Memphis, TN, United States
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Karl D.,Endocrine Clinic | Zhou R.,Medpace Inc. | Vlajnic A.,Sanofi S.A. | Riddle M.,Oregon Health And Science University
Diabetic Medicine | Year: 2012

Aims To evaluate whether fasting plasma glucose values measured early during insulin therapy can identify patients with Type2 diabetes who may not achieve adequate glycaemic control after 6months and will require additional treatment. Methods Patient-level data from seven prospective, randomized, controlled studies using treat-to-target methods were pooled to evaluate the efficacy of insulin glargine. Fasting plasma glucose was measured at baseline, week6 or 8 (6/8) and week12. HbA1c was measured at week24 to assess glycaemic control. Results One thousand and thirty-six patients (56% male, 81% white) were included in the analysis (mean age 56.3years; duration of diabetes 8.4years). Baseline mean fasting plasma glucose was 11.2mmol/l and mean HbA1c was 73mmol/mol (8.8%). After 24weeks of treatment, mean HbA1c decreased to 53mmol/mol (7.0%); 56% of patients reached a target HbA1c≤53mmol/mol (7.0%). Significant correlations with week24 HbA1c were obtained for fasting plasma glucose measured at week6/8 and week12 (r=0.32; P<0.0001 for both). Patients with fasting plasma glucose >10mmol/l at week6/8 or week12 were significantly less likely to achieve the HbA1c target at the end of treatment than patients with fasting plasma glucose <8.9mmol/l (P<0.0001 for both). If fasting plasma glucose was >10mmol/l at week 6/8 or week12, patients had only a 27% chance of reaching the HbA1c goal. Conclusions Fasting plasma glucose remaining >10mmol/l after 6-12weeks of glargine therapy indicates that reaching target HbA1c≤53mmol/mol (7.0%) is unlikely and calls for individualized attention to consider further therapeutic options. © 2012 The Authors. Diabetic Medicine © 2012 Diabetes UK.


Savage M.O.,William Harvey Research Institute | Cohen L.,Childrens Hospital Boston | Cohen A.J.,Endocrine Clinic | Cohen P.,Mattel Childrens Hospital UCLA | Saenger P.H.,Yeshiva University
Pediatric Endocrinology Reviews | Year: 2010

Defects in the growth hormone (GH)-insulin-like growth factor (IGF)-I axis may cause GH resistance characterized by IGF-I deficiency and growth failure. The range of defects causing GH resistance is broad as are their biochemical and phenotypical characteristics. We propose that GH-IGF-I axis defects form a continuum of clinical and biochemical effects ranging from GH deficiency to GH resistance. The pathophysiology of GH resistance is described followed by a scheme for investigation of the child with severe short stature and normal GH secretion. We critically discuss GH therapy for such patients and define acceptable growth responsiveness. Finally we discuss therapy with IGF-I within the limits of the USA Food and Drug Administration and European Medicines Agency labels for GH resistance.


Kanazirev B.,Medical University-Varna | Hristozov K.,Endocrine Clinic | Bachvarova M.,Medical University-Varna | Georgieva G.,Medical University-Varna | Dimova M.,Medical University-Varna
Endokrinologya | Year: 2011

The cardiovascular signs and symptoms of thyroid disease are some of the most profound and clinically relevant findings that accompany hyperthyroidism. On the basis of the understanding of the cellular mechanisms of thyroid hormone action on the heart and cardiovascular system, it is possible to explain the changes in cardiac output, cardiac contractility, blood pressure, vascular resistance, and rhythm disturbances that result from thyroid dysfunction. The importance of the recognition of the effects of thyroid disease on the heart also derives from the observation that restoration of normal thyroid function most often reverses the abnormal cardiovascular hemodynamics.

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