Older people with diabetes may be less capable of managing the disease than the younger ones as a result of increased risk of both physical and cognitive impairment. This study provided further evidence for the need of an international consensus statement regarding care of diabetes in older people.
Hereditary angioedema (HAE) is characterized by recurrent edema attacks in various organs causing discomfort and pain [1]. Managing and preventing recurrent attacks in patients with HAE is a clinical challenge that becomes considerably more complicated during pregnancy. The present report describes the management of a patient with type I HAE over the course of two pregnancies. The patient provided consent for publication.The patient had been diagnosed with type I HAE at 15 years of age and the disease was controlled with danazol. At 33 years of age the patient expressed an interest in trying to conceive, and danazol was discontinued. After conception, the patient experienced an increased frequency and severity of HAE attacks, occurring every 5-7 days in her first and second trimesters. The majority of these attacks were abdominal, causing severe pain and vomiting. These attacks were successfully managed in the emergency department with an intravenous infusion of 1500-2000 U of purified C1 esterase inhibitor (Berinert; CSL Behring, King of Prussia, PA, USA), analgesics, and antiemetics. The patient was hospitalized twice during the first trimester and once during the second trimester owing to persistent abdominal symptoms that did not completely resolve with management in the emergency department. In the third trimester, the patient started receiving 1500 U of C1 inhibitor (C1-INH) every 5 days as prophylactic therapy and had no further HAE attacks. At term, the patient was treated with a prophylactic dose of C1-INH given prior to induction for a vaginal delivery of a healthy male neonate weighing 2780 g that was HAE-negative on further testing. After delivery, the patient was restarted on danazol 100 mg twice daily for prevention of HAE attacks and thus was unable to breastfeed.Two years after her first delivery, the patient discussed with her physicians and planned for a second pregnancy. She discontinued danazol and initiated C1-INH prophylactic therapy (initially 500 U weekly and then increased to 1000 U weekly). A portacath catheter was inserted to facilitate recurrent intravenous administration of C1-INH. Once she became pregnant, the patient developed weekly HAE attacks despite prophylactic C1-INH infusions. On 5 separate occasions the patient attended the emergency department for treatment with C1-INH (1500-2000 U), analgesics, and antiemetics. This increase in her disease activity resulted in her prophylactic regimen being changed from 1000 U twice weekly, to 1500 U twice weekly, to a maximum dose of 2000 U twice weekly by the end of the first trimester (Table 1). The titration of the C1-INH dose resulted in a gradual decline in frequency and severity of HAE attacks, decreasing to every 2-3 weeks by the third trimester without any emergency department treatment needed. At delivery, the patient was treated with 1000 U of C1-INH prior to induction of labor, and vaginally delivered an HAE-positive male neonate weighing 2550 g without complication. After delivery, the patient breastfed for 24 hours before res...
ObjectiveImpaired mitochondrial function may contribute to the onset of contractile dysfunction with insulin resistance/type 2 diabetes. Our aim was therefore to determine alterations in the mitochondrial proteome of a mouse model of obesity/type 2 diabetes.MethodsMitochondrial proteins were isolated from hearts collected from 18- to 20-week-old female db/db mice and compared to matched controls. We performed two-dimensional polyacrylamide gel electrophoresis to determine differentially expressed proteins. Peptides of interest were further analysed by mass spectrometry and Mascot software was employed to identify protein matches.ResultsOur data showed that ATP synthase D chain, ubiquinol cytochrome-C reductase core protein 1 and electron transfer flavoprotein subunit alpha peptide levels were altered with obesity. Moreover, we found coordinate down-regulation of contractile proteins in the obese heart, i.e. α-smooth muscle actin, α-cardiac actin, myosin heavy-chain α and myosin-binding protein C.ConclusionWe propose that decreased contractile protein levels may contribute to contractile dysfunction of hearts from diabetic mice.
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