pseudohypoparathyroidism/offita

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Compound heterozygous mutations in the GNAS gene of a boy with morbid obesity, thyroid-stimulating hormone resistance, pseudohypoparathyroidism, and a prothrombotic state.

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BACKGROUND Pseudohypoparathyroidism type Ia and pseudopseudohypoparathyroidism are characterized by Albright's hereditary osteodystrophy (AHO), respectively, with and without hormone resistance. Both clinical conditions result from decreased expression or function of the alpha-subunit of the

Eating behaviors in obese children with pseudohypoparathyroidism type 1a: a cross-sectional study.

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BACKGROUND Children with pseudohypoparathyroidism type 1a (PHP-1a) develop early-onset obesity. These children have decreased resting energy expenditure but it is unknown if hyperphagia contributes to their obesity. METHODS We conducted a survey assessment of patients 2 to 12 years old with PHP-1a

Early manifestation of obesity and calcinosis cutis in infantile pseudohypoparathyroidism.

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Pseudohypoparathyroidism is a parathyroid hormone resistance condition, characterised by biochemical findings of hypocalcaemia or normocalcaemia with inappropriately elevated parathyroid hormone level and usually with a typical osteodystrophy feature. We report an infant with

Pseudohypoparathyroidism--another monogenic obesity syndrome.

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Obesity is a common feature of pseudohypoparathyroidism (PHP) type 1a, but is usually associated with short stature. We describe two children referred because of hyperphagia and excessive weight gain from early infancy. Tall stature in both children initially confounded the diagnosis of PHP, but on

Energy expenditure in obese children with pseudohypoparathyroidism type 1a.

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BACKGROUND Patients with pseudohypoparathyroidism type 1a (PHP-1a) develop early-onset obesity. The abnormality in energy expenditure and/or energy intake responsible for this weight gain is unknown. OBJECTIVE The aim of this study was to evaluate energy expenditure in children with PHP-1a compared

Defective stimulation of adipocyte adenylate cyclase, blunted lipolysis, and obesity in pseudohypoparathyroidism 1a.

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Adipocyte plasma membranes were isolated from four patients with type 1a pseudohypoparathyroidism, a disease in which deficiency of the stimulatory guanine nucleotide binding protein Gs has been reported, and from controls. Stimulation of adenylate cyclase by isoproterenol was defective, whereas

Pseudohypoparathyroidism type 1A and morbid obesity in infancy.

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OBJECTIVE To describe an infant with early excessive weight gain as the principle manifestation of pseudohypoparathyroidism (PHP) type 1a and Albright hereditary osteodystrophy (AHO). METHODS We describe the clinical and laboratory findings in an infant with early excessive weight gain without

Body mass index differences in pseudohypoparathyroidism type 1a versus pseudopseudohypoparathyroidism may implicate paternal imprinting of Galpha(s) in the development of human obesity.

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BACKGROUND Obesity is a prominent feature of Albright hereditary osteodystrophy (AHO), a disorder caused by heterozygous GNAS mutations that disrupt the stimulatory G protein alpha-subunit Galpha(s). Because Galpha(s) is paternally imprinted in certain hormone target tissues, maternal inheritance of

Obesity and calcinosis cutis: characteristic early signs of infantile pseudohypoparathyroidism.

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Pseudo-pseudohypoparathyroidism: report of a case with associated cardiopulmonary syndrome of obesity.

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Pseudohypoparathyroidism, obesity, and type 2 diabetes. A hypothesis.

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Identification of a novel mutation in a pseudohypoparathyroidism family.

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Pseudohypoparathyroidism type Ia (PHP Ia) is defined as a series of disorders characterized by multihormone resistance in end-organs and Albright hereditary osteodystrophy (AHO) phenotype. PHP Ia is caused by heterozygous inactivating mutations in GNAS, which encodes the stimulatory G-protein alpha

Classic and Non-Classic Features in Pseudohypoparathyroidism: Case Study and Brief Literature Review.

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Pseudohypoparathyroidism is a rare condition that is due to a defect in the stimulatory G-protein coupled receptor, resulting in end-organ resistance to parathyroid hormone. Hereditary forms of pseudohypoparathyroidism present with certain classic features such as obesity, short stature,

Spinal cord compression in pseudohypoparathyroidism.

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BACKGROUND Spinal cord compression associated with pseudohypoparathyroidism (PHP) is an increasingly reported sequelae of the underlying metabolic syndrome. The association of neurologic dysfunction with PHP is not well appreciated. We believe this to be secondary to a combination of underlying

What to consider when pseudohypoparathyroidism is ruled out: iPPSD and differential diagnosis.

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Pseudohypoparathyroidism (PHP) is a rare disease whose phenotypic features are rather difficult to identify in some cases. Thus, although these patients may present with the Albright's hereditary osteodystrophy (AHO) phenotype, which is characterized by small stature, obesity with a rounded face,

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