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OBJECTIVE Trigger finger (TF) is a hand disorder causing the fingers to painfully lock in flexion. Diabetes is a known risk factor; however, whether strict glycemic control effectively lowers risk of TF is unknown. Our aim was to examine whether high HbA1c was associated with increased risk of TF among individuals with diabetes. RESEARCH DESIGN AND METHODS The Swedish National Diabetes Register (NDR) was cross-linked with the health care register of the Region of Skåne in southern Sweden. In total, 9,682 individuals with type 1 diabetes (T1D) and 85,755 individuals with type 2 diabetes (T2D) aged ≥18 years were included from 2004 to 2019. Associations between HbA1c and TF were calculated with sex-stratified, multivariate logistic regression models with 95% CIs, with adjustment for age, duration of diabetes, BMI, and systolic blood pressure. RESULTS In total, 486 women and 271 men with T1D and 1,143 women and 1,009 men with T2D were diagnosed with TF. Increased levels of HbA1c were associated with TF among individuals with T1D (women OR 1.26 [95% CI 1.1–1.4], P = 0.001, and men 1.4 [1.2–1.7], P < 0.001) and T2D (women 1.14 [95% CI 1.2–1.2], P < 0.001, and men 1.12 [95% CI 1.0–1.2], P = 0.003). CONCLUSIONS Hyperglycemia increases the risk of developing TF among individuals with T1D and T2D. Optimal treatment of diabetes seems to be of importance for prevention of diabetic hand complications such as TF.

OBJECTIVE To evaluate the frequency of autoimmune markers (islet cell antibodies [ICA] and glutamic acid decarboxylase antibodies [GADA]) and clinical features in newly diagnosed people with diabetes aged 40–75 years. RESEARCH DESIGN AND METHODS Two hundred fifty-nine consecutive patients (aged 40–75 years) with newly suspected diabetes diagnosed during a 2-year period were studied. The diagnosis of newly discovered diabetes was confirmed in 203 patients. Gender, BMI, HbAic, fasting C-peptide, ICA, and GADA were evaluated. The frequency of obesity was estimated using two different sets of criteria: 1) National Diabetes Data Group (NDDG) criteria, and 2) criteria based on a Swedish reference population. RESULTS The annual incidence of diabetes was 106 per 100,000 people. The incidence of diabetes in those patients who were 40–54 years old was significantly higher in men than in women (odds ratio: 2.16; P = 0.001). ICA were detected in 16 of 203 patients (8%), whereas 17 of 203 patients (8%) were GADA+; 10 of 203 (5%) patients were positive for both ICA and GADA. Among the 203 diabetic patients, 19 (9.4%) were classified as having IDDM, giving an IDDM incidence of 10 per 100,000 people aged 40–75 years. The frequency of obesity in NIDDM was high but varied with its definition; the frequency of obesity was highest (P < 0.001) when NDDG criteria, and not Swedish reference values, were used (57 of 75 [76%] vs. 40 of 75 [53%] for women and 66 of 109 [61%] vs. 45 of 109 [41%] for men). CONCLUSIONS A striking male preponderance was found among incident cases of diabetes in people aged 40–54 years. Autoimmune markers were detected in 10% of incident cases of diabetes in people aged 40–75 years. Using a conservative estimation, as many as 10 of 100,000 middle-aged and elderly subjects developed IDDM. The frequency of obesity in NIDDM was high but this was also the case in the reference population.

OBJECTIVE— To determine the effects of islet cell antibodies on β-cell function during the first 3 yr after diagnosis in type II diabetic patients. RESEARCH DESIGN AND METHODS— β-cell function in type II diabetic patients with (n = 11, 50 ± 5 yr of age) and without (n = 10, 52 ± 4 yr of age) ICA was followed prospectively and compared with β-cell function in type I adult diabetic patients (n = 17, 37 ± 5 yr of age) and in healthy control subjects (n = 34, age 45 ± 3 yr). β-cell function was evaluated as fasting C-peptide, 1 + 3 min C-peptide after intravenous glucose, and ∆ C-peptide after glucagon. RESULTS— Fasting C-peptide was equal in type II diabetic patients with ICA (0.30 ± 0.03 nM) and type I diabetic patients (0.24 ± 0.03 nM) at diagnosis, and decreased (P < 0.05) during 3 yr in these groups but not in type II diabetic patients without ICA. At diagnosis, type II diabetic patients with ICA showed a 1 + 3 min C-peptide (0.92 ± 0.17 nM) lower (P < 0.001) than control subjects but higher (P < 0.05) than type I diabetic patients (0.53 ± 0.11 nM). After 1 yr, 1 + 3 min C-peptide in type II diabetic patients with ICA had decreased (P < 0.05) to 0.18 ± 0.11 nM and was equal to type I diabetic patients (0.38 ± 0.10 nM). ∆ C-peptide after glucagon was equally impaired in type II diabetic patients with ICA (0.38 ± 0.06 nM) and type I diabetic patients (0.35 ± 0.11 nM) at diagnosis. After 3 yr, type II diabetic patients with ICA had fasting C-peptide of 0.09 ± 0.04 nM, 1 + 3 min C-peptide of 0.18 ± 0.10 nM, and ∆ C-peptide after glucagon of 0.20 ± 0.09 nM, values equal to type I diabetic patients but lower (P < 0.01) than in type II diabetic patients without ICA, whose values remained unchanged; fasting C-peptide of 0.97 ± 0.17 nM, 1 + 3 min C-peptide of 2.31 ± 0.50 nM, and ∆ C-peptide after glucagon of 1.76 ± 0.28 nM. CONCLUSIONS— In patients considered type II diabetic with ICA, β-cell function progressively decreased after diagnosis, and after 3 yr was similar to type I diabetic patients, whereas β-cell function in type II diabetic patients without ICA was unchanged.

OBJECTIVE To evaluate proinsulin secretion in different types of NIDDM. RESEARCH DESIGN AND METHODS Proinsulin and insulin were evaluated at diagnosis of diabetes and 3 years later (fasting and after stimulation with intravenous glucose and glucagon) in 10 NIDDM patients without islet cell antibodies (ICAs) at diagnosis (age 52 ± 4 years), 11 NIDDM patients with ICAs at diagnosis (age 50 ± 5 years), and 21 healthy control subjects (age 53 ± 4 years). RESULTS At diagnosis, fasting proinsulin was higher in NIDDM patients without ICAs than in control subjects (39.6 ± 10.0 vs. 12.8 ± 1.6 pmol/l, P < 0.01). Proinsulin response to intravenous glucose decreased in NIDDM patients with ICAs (from 35.6 ± 6.2 to 13.5 ± 5.4 pmol/l, P < 0.05), but remained unchanged in those without ICAs. At 3 years after diagnosis, fasting proinsulin (10.0 ± 3.7 vs. 59.1 ± 17.0 pmol/l) and proinsulin responses to intravenous glucose (13.5 ± 5.4 vs. 103.9 ± 35.1 pmol/l) and to intravenous glucagon (7.4 ± 3.9 vs. 36.0 ± 7.7 pmol/l) were much lower (P < 0.01) in NIDDM patients with ICAs than in those without ICAs. CONCLUSIONS After diagnosis of diabetes, proinsulin secretion decreases significantly in NIDDM patients with ICAs and remains constant in those without.

OBJECTIVE To evaluate the relationship between islet cell antibodies (ICAs) and the cardiovascular risk profile 5 years after clinical diagnosis of NIDDM. RESEARCH DESIGN AND METHODS Five years after clinical diagnosis, we evaluated blood pressure (BP) and lipids in 17 NIDDM patients with ICA at diagnosis (age 60 ± 4 years) and 133 NIDDM patients without ICA at diagnosis (age 61 ± 1 year). Urinary albumin excretion was evaluated in a subset of 12 NIDDM patients with ICA at diagnosis (age 60 ± 4 years) and 82 NIDDM patients without ICA at diagnosis (age 61 ± 1 year). RESULTS NIDDM patients without ICA showed higher BP (140/86 ± 2/1 mmHg vs. 128/79 ± 3/2 mmHg; P < 0.05), total cholesterol (6.10 ± 0.11 vs. 5.09 ± 0.29 mmol/l; P < 0.01), LDL-to-HDL ratio (3.85 ± 0.14 vs. 2.49 ± 0.18; P < 0.001), and triglycerides (2.58 ± 0.24 vs. 0.90 ± 0.06 mmol/l; P < 0.001), lower HDL cholesterol (1.08 ± 0.03 vs. 1.40 ± 0.08 mmol/l; P < 0.001), and higher urinary albumin excretion (0.16 ± 0.06 vs. 0.01 ± 0.01 g/24 h; P < 0.05) than NIDDM patients with ICA. Among NIDDM patients without ICA, no differences concerning BP or lipids were found between obese and nonobese patients. CONCLUSIONS ICA at diagnosis of NIDDM is a marker of more favorable cardiovascular risk profile 5 years after clinical diagnosis.