264 research outputs found
β-Cell Glucose Sensitivity to Assess Changes in β-Cell Function in Recent-Onset Stage 3 Type 1 Diabetes
No full textFollowing a diagnosis of type 1 diabetes (T1D), persisting C-peptide secretion leads to improved glycemic control and outcomes. Residual β-cell function is often assessed with serial mixed-meal tolerance tests, but these tests do not correlate well with clinical outcomes. Herein, we instead use β-cell glucose sensitivity (βGS) to assess changes in β-cell function, incorporating insulin secretion for a given serum glucose into the assessment of β-cell function. We evaluated changes in βGS in individuals enrolled in the placebo arm of 10 T1D trials performed at diabetes onset. We found that βGS showed a more rapid decline in children, as compared with adolescents and adults. Individuals in the top quartile of βGS baseline distribution had a slower rate in loss of glycemic control time over time. Notably, half of this group were children and adolescents. Finally, to identify predictors of glycemic control throughout follow-up, we ran multivariate Cox models and found that incorporating βGS significantly improved the overall model. Taken together, these data suggest that βGS may be of great utility in predicting those more likely to have a more robust clinical remission and may be of use in design of new-onset diabetes clinical trials and in evaluating response to therapies.
Article highlights: We undertook this study to better predict β-cell loss following type 1 diabetes diagnosis. We set out to answer whether β-cell glucose sensitivity (βGS) improves means to evaluate β-cell function postdiagnosis and whether βGS correlates with clinical outcomes. We found that βGS declines faster in children, subjects in the top baseline quartile of βGS exhibit slower β-cell decline (half are children), and incorporating βGS into multivariate Cox models for glycemic improves the model. The implications of our findings are that βGS predicts those likely to have robust clinical remissions and may help with clinical trials design
sj-docx-1-dst-10.1177_19322968221139873 – Supplemental material for Real-Time Continuous Glucose Monitoring in Adolescents and Young Adults With Type 2 Diabetes Can Improve Quality of Life
No full textSupplemental material, sj-docx-1-dst-10.1177_19322968221139873 for Real-Time Continuous Glucose Monitoring in Adolescents and Young Adults With Type 2 Diabetes Can Improve Quality of Life by Hannah Chesser, Shylaja Srinivasan, Cassidy Puckett, Stephen E. Gitelman and Jenise C. Wong in Journal of Diabetes Science and Technology</p
A case report of Gitelman syndrome resulting from two novel mutations in SLC12A3 gene
No full textAbstractIntroductionHypokalaemia is a common clinical problem. A potential but commonly overlooked cause of hypokalaemia is Gitelman syndrome.Material and methodsA 26-year-old man was admitted to the hospital due to syncope with general and muscular weakness and muscle cramps. The patient's history revealed previous recurrent syncope events associated to hypokalaemia with the lowest serum potassium value being 2.6mmol/l. At admission, blood pressure was normal and no changes were found at physical examination. Laboratory tests showed mild hypokalaemia (3.0mmol/l), hypomagnesaemia (1.36mg/dl), hypocalciuria (< 40mg/24h), and metabolic alkalosis (HCO3− 29.7mmol/l, BE 5.3mmol/l).ResultsFurther laboratory tests (FeK, TTKG) confirmed inappropriate kaliuresis. Conn's disease was excluded by hormonal and imaging assessments. Genetic testing was performed and two novel heterozygous mutations: c.35_36insA and c.1095+5G>A were found in transcript NM_000339.2 in SLC12A3 gene.ConclusionThe patient was diagnosed with Gitelman syndrome and was treated with supplements of potassium and magnesium
Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome: an international cross-sectional study
No full textBACKGROUND: Small cohort studies have reported high parathyroid hormone (PTH) levels in patients with Bartter syndrome and lower serum phosphate levels have anecdotally been reported in patients with Gitelman syndrome. In this cross-sectional study, we assessed PTH and phosphate homeostasis in a large cohort of patients with salt-losing tubulopathies. METHODS: Clinical and laboratory data of 589 patients with Bartter and Gitelman syndrome were provided by members of the European Rare Kidney Diseases Reference Network (ERKNet) and the European Society for Pediatric Nephrology (ESPN). RESULTS: 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I & II had the highest median PTH level (7.5 pmol/l) and 56% had hyperparathyroidism (PTH >7.0 pmol/l). Serum calcium was slightly lower in Bartter syndrome type I & II patients with hyperparathyroidism (2.42 vs. 2.49 mmol/l; p = 0.038) compared to those with normal PTH levels and correlated inversely with PTH (rs -0.253; p = 0.009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate - standard deviation score < -2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with TmP/GFR (rs 0.699; p < 0.001), suggesting renal phosphate wasting. CONCLUSIONS: Hyperparathyroidism is frequent in patients with Bartter syndrome type I & II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting
Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome: an international cross-sectional study
No full textBartter syndrome; Parathyroid hormone; PhosphateSíndrome de Bartter; Hormona paratiroidea; FosfatoSíndrome de Bartter; Hormona paratiroïdal; FosfatBackground
Small cohort studies have reported high parathyroid hormone (PTH) levels in patients with Bartter syndrome and lower serum phosphate levels have anecdotally been reported in patients with Gitelman syndrome. In this cross-sectional study, we assessed PTH and phosphate homeostasis in a large cohort of patients with salt-losing tubulopathies.
Methods
Clinical and laboratory data of 589 patients with Bartter and Gitelman syndrome were provided by members of the European Rare Kidney Diseases Reference Network (ERKNet) and the European Society for Paediatric Nephrology (ESPN).
Results
A total of 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I and II had the highest median PTH level (7.5 pmol/L) and 56% had hyperparathyroidism (PTH >7.0 pmol/L). Serum calcium was slightly lower in Bartter syndrome type I and II patients with hyperparathyroidism (2.42 versus 2.49 mmol/L; P = .038) compared to those with normal PTH levels and correlated inversely with PTH (rs −0.253; P = .009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate—standard deviation score < −2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with tubular maximum reabsorption of phosphate/glomerular filtration rate (TmP/GFR) (rs 0.699; P < .001), suggesting renal phosphate wasting.
Conclusions
Hyperparathyroidism is frequent in patients with Bartter syndrome type I and II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting.This project has been supported by the European Reference Network for Rare Kidney Diseases (ERKNet), which is partly co-funded by the European Union within the framework of the Third Health Programme ‘ERN-2016-Framework Partnership Agreement 2017–2021’. This work is generated within the European Society for Paediatric Nephrology working group on inherited renal disorders. This work was supported by an Innovation Grant 19OI06 from the Dutch Kidney Foundation (to T.N.)
Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome: an international cross-sectional study
No full textBACKGROUND: Small cohort studies have reported high parathyroid hormone (PTH) levels in patients with Bartter syndrome and lower serum phosphate levels have anecdotally been reported in patients with Gitelman syndrome. In this cross-sectional study, we assessed PTH and phosphate homeostasis in a large cohort of patients with salt-losing tubulopathies.
METHODS: Clinical and laboratory data of 589 patients with Bartter and Gitelman syndrome were provided by members of the European Rare Kidney Diseases Reference Network (ERKNet) and the European Society for Paediatric Nephrology (ESPN).
RESULTS: A total of 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I and II had the highest median PTH level (7.5 pmol/L) and 56% had hyperparathyroidism (PTH >7.0 pmol/L). Serum calcium was slightly lower in Bartter syndrome type I and II patients with hyperparathyroidism (2.42 versus 2.49 mmol/L; P = .038) compared to those with normal PTH levels and correlated inversely with PTH (rs -0.253; P = .009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate-standard deviation score < -2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with tubular maximum reabsorption of phosphate/glomerular filtration rate (TmP/GFR) (rs 0.699; P < .001), suggesting renal phosphate wasting.
CONCLUSIONS: Hyperparathyroidism is frequent in patients with Bartter syndrome type I and II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting
From coal to steel: The formation of an independent workers' movement in the Soviet Union, 1989-1991.
No full textThe dissertation addresses two related questions, both concerning Soviet coal miners, the first group to lead mass strikes and create an independent workers' movement in that country in over sixty years. The first question asks why steelworkers, often located in mining communities, did not join the miners in striking and forming a "workers' movement." The second question asks how the miners, once mobilized, transformed their demands in less than two years from supporting "perestroika from below," to demanding that Gorbachev resign and the Soviet Union be dismantled. In answering the first question, the thesis provides case studies of two steel plants, located in the two major coal basins of Siberia and Eastern Ukraine. The dissertation argues that as a result of the centrally planned shortage economy, workers and managers in state enterprises were placed in a position of "mutual dependence:" managers being dependent on workers in a labor short economy, and workers being dependent on managers for the provision of goods and services difficult to otherwise obtain. It is held that workers were in a collective action problem, where most would gain by striking, but organizers of unsuccessful strikes risked losing access to vital goods and services. The provision of enterprise goods and services varied between industries, with coal miners paid with higher wages and fewer "in-kind" benefits relative to steelworkers, making them less dependent on management's largess. In answering the second question on the miners' radicalization, the rational choice approach is dropped for an analysis focusing on institutional and cultural factors. After mobilization, the miners' movement became so rapidly political, it is argued, because of the "fusion" of politics and economics in state socialist societies, whereby the very visible hand of the state is perceived as squeezing the worker at the factory, and distributing that product throughout society. Moreover, the relationship of workers to the state was interpreted through the cultural frameworks of the once-dominant ideology, as miners employed such concepts as a labor theory of value to argue that, subsidies notwithstanding, they were being exploited by the state and would be better served by the market.PhDPolitical ScienceUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/103740/1/9409669.pdfDescription of 9409669.pdf : Restricted to UM users only
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Opinion polling in Central and Eastern Europe under communism
No full textWhilst political opinion polling occupies a well-entrenched position within contemporary capitalist political systems, the same cannot be said for the countries of Central and Eastern Europe. This article focuses primarily on the development of political opinion polling in these countries in the period prior to the collapse of communist regimes at the end of 1989. Polling was a feature of these communist-led societies, although it was limited in terms of its activities, the scope of issue coverage, and its ability to measure public opinion effectively. The major focus of the discussion concentrates on the methodological issues and problems confronting opinion pollsters in these societies during this time
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