Purpose: The impact of GH/IGF-1 levels on skeletal muscle in acromegaly is still controversial. Temporal (TMT) and masseter muscle (MMT) thickness has been recently demonstrated as a reliable measure of muscle mass. We aimed to investigate the relationship between TMT, MMT and clinical/biochemical characteristics in patients with acromegaly.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2024
Purpose: To evaluate the impact of pasireotide (PAS) therapy on hormonal and glycometabolic outcome in patients with acromegaly previously treated with combination medical therapies or unconventional dosages of first-generation somatostatin receptor ligands (fg-SRLs).
Methods: Retrospective study carried out in two referral centers for pituitary diseases. Twenty-one acromegalic patients were switched to PAS (12 had biochemical control, 9 were uncontrolled).
J Endocrinol Invest
January 2024
Purpose: Diabetic striatopathy (DS) is a rare complication of poorly controlled diabetes mellitus (DM), characterized by hyperglycemia associated with chorea/ballism and characteristic reversible basal ganglia abnormalities on computed tomography (CT) and/or magnetic resonance imaging (MRI). We propose a narrative review of the literature on this topic, currently unknown to most, and about which physicians should be aware. We intend to summarize, critically review, and take to mean the evidence on this disorder, describing its typical features.
View Article and Find Full Text PDFBackground: Diabetic striatopathy is defined as a state of hyperglycemia associated with chorea/ballism, striatal hyperdensity at CT, or hyperintensity at T1-weighted MRI. It is considered a rare complication of uncontrolled diabetes but prevalence data are scarce.
Objectives: Characterize diabetic striatopathy prevalence in the population afferent to the largest teaching hospital in Genova (Liguria, Italy) and investigate the role of glycated hemoglobin level in predicting the risk.
This paper describes a biological test of the hypothesis that one or more components of the intracellular nucleotide pool represent a significant target for the mutagenic effects of alkylating agents. In other words, we ask whether mutagenesis can occur either through alkylation of susceptible nucleotide residues in DNA, or through alkylation of a free nucleotide, followed by its incorporation into DNA. Our approach is based upon the premise that if a nucleotide pool is a mutagenic target, then transient expansion of that pool should increase the target size and enhance mutagenesis following subsequent treatment with an alkylating agent.
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