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Query: UMLS:C0011854 (type 1 diabetes)
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Anorexia nervosa is a syndrome with multifactorial etiology in which several genetic, biologic, psychological and social factors are involved. Patients affected by anorexia nervosa (AN) may develop multiple endocrine abnormalities, e.g. amenorrhea, hypothalamus-pituitary-adrenal axis hyperactivity, low T3 syndrome and peculiar changes of somatotroph axis function. These endocrine abnormalities are also found after prolonged starvation and may represent an adaptive response developed in order to save energy and proteins. It is still a matter of debate whether these endocrine changes are etiologic or secondary. In fact, several evidences suggest the existence in AN of hypothalamus functional alterations, which may be involved in the development and maintenance of the food intake disorder; on the other hand, the increased CRH secretion seems to be secondary to malnutrition as well as GH hypersecretion coupled to low IGF-I levels; the latter is a common finding in AN, as well as in other undernutrition and malabsorption conditions, type 1 diabetes mellitus, liver cirrhosis and catabolic states. Hypothalamic amenorrhea, which is one of the diagnostic criteria for AN, is not linked only to the reduction of body weight but reflects also deep alterations of gonadotropin secretory pattern. Low T3 syndrome is frequently found in AN; on the other hand, an iodide-induced hypothyroidism is quite uncommon. T3 reduction in AN seems to be an adaptive response to prolonged starvation; however the presence of a simultaneous central dysregulation cannot be excluded. Finally, AN patients frequently show defects in urinary concentration or dilution with inappropriate secretion of antidiuretic hormone, which may be due to intrinsic defects in the neurohypophysis or to abnormalities of its regulatory afferent neurons.
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PMID:[Endocrine abnormalities in anorexia nervosa]. 1271 47

GH hypersecretory states include organic and functional causes. Among functional GH hypersecretory states, enhanced somatotroph secretion physiologically occurs at birth associated with reduced IGF-I levels reflecting the still immature sensitivity of liver to circulating GH levels; this may also occur in women exposed to oral extrogens. Pathophysiological conditions of GH hypersecretion are generally associated with congenital or acquired/functional conditions of peripheral GH insensitivity. Genetic alterations of the GH receptor lead to the so called Laron's syndrome. On the other hand, a relevant number of clinical conditions (malnutrition, malabsorption, anorexia nervosa, liver cirrhosis, renal failure, Type 1 diabetes mellitus) are associated with acquired GH insensitivity and a more or less pronounced GH hypersecretion. Both organic and acquired conditions of GH insensitivity show low IGF-I synthesis and release and therefore lack the negative IGF-I feedback action on somatotroph function. GH hypersecretion may be associated with renal failure; however, in this case, the alteration in the metabolic clearance rate of GH would also have a role; moreover, IGF-I levels are generally normal in this condition. Hyperthyroidism is another condition connoted by elevated GH levels that reflects a true GH hypersecretory state and is, in fact, associated with high-normal IGF-I levels; this peculiar condition is likely to be reflecting the stimulatory effect of thyroid hormones on both GH and IGF-I secretion and is promptly reversed by treatment-induced euthyroidism. Apart from these "functional" hypersecretory state, the classic organic GH hypersecretory state is represented by acromegaly or giantism. In these conditions GH hypersecretion is generally sustained by a pituitary adenoma hypersecreting GH alone or together with another pituitary hormone, mostly PRL; less frequently GH hypersecretion may be due to ectopic GHRH hypersection. Exaggerated GH secretion elicits exaggerated IGF-I synthesis and secretion that is, in turn, responsible for the large majority of endocrine signs and symptoms. In the appropriate clinical context of acromegalic features, evidence of concomitant marked GH and IGF-I hypersecretion at baseline demonstrates active acromegaly or giantism and indicates the need for magnetic resonance imaging in order to verify the presence of a pituitary tumor. However, as random measurement of basal GH levels is not reliable for definite diagnosis of acromegaly, it is considered mandatory to rely on the lack of GH suppression below 1 microg/l during oral glucose tolerance test (OGTT) coupled with elevated IGF-I levels. The same criteria are assumed, at present, to define true cure of the disease after (or under) treatment. There is consensus about the assumption that concomitant normalization or persistent abnormality of both OGTT-induced GH nadir and IGF-I levels define a successfully or a poorly controlled disease status, respectively. On the other hand, acromegalic patients with GH nadir above 1 microg/l or IGF-I levels persistently elevated are inadequately controlled and their disease should not be considered inactive. It has been clearly demonstrated that an extended exposure to GH and IGF-I excess level, even if slight, has a very harmful effect on patients; therefore early diagnosis of acromegaly and appropriate definition of its cure are of fundamental extreme in order to plan a prompt and appropriate therapeutic intervention(s) guaranteed also by the continuous improvement in the therapeutic tools available to treat this systemic disease.
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PMID:Hormonal diagnosis of GH hypersecretory states. 1549 57

Adipose tissue is a hormonally active tissue, producing adipocytokines which may influence activity of other tissues. Adiponectin, abundantly present in the plasma increases insulin sensitivity by stimulating fatty acid oxidation, decreases plasma triglycerides and improves glucose metabolism. Adiponectin levels are inversely related to the degree of adiposity. Anorexia nervosa and type 1 diabetes are associated with increased plasma adiponectin levels and higher insulin sensitivity. Decreased plasma adiponectin levels were reported in insulin-resistant states, such as obesity and type 2 diabetes and in patients with coronary artery disease. Activity of adiponectin is associated with leptin, resistin and with steroid and thyroid hormones, glucocorticoids, NO and others. Adiponectin suppresses expression of extracellular matrix adhesive proteins in endothelial cells and atherosclerosis potentiating cytokines. Anti-atherogenic and anti-inflammatory properties of adiponectin and the ability to stimulate insulin sensitivity have made adiponectin an important object for physiological and pathophysiological studies with the aim of potential therapeutic applications.
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PMID:Adiponectin, an adipocyte-derived protein. 1554 26

In anorexia nervosa, under-nutrition and weight regulatory behaviours such as vomiting and laxative abuse can lead to a range of biochemical problems. Hypokalaemia is the most common electrolyte abnormality. Metabolic alkalosis occurs in patients who vomit or abuse diuretics and acidosis in those misusing laxatives. Hyponatraemia is often due to excessive water ingestion, but may also occur in chronic energy deprivation or diuretic misuse. Urea and creatinine are generally low and normal concentrations may mask dehydration or renal dysfunction. Abnormalities of liver enzymes are predominantly characterized by elevation of aminotransferases, which may occur before or during refeeding. The serum albumin is usually normal, even in severely malnourished patients. Amenorrhoea is due to hypogonadotrophic hypogonadism. Reduced concentrations of free T4 and free T3 are frequently reported and T4 is preferentially converted to reverse T3. Cortisol is elevated but the response to adrenocorticotrophic hormone is normal. Hypoglycaemia is common. Hypercholesterolaemia is a common finding but its significance for cardiovascular risk is uncertain. A number of micronutrient deficiencies can occur. Other abnormalities include hyperamylasaemia, hypercarotenaemia and elevated creatine kinase. There is an increased prevalence of eating disorders in type 1 diabetes and the intentional omission of insulin is associated with impaired metabolic control. Refeeding may produce electrolyte abnormalities, hyper- and hypoglycaemia, acute thiamin depletion and fluid balance disturbance; careful biochemical monitoring and thiamin replacement are therefore essential during refeeding. Future research should address the management of electrolyte problems, the role of leptin and micronutrients, and the possible use of biochemical markers in risk stratification.
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PMID:The clinical biochemistry of anorexia nervosa. 2234 51

We here report a case of diabetic ketoacidosis at onset of type 1 diabetes after a prolonged period of starvation due to anorexia nervosa. A 53-year-old female with a history of anorexia nervosa was admitted to the psychiatric clinic due to psychotic behaviour and inability to take care of herself. Twenty-four hours after admission she was transferred to the clinic of internal medicine due to altered mental status, and laboratory screening revealed a pH of 6.895 and blood glucose concentration of 40 mmol/L. Due to the unusual combination of prolonged starvation and diabetic ketoacidosis we implemented some modifications of existing treatment guidelines and some special considerations regarding nutrition in order to prevent a re-feeding syndrome.
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PMID:Severe diabetic ketoacidosis in combination with starvation and anorexia nervosa at onset of type 1 diabetes: a case report. 2354 63

The coexistence of Type 1 Diabetes Mellitus and anorexia nervosa results in an increased incidence of known diabetic complications such as retinopathy and nephropathy, presumably because blood glucose is difficult to control within the throes of comorbid anorexia nervosa. In addition, even when a diabetic patient with anorexia nervosa has committed to resolving his or her eating disorder, glucose control is again difficult and fraught with complexity and peril as will be highlighted in the following case report. Prudence dictates that strict glucose control is not indicated for the relatively short period of time that constitutes the early stage of refeeding in a patient with severe anorexia nervosa. Rather, "permissive hyperglycemia" may be the more optimal course to pursue, as a clinical strategy which is considerate of both the criticality of the refeeding treatment plan and of the long-term nature of the diabetic illness.
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PMID:Anorexia nervosa complicated by diabetes mellitus: the case for permissive hyperglycemia. 2471 47

Eating problems in adolescents with type 1 diabetes (T1D) can be divided into two groups. The first includes the diagnosed eating disorders (EDs), i.e., diseases specifically identified by defined signs and symptoms for which a degree of severity has been established, such as anorexia nervosa, bulimia nervosa, binge-eating disorder, pica, and rumination. The second is the group of disordered eating symptoms (DES), which include behaviors such as dieting for weight loss, binge eating, self-induced vomiting, excessive exercise, and laxative or diuretic use; these behaviors cannot be categorized as complete diseases, and, although apparently mild, they must be closely evaluated because they can evolve into true EDs. In this review, present knowledge about the clinical relevance of EDs and DES and the possible preventive and therapeutic measures used to reduce their impact on the course of T1D will be discussed. As adolescents with diabetes are at higher risk of eating disturbances and consequently for higher rates of disease complications, care providers should pay attention to clinical warning signs that raise suspicion of disturbed eating to refer these patients early to an expert in nutrition and mental health disorders. To ensure the best care for adolescents with T1D, diabetes teams should be multidisciplinary and include a pediatric diabetologist, a skilled nurse, a dietician, and a psychologist.
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PMID:Eating Disorders and Disordered Eating Symptoms in Adolescents with Type 1 Diabetes. 2882 8

Background Adolescents with type 1 diabetes mellitus (T1DM) are at an increased risk of eating disturbances. The aim of this study was to evaluate whether the risk of a disordered eating behavior (DEB) also applies to the well sibling sharing the same environment. Methods Well siblings were included if they were 10-18 years old, had a sibling with a T1DM diagnosis for at least 6 months and lived with the sibling during the illness. The control group was comprised of healthy participants recruited from the outpatient clinic with no family history of T1DM. Participants completed a four-part questionnaire concerning their eating behaviors that was developed by the study team. This survey aimed to evaluate the dietary habits and eating patterns. All participants completed the Eating Attitudes Test-26 (EAT-26) and a 24-h food dietary recall. Any participant with a high EAT-26 score or that seemed to be at risk according to the questionnaire was re-evaluated. Results Eight cases (33.3%) in the well sibling group had either a total and/or subgroup pathological score. Three of them were found to have DEB and one case was diagnosed with anorexia nervosa (AN). In the control group, five cases (17.2%) had either a total and/or subgroup pathological score. Three of these cases were found to have DEB, no cases were diagnosed with an eating disorder. There were no statistically significant differences in the EAT-26 scores between the groups. Conclusions Although a direct relationship was not observed, the probability of having a pathologic EAT-26 score was higher in the group with a sibling with T1DM.
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PMID:Can having a sibling with type 1 diabetes cause disordered eating behaviors? 2987 93


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