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91.
Aileen K. Wang Shweta Sharma Paul Kim Karen Mrejen-Shakin 《Indian Journal of Critical Care Medicine》2014,18(7):456-460
We report a case of symptomatic hypomagnesaemia in medical intensive care unit that is strongly related to proton pump inhibitors (PPIs) and provide literature review. A 65-year-old male with severe gastroesophageal reflux on omeprazole 20 mg orally twice a day, who presented to the hospital with abdominal pain, nausea, diarrhea, and new onset seizures. On admission, his serum magnesium level was undetectable. Electrocardiogram showed a new right bundle branch block with a prolonged QT interval. The hypomagnesemia was corrected with aggressive magnesium supplementation and hypomagnesemia resolved only after the PPI was stopped. Neurologic and cardiac abnormalities were corrected. This is a life-threatening case of an undetectable magnesium level strongly associated with PPI use. In critically, ill patients with refractory hypomagnesemia, we advocate considering changing gastrointestinal prophylaxis from a PPI to a histamine-receptor blocker. 相似文献
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Pradeep Kumar Sharma Bhaskar Saikia Rachna Sharma Kumar Ankur Praveen Khilnani Vinay Kumar Aggarwal Hae Cheong 《Indian journal of pediatrics》2014,81(10):1095-1098
Bartter syndrome is a group of inherited, salt-losing tubulopathies presenting as hypokalemic metabolic alkalosis with normotensive hyperreninemia and hyperaldosteronism. Around 150 cases have been reported in literature till now. Mutations leading to salt losing tubulopathies are not routinely tested in Indian population. The authors have done the genetic analysis for the first time in the Bartter syndrome on two cases from India. First case was antenatal Bartter syndrome presenting with massive polyuria and hyperkalemia. Mutational analysis revealed compound heterozygous mutations in KCNJ1(ROMK) gene [p(Leu220Phe), p(Thr191Pro)]. Second case had a phenotypic presentation of classical Bartter syndrome however, genetic analysis revealed only heterozygous novel mutation in SLC12A gene p(Ala232Thr). Bartter syndrome is a clinical diagnosis and genetic analysis is recommended for prognostication and genetic counseling. 相似文献
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Kai-Ting Yang Jennifer-Ann Bayan Ni Zeng Richa Aggarwal Lina He Zhechu Peng Anketse Kassa Melissa Kim Zhiou Luo Zhenrong Shi Vivian Medina Keerthi Boddupally Bangyan L. Stiles 《Diabetologia》2014,57(2):352-361
Aims/hypothesis
Adult beta cells have a diminished ability to proliferate. Phosphatase and tensin homologue (PTEN) is a lipid phosphatase that antagonises the function of the mitogenic phosphatidylinositol 3-kinase (PI3K) pathway. The objective of this study was to understand the role of PTEN and PI3K signalling in the maintenance of beta cells postnatally.Methods
We developed a Pten lox/lox; Rosa26 lacZ; RIP-CreER + model that permitted us to induce Pten deletion by treatment with tamoxifen in mature animals. We evaluated islet mass and function as well as beta cell proliferation in 3- and 12-month-old mice treated with tamoxifen (Pten deleted) vs mice treated with vehicle (Pten control).Results
Deletion of Pten in juvenile (3-month-old) beta cells significantly induced their proliferation and increased islet mass. The expansion of islet mass occurred concomitantly with the enhanced ability of the Pten-deleted mice to maintain euglycaemia in response to streptozotocin treatment. In older mice (>12 months of age), deletion of Pten similarly increased islet mass and beta cell proliferation. This novel finding suggests that PTEN-regulated mechanisms may override the age-onset diminished ability of beta cells to respond to mitogenic stimulation. We also found that proteins regulating G1/S cell-cycle transition, such as cyclin D1, cyclin D2, p27 and p16, were altered when PTEN was lost, suggesting that they may play a role in PTEN/PI3K-regulated beta cell proliferation in adult tissue.Conclusions/interpretation
The signals regulated by the PTEN/PI3K pathway are important for postnatal maintenance of beta cells and regulation of their proliferation in adult tissues. 相似文献98.
Shweta Urva PhD Tamer Coskun MD Corina Loghin MD Xuewei Cui PhD Emily Beebe BS Libbey O'Farrell BS Daniel A. Briere MS Charles Benson MD Michael A. Nauck MD Axel Haupt MD 《Diabetes, obesity & metabolism》2020,22(10):1886-1891
The effect of dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist (RA) tirzepatide on gastric emptying (GE) was compared to that of GLP-1RAs in non-clinical and clinical studies. GE was assessed following acute and chronic treatment with tirzepatide in diet-induced obese mice versus semaglutide or long-acting GIP analogue alone. Participants [with and without type 2 diabetes (T2DM)] from a phase 1, 4-week multiple dose study received tirzepatide, dulaglutide or placebo. GE was assessed by acetaminophen absorption. In mice, tirzepatide delayed GE to a similar degree to that achieved with semaglutide; however, these acute inhibitory effects were abolished after 2 weeks of treatment. GIP analogue alone had no effect on GE or on GLP-1's effect on GE. In participants with and without T2DM, once-weekly tirzepatide (≥5 and ≥4.5 mg, respectively) delayed GE after a single dose. This effect diminished after multiple doses of tirzepatide or dulaglutide in healthy participants. In participants with T2DM treated with an escalation schedule of tirzepatide 5/5/10/10 or 5/5/10/15 mg, a residual GE delay was still observed after multiple doses. These data suggest that tirzepatide's activity on GE is comparable to that of selective GLP-1RAs. 相似文献
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