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Sleep–Wake Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Margaret Kay-Stacey, Eunice Torres-Rivera, Phyllis C. Zee
Must demonstrate at least one of the following: Cognitive dysfunction.Altered perceptionEating disorder: either hyperphagia or anorexia.Disinhibited behavior (e.g. hypersexuality).Between episodes, the patient has normal alertness, cognitive function, behavior, and mood.
Etiology and Prevalence of Obesity
Published in Claude Bouchard, The Genetics of Obesity, 2020
Most patients with PWS are short and have an adult height which averages 59 inches in girls and 61 inches in boys. Body weight is increased to a mean of 80 kg in girls and 98 kg in boys.20 Affected individuals are mentally retarded, but the degree of this retardation is highly variable. Hyperphagia is characteristic of these individuals, and emotional problems — including temper tantrums — are well known, particularly related to food. Levels of pancreatic polypeptide are low, and Zipf and his colleagues have provided suggestive evidence that pancreatic polypeptide can lower food intake, particularly in girls with PWS.23 Scoliosis has been observed in many patients, but bone age is usually the same as the chronological age or only slightly retarded. Advanced dental caries and hypoplastic enamel have been observed, as has dysplasia of the hip.20 The profound hypotonia present at birth usually improves somewhat during the first 2 or 3 years of life.
α-Mannosidosis (β-Mannosidosis)
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Hydrocephalus has been reported [28] and spastic paraplegia [29], as well as ataxia [7]. Progressive cerebellar ataxia of late adolescent onset was the initial clinical manifestation is three adult siblings [30]. They also displayed nystagmus, dysarthria, and positive Babinski responses. Hyperphagia has been observed [17]. Cardiovascular abnormality has been manifested by premature ventricular contractions and a shortened PR interval on electrocardiogram (EKG) [31]. Magnetic resonance imaging (MRI) findings have included cerebellar atrophy and abnormal signal in the white matter. A patient with delusions and hallucinations had cerebellar atrophy and periventricular white matter changes on MRI [32]. In a series of 35 patients, [33] with a milder type 2 phenotype, all were socially dependent and unable to care for themselves. Regardless of the phenotype degeneration with time appears to be the rule.
Food addiction among morbidly obese patients: prevalence and links with obesity complications
Published in Journal of Addictive Diseases, 2022
Mickaël Som, Aymery Constant, Teycir Zayani, Estelle Le Pabic, Romain Moirand, David Val-Laillet, Ronan Thibault
In the US general population, Schulte and Gearhardt19 reported that 15% potentially had food addiction. Pursey et al.18 found that 19.9% of overweight and obese patients had food addiction. In our study, the prevalence was higher, probably because only obese patients with a BMI ≥ 35 were included. However, another study conducted in France found that 16.5% of patients eligible for obesity surgery had FA.30 The difference could be due to the fact that they used the YFAS 1.0, which offers fewer classification criteria than the YFAS 2.0 version. Among obese patients, the prevalence of FA was reported to be 17.2%,21 25%,20 and 40%22 among patients eligible for obesity surgery. The prevalence could be even higher in the case of eating disorders:23,24 57% among patients with bulimic hyperphagia,31 41%31 and up to 96% among patients with binge-eating disorders and bulimia respectively.32 Interestingly, no differences were found in the prevalence of FA between male and female subjects. Even if obesity is known to be more prevalent among female patients, male patients should also be screened for FA.
Effectiveness and safety of sodium–glucose co-transporter-2 inhibitors in Thai adults with type 2 diabetes mellitus: a real-world study
Published in Current Medical Research and Opinion, 2020
Chutintorn Sriphrapradang, Yotsapon Thewjitcharoen, Supawan Buranapin, Kittisak Sawanyawisuth, Nalin Yenseung, Wisawa Ubonchareon, Laddawan Limpijankit, Thep Himathongkam
SGLT2is led to a net weight loss of 2.3 kg and 2.5 kg after 12 and 24 months of treatment, respectively, in our study. These findings are comparable to results from another study in Asian populations (range, −1.3 to −3.9 kg)24. Typically, SGLT2i associated weight loss is characterized by early and rapid body water and fat loss after approximately 8 weeks of therapy, followed by a slower rate of sustained fat loss25,26. However, in the present study, body weight rebounded in the third year of treatment. This weight loss variability in response to SGLT2is is not explained completely by drug–response heterogeneity. Concurrent multiple glucose-lowering agents or medication adherence, which counterbalance the desired weight loss, should also be considered. Less weight loss or even weight gain is reported in people receiving concurrent sulfonylurea, thiazolidinediones or insulin, suggesting that the real-world use of drugs causing weight gain is relatively common in Thailand27. Diabetes medications associated with weight loss benefit, such as GLP-1RAs, were prescribed in only 3.1% of the participants in this study. Additionally, attenuated weight loss could be secondary to compensatory hyperphagia28. Unfortunately, food intake records were not available in this study. Studies examining the responses in weight responders and non-responders to SGLT2i treatment may help determine future therapeutic approaches.
Prader-Willi syndrome and Angelman syndrome: Visualisation of the molecular pathways for two chromosomal disorders
Published in The World Journal of Biological Psychiatry, 2019
Friederike Ehrhart, Kelly J. M. Janssen, Susan L. Coort, Chris T. Evelo, Leopold M. G. Curfs
The arcuate nucleus of the hypothalamus is a major site for leptin action (Mercer et al. 2013). Neurons expressing neuropeptide Y (NPY) and agouti-related peptide (AgRP), as well as neurons expressing POMC are located there. Upon activation, NPY/AgRP neurons stimulate food intake, whereas POMC neurons reduce food intake. Leptin is secreted by adipose tissue in order to regulate fat storage (Myers et al. 2000). It is capable of stimulating POMC neurons, but Varela and Horvath (2012) found that the leptin-mediated depolarisation of POMC neurons is disturbed when MAGEL2 is lost, meaning that food intake is being less repressed. This could be another explanation for hyperphagia. Research by Maillard et al. (2016) stated that loss of MAGEL2 in mice leads to a disruption of hypothalamic feeding circuits in general, which is in line with the results of Varela and Horvath. Furthermore, after POMC neurons would be depolarised, neuropeptide precursor POMC is cleaved to α-melanocyte stimulating hormone (Belgardt et al. 2009). This peptide activates receptors on neuron populations that are located in the PVN. In this way, the reduced volume of the PVN, and the reduced activation of and secretion by POMC neurons, might have a relation.