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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothalamic obesity (HyOb) is a complex neuroendocrine disorder caused by damage to the hypothalamus, which results in disruption of energy regulation. The key hypothalamic areas of energy regulation are the ARC (arcuate nucleus), the VMH (ventromedial hypothalamus), the PVN (paraventriculer nuclei) and the LHA (lateral hypothalamic area). These pathways can be disrupted mechanically by hypothalamic tumors, neurosurgery, inflammatory disorders, radiotherapy and trauma or functionally as such seen in genetic diseases. Rapid weight gain and severe obesity are the most striking features of HyOb and caused by hyperphagia, reduced basal metabolic rate (BMR) and decreased physical activity. HyOb is usually unresponsive to diet and exercise. Although, GLP-1 and its anologs seem to be a new agent, there is still no curative treatment. Thus, prevention is of prime importance and the clinicians should be alert and vigilant in patients at risk for development of HyOb.
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PMID:Hypothalamic obesity in children: pathophysiology to clinical management. 2578 73

Kumbhakarna was brother of the evil Raavana in the mythological tale of Ramayana. According the legend, Kumbhakarna had an insatiable appetite and thirst and used to sleep for great lengths of time. He also had an uncontrollable temper, which was feared by many. It is our assessment that Kumbhakarna possibly suffered from hypothalamic obesity. Hypothalamic obesity can be defined as significant polyphagia and weight gain that occurs because of structural or function involvement of the ventromedial nucleus of the hypothalamus bilaterally. The characteristic features are obesity associated with polyphagia. Somnolence is present in 40% of cases. Sham rage is a characteristic behavioral abnormality seen in these patients. All these symptoms are described in the mythological text while describing Kumbhakarna. The episodic nature of Kumbhakarna's symptoms can also be explained by another hypothalamic syndrome called Klein-Levine syndrome. This syndrome is characterized by with periodic episodes of somnolence, hyperphagia and hypersexuality along with other behavioral and cognitive difficulties.
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PMID:Kumbhakarna: Did he suffer from the disorder of the hypothalamus? 2593 5

Hypothalamic obesity (HO) occurs in patients with tumors and lesions in the medial hypothalamic region. Hypothalamic dysfunction can lead to hyperinsulinemia and leptin resistance. This review is focused on HO caused by craniopharyngiomas (CP), which are the most common childhood brain tumors of nonglial origin. Despite excellent overall survival rates, CP patients have substantially reduced quality of life because of significant long-term sequelae, notably severe obesity in about 50% of patients, leading to a high rate of cardiovascular mortality. Recent studies reported that both hyperphagia and decreased energy expenditure can contribute to severe obesity in HO patients. Recognized risk factors for severe obesity include large hypothalamic tumors or lesions affecting several medial and posterior hypothalamic nuclei that impact satiety signaling pathways. Structural damage in these nuclei often lead to hyperphagia, rapid weight gain, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue. To date, most efforts to treat HO have shown disappointing long-term success rates. However, treatments based on the distinct pathophysiology of disturbed energy homeostasis related to CP may offer options for successful interventions in the future.
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PMID:Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention. 2637 Oct 51

Childhood-onset craniopharyngiomas (CP) are rare embryonal malformations of low-grade histological malignancy. Hypothalamic involvement and/or treatment-related lesions result in impaired physical and social functionality and severe neuroendocrine sequelae. Quality of life in CP with hypothalamic involvement is impaired by severe obesity, physical fatigue, reduced motivation, dyspnea, diarrhea, and non-optimal psychosocial development. 567 CI patients have been recruited between 1998 and 2010 in the German Craniopharyngioma Registry. Only 5 of 567 patients (<1%) presented without confirmed signs of relapse/progression, visual impairment, and endocrine deficiencies during longitudinal follow-up of more than 5 years. Hypothalamic obesity in CP is associated with a severe increase in BMI during the early post-operative period. Patients with CP involving hypothalamic structures show reduced 10-years overall survival, whereas overall and progression-free survival rates are not related to the degree of surgical resection. Accordingly, gross-total resection should be avoided in cases of hypothalamic involvement to prevent further hypothalamic damage. As surgical expertise has been shown to have impact on postoperative morbidity, medical societies should establish criteria of adequate professional expertise for the treatment of CP. Based on these criteria, health authorities should organize the certification of centers of excellence authorized for treatment and care of patients with this chronic disease.
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PMID:Craniopharyngioma: long-term consequences of a chronic disease. 2652 17

Hypothalamic obesity is often complicated in patients with craniopharyngioma due to hypothalamic damage by the tumor itself, treatment modalities, and associated multiple pituitary hormone deficiency. Hypothalamic obesity causes secondary diseases such as nonalcoholic fatty liver disease (NAFLD) and diabetes mellitus (DM). We report a 19-year-old female who was diagnosed with craniopharyngioma, developed hypothalamic obesity after tumor resection, and progressed to hepatopulmonary syndrome. She manifested NAFLD 1 year after tumor resection. Two years later, the craniopharyngioma recurred, and she underwent a second resection. Three years after her second operation, she was diagnosed with type 2 DM, after which she did not visit the outpatient clinic for 2 years and then suddenly reappeared with a weight loss of 25.8 kg that had occurred over 21 months. One month later, she presented to the Emergency Department with dyspnea. Laboratory findings revealed liver dysfunction and hypoxia with increased alveolar artery oxygen gradient. Liver biopsy showed portal hypertension and micronodular cirrhosis. Echocardiography and a lung perfusion scan demonstrated a right to left shunt. She was finally diagnosed with hepatopulmonary syndrome and is currently awaiting a donor for liver transplantation. Patients surviving craniopharyngioma need to be followed up carefully to detect signs of hypothalamic obesity and monitored for the development of other comorbidities such as DM, NAFLD, and hepatopulmonary syndrome.
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PMID:Hepatopulmonary syndrome caused by hypothalamic obesity and nonalcoholic fatty liver disease after surgery for craniopharyngioma: a case report. 2960 50

Hypothalamic obesity (HO) is a rare and serious disease of various origins: tumor, traumatism, radiotherapy, vascular, genetic, or even psychotropic drug use. HO usually begins in childhood with eating disorders and progresses with an aggregate of severe comorbidities. Transition from pediatric to adult health care is a critical period to assure weight stability and a good management of comorbidities. In case of loss to follow-up, there is an increased risk of major weight gain and long-term complications with severe obesity. To minimize this risk, pediatric and adult specialists must work together to prepare, supervise, and monitor transition. Transition ideally involves the patient, parents, and care providers with a good communication between pediatric and adult teams from expert centers. Maintaining a diet and physical activity management plan, acquisition of autonomy for hormone replacement therapy and management of psychosocial consequences of obesity are fundamental issues in patients with HO. Patient associations and specialized diet center weight loss programs can help as well as group approaches.
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PMID:Management of Hypothalamic Obesity during Transition from Childhood to Adulthood. 2988 2

Hypothalamic obesity is a clinical syndrome characterized by severe and refractory obesity that is caused by hypothalamic function impairment. Recently, bariatric surgery has been attempted for patients with hypothalamic obesity after craniopharyngioma, but experiences have not yet been accumulated in other hypothalamic disorders. Here, we report the case of a 39-year-old male patient with panhypopituitarism who received laparoscopic sleeve gastrectomy (LSG) after intracranial germinoma treatment. The patient was diagnosed with intracranial germinoma at age 15 and achieved complete remission after radiotherapy (total 50 Gy). He was obese during diagnosis [body mass index (BMI), 29.2 kg/m2], and his obesity gradually worsened after the intracranial germinoma treatment, and LSG was considered when his BMI was 48.6 kg/m2. After 1 month of hospitalized diet-exercise program, LSG was performed. After LSG, his BMI gradually decreased and reached 38.8 kg/m2 on the day of discharge (6 weeks after the surgery). Five months after LSG, his insulin resistance improved, but insulin hypersecretion remained. Fifteen months after the surgery, his BMI was 31.2 kg/m2, with marked decrease in visceral and subcutaneous fat areas (from 393.8 cm2 and 168.2 cm2 before the surgery to 111.5 cm2 and 56.3 cm2, respectively.). To our knowledge, this is the first case of LSG for hypothalamic obesity after intracranial germinoma treatment. Although the pathophysiology of hypothalamic obesity is different from that of primary obesity, LSG could be a successful therapeutic choice for patients with hypothalamic obesity after the intracranial germinoma treatment.
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PMID:Laparoscopic Sleeve Gastrectomy on Severe Obesity after Intracranial Germinoma Treatment: A Case Report. 3177 1


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