glucosidase/muntah

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Pneumatosis cystoides intestinalis induced by the alpha-glucosidase inhibitor complicated from sigmoid volvulus in a diabetic patient.

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We present the case of a diabetic patient on treatment with acarbose who had presented a sigmoid volvulus with localized cystic pneumatosis of the sigmoid colon.A 72-year-old patient with a medical history of atrial fibrillation, DNID in treatment since 10

Three diabetic cases of acute dizziness due to initial administration of voglibose.

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We observed 3 diabetic patients with intolerable dizziness followed by nausea and vomiting immediately after an initial administration of the alpha-glucosidase inhibitor, voglibose. These symptoms did not recur after discontinuation of the drug. Adverse effects as observed in these cases have not

Glycogen storage disease type II in the Lapland dog.

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A newly recognized inherited metabolic disease in the Lapland dog is described. The metabolic defect is a deficiency of acid-alpha-glucosidase, a lysosomal hydrolase. The clinical picture is dominated by vomiting related to megaoesophagus, and progressive muscle weakness leading to exhaustion and

Hesperidin-3'-o-methylether is more potent than hesperidin in phosphodiesterase inhibition and suppression of ovalbumin-induced airway hyperresponsiveness.

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Hesperidin is present in the traditional Chinese medicine, "Chen Pi," and recently was reported to have anti-inflammatory effects. Therefore, we were interested in comparing the effects of hesperidin and hesperidin-3'-O-methylether on phosphodiesterase inhibition and airway hyperresponsiveness (AHR)

A randomized study of alglucosidase alfa in late-onset Pompe's disease.

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BACKGROUND Pompe's disease is a metabolic myopathy caused by a deficiency of acid alpha glucosidase (GAA), an enzyme that degrades lysosomal glycogen. Late-onset Pompe's disease is characterized by progressive muscle weakness and loss of respiratory function, leading to early death. We conducted a

Pompe disease: dramatic improvement in gastrointestinal function following enzyme replacement therapy. A report of three later-onset patients.

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Pompe disease is a lysosomal storage disease due to deficient acid α-glucosidase (GAA) activity. Infants with the classic infantile-onset subtype present with severe hypotonia and cardiomegaly, and most expire in the first year of life, whereas the severity of the muscle-based manifestations in

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