ABSTRACT
We present the case series of two women aged 35 and 60â¯years who presented to our emergency department with severe vomiting, nausea, and malaise. Their symptoms started approximately 2â¯h after the ingestion of home-made mixed vegetables with freshly picked vegetables and leaves from the patients' garden, of which one was supposed to be borage. An electrocardiogram revealed diffuse ST-segment depression with down-up sloping in both patients. We supposed an accidental confusion of wild borage (Borago officinalis) with foxglove (Digitalis purpurea). Both patients were subsequently admitted to the intermediate-care-unit for close monitoring and continuous activated charcoal administration. Digitoxin serum concentrations were elevated in both patients (40.9 and >50â¯ng/ml, respectively - reference therapeutic range 8-18â¯ng/ml). The younger woman, despite the relatively lower serum digitoxin concentrations, presented a single episode of advanced atrioventricular block and long-lasting sinus bradycardia. Both showed a complete recovery. Although not uncommon, our case series reiterates the fact that such plant misclassifications are potentially life-threating and warrant the treating physicians' full attention. Learning objective: Plant poisoning is a frequent reason for consultation of poison information centers and may result in life-threatening cardiac arrhythmias. Confusion of foxglove leaves (Digitalis purpurea) with borage leaves (Borago officinalis L.), which is a popular food ingredient for mixed salads, is not uncommon. Without a dedicated medical history, such cases are difficult to diagnose and warrant the treating physicians' full attention and the involvement of a local poison information center.
ABSTRACT
Genetic factors play an important role in the pathogenesis of type 2 diabetes. The relevance to type 2 diabetes of the common polymorphism Glu23Lys in the potassium inward rectifier 6.2 (KIR6.2) gene is still controversial. The aim of this study was to assess whether this polymorphism influences beta-cell function, alpha-cell function, or insulin action. We therefore studied 298 nondiabetic subjects using an oral glucose tolerance test (OGTT) and 75 nondiabetic subjects using a hyperglycemic clamp (10 mmol/l) with additional glucagon-like peptide (GLP)-1 and arginine stimulation. The prevalence of the Lys allele was approximately 37%, and the Lys allele was associated with higher incremental plasma glucose during the OGTT (P = 0.03, ANOVA). Neither first- nor second-phase glucose-stimulated C-peptide secretion was affected by the presence of the polymorphism; nor were maximal glucose-, GLP-1-, or arginine-induced C-peptide secretion rates; nor was insulin sensitivity (all P > 0.7). However, the relative decrease in plasma glucagon concentrations during the 10 min after the glucose challenge was reduced in carriers of the Lys allele (10 +/- 3% decrease from baseline in Lys/Lys, 18 +/- 2% in Glu/Lys, and 20 +/- 2% in Glu/Glu; P = 0.01, ANOVA). In conclusion, our findings suggest that the common Glu23Lys polymorphism in KIR6.2 is not necessarily associated with beta-cell dysfunction or insulin resistance but with diminished suppression of glucagon secretion in response to hyperglycemia. Our findings thus confirm its functional relevance for glucose metabolism in humans.