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Manuel Puig-Domingo

Researcher at Autonomous University of Barcelona

Publications -  48
Citations -  1307

Manuel Puig-Domingo is an academic researcher from Autonomous University of Barcelona. The author has contributed to research in topics: Population & Type 2 diabetes. The author has an hindex of 16, co-authored 46 publications receiving 946 citations. Previous affiliations of Manuel Puig-Domingo include Carlos III Health Institute & Hospital de Sant Pau.

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New splice site acceptor mutation in AIRE gene in autoimmune polyendocrine syndrome type 1.

TL;DR: A novel homozygous mutation in the splice site acceptor (SSA) of intron 5 (c.653-1G>A) in two siblings with different clinical outcomes of APS-1 is identified, highlighting the possibility to suspect mutations in the AIRE gene in cases of childhood chronic candidiasis and/or hypoparathyroidism otherwise unexplained.
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One year of the pandemic - how European endocrinologists responded to the crisis: a statement from the European Society of Endocrinology.

TL;DR: In this paper, the major characteristics of the response of European endocrinologists to the pandemic including disclosure of the endocrine phenotype of COVID-19 with diabetes, obesity and hypovitaminosis D playing a key role in this clinical setting with its huge implication for the prevention and management of the disease.
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Breaking Therapeutic Inertia in Type 2 Diabetes: Active Detection of In-Patient Cases Allows Improvement of Metabolic Control at Midterm

TL;DR: Active detection of hyperglycaemia in patients admitted in conventional surgical beds permits the identification of T2D patients with SCGC as well as previously unknown cases.
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Leptin and thyrotropin relationship is modulated by smoking status in euthyroid subjects.

TL;DR: Leptin is an independent predictor of TSH concentration variations only in euthyroid smoker subjects of both sexes at all ranges of BMI, but not in nonsmokers.
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Why don't corticotroph tumors always produce Cushing's disease?

TL;DR: It is found that the lack of secretory activity of these tumors is related to an impaired processing of POMC and a high degradation of ACTH, with the macro functioning corticotroph tumor behaving as an intermediate state between micro functioning and silent corticOTroph tumors.