glucosidase/glavobolja

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A complex craniovertebral junction malformation in a patient with late onset glycogenosis 2.

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Glycogenosis II (GSDII) is an autosomal recessive lysosomal storage disorder resulting from deficiency of acid alpha-glucosidase and subsequent lysosomal accumulation of glycogen in skeletal, cardiac and smooth muscles. The late-onset form is characterized by wide variability of the phenotypical

A study on the safety and efficacy of reveglucosidase alfa in patients with late-onset Pompe disease.

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Late-onset Pompe disease is a rare genetic neuromuscular disorder caused by lysosomal acid alpha-glucosidase (GAA) deficiency that ultimately results in mobility loss and respiratory failure. Current enzyme replacement therapy with recombinant human (rh)GAA has demonstrated efficacy in subjects with

Neurological Manifestation of Incretin-Based Therapies in Patients with Type 2 Diabetes: A Systematic Review and Network Meta-Analysis.

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As a new class of antidiabetic drug, incretin-based therapies, which include dipeptidyl peptidase-4 inhibitors (DPP-4Is) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs), have raised concerns about symptoms of withdrawal in patients with type 2 diabetes mellitus (T2DM), such as dizziness

A Case of Adult-onset Pompe Disease with Cerebral Stroke and Left Ventricular Hypertrophy.

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BACKGROUND Pompe disease is an autosomal recessive glycogen storage disorder caused by a deficiency of the lysosomal glycogen-hydrolyzing enzyme acid α-glucosidase. The adult-onset form, late-onset Pompe disease, has been characterized by glycogen accumulation, primarily in skeletal and smooth

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