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Lili Liu, Zhuo Shao, Ying Xia, Jiabi Qin, Yang Xiao, Zhiguang Zhou and Zubing Mei

Objective: Combined treatment with an incretin-based drug, such as a glucagon-like peptide 1 receptor agonist (GLP-1 RA) or a dipeptidyl peptidase-4 (DPP-4) inhibitor, and basal insulin is a new strategy for improving glucose control in type 1 diabetes mellitus (T1DM). We performed a meta-analysis to assess the effect of this combined treatment on glycaemic control, insulin dose, severe hypoglycaemia, weight gain, and gastrointestinal side effects in T1DM patients.

Methods: We searched PubMed, EMBASE and the Cochrane Library for relevant studies published before July 16, 2018. The primary outcome was glycosylated haemoglobin (HbA1c). Secondary outcomes included total daily insulin dose, body weight, severe hypoglycaemia and gastrointestinal side effects.

Results: Nine randomized controlled trials (RCTs) involving 2389 patients were ultimately included in the meta-analysis. The pooled data suggested that incretin-based therapy was associated with a reduction in HbA1c levels [weighted mean difference (WMD) -0.17%, 95% confidence interval (CI) -0.24 to -0.11, P<0.001)], total daily insulin dose (WMD -5.53 IU/day, 95% CI -8.89 to -2.17, P=0.001) and body weight (WMD -3.24 kg, 95% CI -4.43 to -2.04, P<0.001). Incretins did not increase the risk of severe hypoglycaemia [odds ratio (OR) 0.83, 95% CI 0.60 to 1.16, P=0.287] but increased the occurrence of gastrointestinal side effects (OR 3.46, 95% CI 2.20 to 5.45 P<0.001).

Conclusions: In T1DM patients, GLP-1 RAs, but not DPP-4 inhibitors, combined with insulin appear to be an effective therapy but may increase the occurrence of gastrointestinal side effects.

Open access

Peng Fan, Chao-Xia Lu, Di Zhang, Kun-Qi Yang, Pei-Pei Lu, Ying Zhang, Xu Meng, Su-Fang Hao, Fang Luo, Ya-Xin Liu, Hui-Min Zhang, Lei Song, Jun Cai, Xue Zhang and Xian-Liang Zhou

Liddle syndrome (LS), a monogenetic autosomal dominant disorder, is mainly characterized by early-onset hypertension and hypokalemia. Clinically, misdiagnosis or missing diagnosis is common, since clinical phenotypes of LS are variable and nonspecific. We report a family with misdiagnosis of primary aldosteronism (PA), but identify as LS with a pathogenic frameshift mutation of the epithelial sodium channel (ENaC) β subunit. DNA samples were collected from a 32-year-old proband and 31 other relatives in the same family. A designed panel including 41 genes associated with monogenic hypertension was screened using next-generation sequencing. The best candidate disease-causing variants were verified by Sanger sequencing. Genetic analysis of the proband revealed a novel frameshift mutation c.1838delC (p.Pro613Glnfs*675) in exon 13 of SCNN1B. This heterozygous mutation involved the deletion of a cytosine from a string of three consecutive cytosines located at codons 612 to 613 and resulted in deletion of the crucial PY motif and elongation of the β-ENaC protein. The identical mutation was also found in 12 affected family members. Amiloride was effective in alleviating LS for patients. There were no SCNN1A or SCNN1G mutations in this family. Our study emphasizes the importance of considering LS in the differential diagnosis of early-onset hypertension. The identification of a novel frameshift mutation of SCNN1B enriches the genetic spectrum of LS and has allowed treatment of this affected family to prevent severe complications.