate and/or blood pressure and alterations in dietary intake (like anorexia). We present a rare case of anorexia–cachexia syndrome like a manifestation of neuroendocrine dysfunction in a patient with a papillary craniopharyngioma. Anorexia–cachexia syndrome is a complex metabolic process associated with underlying illness and characterized by loss of muscle with or without loss of fat mass and can occur in a number of diseases like cancer neoplasm, non-cancer neoplasm, chronic disease or immunodeficiency states like HIV/AIDS. The role of cytokines and anorexigenic and orexigenic peptides are important in the etiology. The anorexia–cachexia syndrome is a clinical entity rarely described in the literature and it leads to important function limitation, comorbidities and worsening prognosis.

          Learning points:
          • Suprasellar lesions can result in pituitary and hypothalamic dysfunction.

          • The hypothalamic neuroendocrine dysfunction is commonly related with obesity, behavioral changes, disturbed circadian rhythm and sleep irregularities, but rarely with anorexia–cachexia.

          • Anorexia–cachexia syndrome is a metabolic process associated with loss of muscle, with or without loss of fat mass, in a patient with neoplasm, chronic disease or immunodeficiency states.

          • Anorexia–cachexia syndrome results in important function limitation, comorbidities that influence negatively on treatment, progressive clinical deterioration and bad prognosis that can lead the patient to death.

          • Anorexia–cachexia syndrome should be suspected in patients with emaciation and hypothalamic lesions.

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          Most cited references35

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          Anatomy and regulation of the central melanocortin system.

          Roger Cone (2005)
          The central melanocortin system is perhaps the best-characterized neuronal pathway involved in the regulation of energy homeostasis. This collection of circuits is unique in having the capability of sensing signals from a staggering array of hormones, nutrients and afferent neural inputs. It is likely to be involved in integrating long-term adipostatic signals from leptin and insulin, primarily received by the hypothalamus, with acute signals regulating hunger and satiety, primarily received by the brainstem. The system is also unique from a regulatory point of view in that it is composed of fibers expressing both agonists and antagonists of melanocortin receptors. Given that the central melanocortin system is an active target for development of drugs for the treatment of obesity, diabetes and cachexia, it is important to understand the system in its full complexity, including the likelihood that the system also regulates the cardiovascular and reproductive systems.
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            Depressive disorders and immunity: 20 years of progress and discovery.

            Since the inception of Brain, Behavior and Immunity twenty years ago, many exciting developments have occurred regarding the relationship between depression and the immune system. These developments have increasingly put the field of psychoneuroimmunology into a clinical context with important translational implications. Initial studies focused on the impact of depression on relatively narrowly defined immunologic endpoints, which ultimately found their relevance in studies examining the effect of depression on immunologically-based diseases including infectious illnesses, autoimmune disorders, and cancer as well as more recently cardiovascular disease. Mechanistic studies have also greatly contributed to an understanding of those facets of depression, which might mediate these effects. More recently, the reciprocal influences of the immune system on the brain and behavior including depression have taken center stage. Increasing data now indicate that activated inflammatory processes can influence multiple aspects of CNS function including neurotransmitter metabolism, neuroendocrine function, and information processing leading to behavioral changes in humans that bespeak depression. These latter developments have intrigued scientists investigating the pathophysiology of depression and warrant consideration as some of the most exciting new developments in psychiatry in the past 20 years. What the future holds is a world of promise as multiple translational targets derived from the cytokine model of depression work their way into the clinical arena as drug targets for further development. Moreover, the work has served to instantiate brain-immune interactions as an essential component in psychiatric and medical co-morbidities and their impact on health and illness.
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              Endotoxin produces a depressive-like episode in rats.

              Activation of the immune system produces psychological and physiological effects, which resemble the characteristics of depression. The present study was designed to investigate further, in rats, the similarity between the behavioral effects of immune activation and a model of depression in animals. Reduction in the preference for and consumption of saccharin solutions and suppression of sexual behavior were used as models of one essential feature of depression, the inability to experience pleasure (anhedonia). Other measures testing this model were the reduction in food consumption, body weight, locomotor activity, and social interaction. It was found that systemic injection of lipopolysaccharide (endotoxin), which is a potent activator of the immune system, significantly decreased saccharin preference in fluid-deprived rats. Lipopolysaccharide (LPS) also decreased free consumption of saccharin, but not water, in non-deprived rats. Several indices of male sexual behavior were significantly suppressed following LPS administration. Chronic, but not acute, treatment with the tricyclic antidepressant imipramine abolished the suppressive effect of LPS on saccharin preference. Moreover, chronic, but not acute, treatment with imipramine also reduced and facilitated the recovery from the suppressive effects of LPS on food consumption, body weight, social interaction and activity in the open-field test. The results suggest that activation of the immune system in rats produces anhedonia and other depressive-like symptoms, which can be attenuated or completely blocked by chronic treatment with an antidepressant drug.

                Author and article information

                Journal
                Endocrinol Diabetes Metab Case Rep
                Endocrinol Diabetes Metab Case Rep
                EDM
                Endocrinology, Diabetes & Metabolism Case Reports
                Bioscientifica Ltd (Bristol )
                2052-0573
                21 April 2017
                2017
                : 2017
                : 17-0018
                Affiliations
                [1 ]Endocrinology Department
                [2 ]Anatomic Pathology Department , Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Colonia Doctores, Mexico CityMexico
                Author notes
                Correspondence should be addressed to B González-Virla; Email: baldogonzal@ 123456hotmail.com
                Article
                EDM170018
                10.1530/EDM-17-0018
                5409936
                25ab7b91-95ad-49fe-bde7-d500112608c0
                © 2017 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                : 11 March 2017
                : 27 March 2017
                Categories
                Unique/Unexpected Symptoms or Presentations of a Disease

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