diabetes insipidus/fetma

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Severe obesity and diabetes insipidus in a patient with PCSK1 deficiency.

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Non-synonymous mutations affecting both alleles of PCSK1 (proprotein convertase 1/3) are associated with obesity and impaired prohormone processing. We report a proband who was compound heterozygous for a maternally inherited frameshift mutation and a paternally inherited 474kb deletion that

Hypothalamic obesity complicated by adipsic central diabetes insipidus following surgical resection of a craniopharyngioma.

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[Clinical aspects and pathogenesis of two cases of obesity and one case of diabetes insipidus secondary to tuberculous meningitis clinically cured].

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[Association of diabetes insipidus and diencephalohypophyseal obesity].

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Some endocrinological studies on a child with obesity and diabetes insipidus.

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Hyperphagia, obesity and diabetes insipidus due to hypothalamic lesion in a girl.

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Diabetes insipidus and obesity in an Itesot leper child.

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Successful weight loss with protein-sparing modified fast in a morbidly obese boy with panhypopituitarism, diabetes insipidus, and defective thirst regulation.

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A novel ALMS1 splice mutation in a non-obese juvenile-onset insulin-dependent syndromic diabetic patient.

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Insulin-dependent juvenile-onset diabetes may occur in the context of rare syndromic presentations suggesting monogenic inheritance rather than common multifactorial autoimmune type 1 diabetes. Here, we report the case of a Lebanese patient diagnosed with juvenile-onset insulin-dependent diabetes

Hypothalamic sarcoidosis: a new cause of morbid obesity.

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I have described a 21-year-old man who had biopsy-proven hypothalamic sarcoidosis and polyphagia with a weight increase to 393 lb (178.6 kg) on a 5 ft 4 inch frame during a seven-year follow-up. This morbid obesity appears to be due to sarcoid invasion of the satiety center in the ventral medial

Primary treatment regimen and diabetes insipidus as predictors of health outcomes in adults with childhood-onset craniopharyngioma.

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BACKGROUND Craniopharyngiomas are often associated with significant morbidity due to their location and treatment effects. Little is known of the effects of primary treatment regimen and diabetes insipidus (DI), a clinical surrogate of hypothalamic obesity, on health outcomes in adults with

Panhypopituitarism associated with diabetes insipidus in a girl with a suprasellar arachnoid cyst.

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We report on a female patient with a large suprasellar arachnoid cyst (3.5 x 2.5 cm) combined with right optic nerve hypoplasia. She developed growth hormone deficiency and hypothyroidism at the age of 8.5 years, adrenal insufficiency at the age of 11 years, diabetes insipidus and hypogonadotropic

Morbid Obesity as Early Manifestation of Occult Hypothalamic-Pituitary LCH with Delay in Treatment.

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Morbid obesity presents unique challenges in managing additional disease processes. A 16-year-old male with a history of central diabetes insipidus (DI) and hypothyroidism developed destructive lesions in both his right mandible and brain, which were not discovered until the patient presented for

Primary hypothyroidism, precocious puberty and hypothalamic obesity in Langerhans cell histiocytosis.

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A 5 year old girl presented with central diabetes insipidus and primary hypothyroidism. No clinical or radiological evidence of Langerhans cell histiocytosis (LCH) was present. Absent posterior pituitary bright spot was seen in magnetic resonance imaging of the brain. She subsequently developed

[A not very essential obesity: the Rohhad syndrome. Description of two cases and review of the literature].

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Rapid-onset Obesity with Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation (ROHHAD) is a rare and complex pediatric disorder. Children typically show ROHHAD after the first years of life with rapid weight gain and subsequently autonomic nervous system dysregulation (altered pain

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