| 1. |
- Chantzichristos, Dimitrios, 1976, et al.
(författare)
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Incidence, prevalence and seasonal onset variation of Addison's disease among persons with type 1 diabetes mellitus: nationwide, matched cohort studies.
- 2018
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Ingår i: European journal of endocrinology. - 1479-683X. ; 178:1, s. 115-122
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Tidskriftsartikel (refereegranskat)abstract
- We determined the incidence and prevalence of Addison's disease (AD) among persons with or without type 1 diabetes mellitus (T1DM) in nationwide, matched cohort studies.Persons with T1DM were identified from the Swedish National Diabetes Register and each was matched for age, sex, year and county to five controls randomly selected from the general population. Persons with AD were identified from the Swedish National Inpatient Register. Baseline demographics and seasonal onset variation of AD were presented by descriptive statistics. Prevalence and incidence were estimated by proportions and incidence rates, respectively. Times to AD were analyzed using the Cox proportional hazard model.Between 1998 and 2013, 66 persons with T1DM were diagnosed with AD at a mean age (s.d.) of 36.4 (13.0) years among 36 514 persons with T1DM, while 32 were diagnosed with AD at a mean age of 42.7 (15.2) years among 182 570 controls. The difference in mean age at diagnosis of AD between the groups was 6.3 years (P value=0.036). The incidence of AD for a person with or without T1DM was therefore 193 and 18 per million person-years, respectively. The adjusted relative risk increase of developing AD in T1DM was 10.8 (95% CI: 7.1-16.5). The highest incidence of AD was observed during February-March and September-October. The prevalence of AD in persons with or without T1DM in December 2012 was 3410 and 208 per million, respectively. The odds ratio for AD in persons with T1DM vs controls was 16.5 (95% CI: 11.1-24.5).The risk to develop AD among persons with T1DM is more than 10 times higher than in persons without T1DM. Persons with T1DM develop AD at a younger age. The incidence of AD may have a seasonal pattern.
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| 2. |
- Chantzichristos, Dimitrios, 1976, et al.
(författare)
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MANAGEMENT OF ENDOCRINE DISEASE: Disease burden and treatment challenges in patients with both Addison's disease and type 1 diabetes mellitus.
- 2020
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Ingår i: European journal of endocrinology. - 1479-683X. ; 183:1
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Forskningsöversikt (refereegranskat)abstract
- Concurrent type 1 diabetes (T1D) and Addison's disease (AD) is a rare combination of diseases and, in approximately one third of these patients, it is also combined with an autoimmune thyroid disease. Recently, it was shown that patients with both T1D and AD have a higher risk of premature death compared to patients with T1D alone, the most common causes of death being due to diabetic complications and cardiovascular disease. These patients receiving replacement therapies with both insulin and glucocorticoids face an increased risk of hypo- and hyperglycemia, and diabetic ketoacidosis, and have a higher risk of adrenal crisis than patients with AD alone. Treatment challenges include the opposing effects of insulin and glucocorticoids on glucose homeostasis, and the need to balance and synchronize these two treatments. The rarity of this disease combination may explain the paucity of data on outcome and specific treatment strategies in this patient group. Based on this review, we suggest management strategies for their insulin and glucocorticoid replacement therapies and indicate future areas of research.
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| 3. |
- Chantzichristos, Dimitrios, 1976, et al.
(författare)
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Mortality in patients with diabetes mellitus and Addison's disease: a nationwide, matched, observational cohort study.
- 2017
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Ingår i: European journal of endocrinology. - 1479-683X. ; 176:1, s. 31-39
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Tidskriftsartikel (refereegranskat)abstract
- Our hypothesis was that patients with diabetes mellitus obtain an additional risk of death if they develop Addison's disease (AD).Nationwide, matched, observational cohort study cross-referencing the Swedish National Diabetes Register with Inpatient, Cancer and Cause of Death Registers in patients with diabetes (type 1 and 2) and AD and matched controls with diabetes. Clinical characteristics at baseline, overall, and cause-specific mortality were assessed. The relative risk of death was assessed using a Cox proportional hazards regression model.Between January 1996 and December 2012, 226 patients with diabetes and AD were identified and matched with 1129 controls with diabetes. Median (interquartile range) follow-up was 5.9 (2.7-8.6) years. When patients with diabetes were diagnosed with AD, they had an increased frequency of diabetes complications, but both medical history of cancer and coronary heart disease did not differ compared with controls. Sixty-four of the 226 patients with diabetes and AD (28%) died, while 112 of the 1129 controls (10%) died. The estimated relative risk increase (hazard ratio) in overall mortality in the diabetes and AD group was 3.89 (95% confidence interval 2.84-5.32) compared with controls with diabetes. The most common cause of death was cardiovascular in both groups, but patients with diabetes and AD showed an increased death rate from diabetes complications, infectious diseases and unknown causes.Patients with the rare combination of diabetes and AD showed a markedly increased mortality and died more frequently from infections and unknown causes than patients with diabetes alone. Improved strategy for the management of this combination of metabolic disorders is needed.
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| 4. |
- van Raalte, Daniël H, et al.
(författare)
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Exenatide improves β-cell function up to 3 years of treatment in patients with type 2 diabetes: a randomised controlled trial.
- 2016
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Ingår i: European journal of endocrinology. - 1479-683X. ; 175:4, s. 345-52
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Tidskriftsartikel (refereegranskat)abstract
- Glucagon-like peptide (GLP)-1 receptor agonist treatment improves β-cell function. In this study, we investigated whether the improvements are sustained during a 3-year treatment period.Sixty-nine metformin-treated type 2 diabetes patients were randomised to the GLP1 receptor agonist, exenatide (EXE) twice daily (BID) or to insulin glargine (GLAR). β-cell function parameters were derived using the Mari model from standardised breakfast and lunch meals that were administered before treatment, and after 1 and 3years of treatment. EXE was administered before breakfast.Fifty-nine (EXE: n=30; GLAR: n=29) and thirty-six (EXE: n=16; GLAR: n=20) patients completed the meal at 1- and 3-year treatment respectively. After 3years, groups had comparable glycaemic control (HbA1c: EXE 6.6±0.2% and GLAR 6.9±0.2%; P=0.216). Compared with GLAR, at 1 and 3years, EXE induced a stronger reduction in post-breakfast glucose concentrations (P<0.001), with lower C-peptide levels (P<0.001). Compared with GLAR, EXE increased insulin secretion at 8mmol/L glucose throughout the study period (P<0.01). Both treatments improved β-cell glucose sensitivity after 1-year treatment. However, only EXE treatment sustained this improvement for 3years. No consistent changes in other β-cell parameters including rate sensitivity and potentiation were observed.Compared with GLAR, EXE improved the parameters of β-cell function, especially insulin secretion at 8mmol/L glucose and β-cell glucose sensitivity, which was sustained during the 3-year treatment period.
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| 5. |
- van Raalte, Daniël H, et al.
(författare)
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The effect of alogliptin and pioglitazone combination therapy on various aspects of beta-cell function in patients with recent-onset type 2 diabetes.
- 2014
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Ingår i: European journal of endocrinology / European Federation of Endocrine Societies. - 1479-683X. ; 170:4, s. 565-574
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Tidskriftsartikel (refereegranskat)abstract
- Type 2 diabetes (T2DM) management requires continuous treatment intensification due to progressive beta-cell function decline in insulin resistant individuals. Initial combination therapy of a dipeptidyl peptidase (DPP)-4 inhibitor with a thiazolidinedione (TZD) may be rational. We assessed the effects of the DPP-4 inhibitor alogliptin (ALO) combined with the TZD pioglitazone (PIO), versus ALO monotherapy or placebo (PBO), on beta-cell function and glycemic control in T2DM.
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