Perioperative evaluation of glycaemic status in neck dissection: a retrospective analysis at a single hospital centre

Diabetes mellitus is generally considered a risk factor for impaired wound healing. This study aimed to evaluate the glycaemic status of patients undergoing neck dissection and describe its impact on postoperative outcomes, especially wound healing. A retrospective analysis was performed of the preoperative, intraoperative, and postoperative glycaemic data obtained from the medical charts of 60 adult patients who had undergone 64 neck dissections. Nine of the 64 procedures were performed in diabetic patients (14.1%). The average glucose values were: preoperative 5.99 ± 1.25 mmol/l, intraoperative 8.90 ± 2.62 mmol/l, and postoperative 10.01 ± 2.49 mmol/l. All registered preoperative hyperglycaemia cases (eight cases) were diabetic. Postoperative insulin therapy was done in 14 procedures (21.9%). Wound healing complications were found in five patients (7.8%); there was no wound infection. There was no association of wound healing complications with preoperative diabetic status (P = 1.000), preoperative glucose control (P = 1.000), preoperative (P = 0.469), intraoperative (P = 0.248), and postoperative (P = 0.158) glucose values, or with postoperative glucose control (P = 0.577). These data do not support the association of stress-induced hyperglycaemia or diabetes mellitus with postoperative wound healing problems in neck dissection.     

Continuous monitoring of blood sugar in brittle diabetics

Summary The blood glucose was measured continuously for periods of up to twenty-nine hours in five patients. The method, which does not require heparinization of the patient, is described. — Three unstable diabetics were investigated. In two, diabetic control was considerably improved as a result of alterations made to their therapeutic regime following this investigation. The symptoms of the third diabetic patient were due to complications of diabetes rather than to the disease itself. — The results in these three patients are contrasted with those obtained in two acromegalics (one of whom was also diabetic). Attention is drawn to the occurrence of fasting hyperglycaemia in the early hours of the morning in the brittle diabetics and to the rapidity with which the blood glucose rises. It is thought that growth hormone is not directly responsible for this hyperglycaemia, since marked insulin sensitivity is maintained.

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Dauermessung der Blutzuckerspiegel bei labilen Diabetikern

Zusammenfassung Bei 5 Patienten wurden die Blutzuckerspiegel fortlaufend über Zeiträume von bis zu 29 Std. bestimmt. Die Methodik, die keine Heparinisierung des Patienten erforderlich macht, wird beschrieben. Drei nicht stabile Diabetiker wurden untersucht. Bei zwei Patienten besserte sich die Diabetes-Einstellung beträchtlich auf Grund von Änderungen in der Therapie, die auf Grund dieser Untersuchungsergebnisse vorgenommen wurden. Die Symptome des dritten Diabetikers waren in erster Linie auf Diabeteskomplikationen und nicht so sehr auf die Krankheit selbst zurückzuführen. Die Ergebnisse bei diesen drei Patienten werden mit denen von 2 Akromegalen verglichen, von denen einer ebenfalls einen Diabetes aufwies. Es wird besonders auf das Vorkommen einer Nüchtern-Hyperglykämie in den frühen Morgenstunden bei labilen Diabetikern und auf die Geschwindigkeit des Blutzuckeranstieges hingewiesen. Es wird angenommen, daß das Wachstumshormon nicht direkt für diesen Blutzuckeranstieg verantwortlich ist, da die Insulinempfindlichkeit erhalten bleibt.

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Contrôle continu de la glycémie chez des diabétiques instables

Résumé La glycémie a été mesurée continuellement pendant des périodes allant jusqu'à 29 h chez 5 malades. On décrit la méthode qui n'exige pas l'héparinisation du malade.— Trois diabétiques instables ont été étudiés. Chez deux d'entre eux l'équilibre diabétique a été considérablement amélioré par suite des modifications apportées à leur régime thérapeutique qui a suivi cette investigation. Les symptômes du troisième diabétique étaient dus à des complications du diabète plutôt qu'au diabète lui-même. — Les résultats chez ces trois patients sont comparés avec ceux obtenus chez deux acromégales (dont l'un était aussi diabétique). On attire l'attention sur l'apparition de l'hyperglycémie à jeun dans les premières heures de la matinée chez les diabétiques instables et sur la rapidité avec laquelle la glycémie s'élève. On pense que l'hormone de croissance n'est pas directement responsable de cette hyperglycémie, puisqu'une sensibilité marquée à l'insuline est maintenue.

     

The Hyperglycaemic Activity of Some Catecholamines and the Effect of α- and β-Adrenergic Blocking Compounds in the Mouse

In order to classify the receptors involved in the hyperglycaemic response to catecholamines in the mouse, the relative potency of noradrenaline, adrenaline and isoprenaline in the induction of hyperglycaemia has been tested by giving increasing doses from 10 μg/kg to 1 mg/kg of one of the amines intraperitoneally. Following catecholamine administration the maximal concentration of glucose in the blood occurred between 10 and 30 min. and amounted to about 300 mg%. The relative potency was: adrenaline > noradrenaline while isoprenaline was inactive. The antagonistic effect on adrenaline induced hyperglycaemia of the α-adrenergic blocking compounds: phenoxybenzamine HCl (dibenzyline®) and phentolamine (regitin®) and the β-adrenergic blocking compounds: 1-(isopropylamino)-3-(o-phenoxyphenoxy)-2-propanol (Ph QA 33) and propranolol were tested by giving 1 and 10 mg/kg intraperitoneally 30 min. before the administration of adrenaline. Only phentolamine at the highest dose level was capable of preventing the hyperglycaemic response to adrenaline. Phenoxybenzamine, Ph QA 33 and propranolol proved to be inactive. It is concluded that the mechanism of adrenaline induced hyperglycaemia in mice cannot be explained simply by an α- and/or β-receptor activation.     

Vitamin D,Vitamin D-Binding Proteins,and VDR Polymorphisms in Individuals with Hyperglycaemia

Vitamin D reportedly plays an important role in the pathogenesis of diabetes mellitus; however, this role is unclear and debated. This study investigated the association between 25(OH) vitamin D, vitamin D-binding proteins, and vitamin D receptor (VDR) polymorphisms in healthy individuals and those with prediabetes and type 2 diabetes mellitus (T2D) from South Africa. A cross-sectional study was conducted involving subjects of mixed ancestry aged ≥20 years. Males presented with higher mean 25(OH) vitamin D levels than females, while females exhibited significantly higher serum vitamin D-binding protein levels. Significant differences in mean 25(OH) vitamin D levels were observed in normo-glycaemic, prediabetes, screen-detected DM, and known DM individuals. Vitamin D receptor SNPs Fok1 and Taq1 were not associated with glycaemic status. Fok1 was not associated with 25(OH) vitamin D deficiency, while Taq1 was associated with vitamin D insufficiency. This study showed a high prevalence of vitamin D deficiency/insufficiency in this South African population, with decreased vitamin D levels observed in hyperglycaemic individuals, which was not linked to either vitamin D-binding protein or polymorphisms in Fok1 of the VDR gene. These results may be used as a platform for further research into diagnosis and treatment of hyperglycaemia.     

Early postoperative hyperglycaemia is not a risk factor for infectious complications and prolonged in-hospital stay in patients undergoing oesophagectomy: a retrospective analysis of a prospective trial

Introduction  

Treating hyperglycaemia in hospitalized patients has proven to be beneficial, particularly in those with obstructive vascular disease. In a cohort of patients undergoing resection for oesophageal carcinoma (a group of patients with severe surgical stress but a low prevalence of vascular disease), we investigated whether early postoperative hyperglycaemia is associated with increased incidence of infectious complications and prolonged in-hospital stay.     

The prevalence of retinopathy in subjects with and without type 2 diabetes mellitus

Purpose:  To evaluate the prevalence of and risk factors for, retinopathy in a geographically defined population with type 2 diabetes mellitus compared with a control group of subjects without diabetes, matched by age, sex and residence in order to find the retinopathy attributable to type 2 diabetes. Methods:  The study populations are, on one hand, a prevalence cohort of subjects with type 2 diabetes resident in the community of Laxå, Sweden, and on the other a control group, matched by age, gender and residence with those with a diagnosis of type 2 diabetes mellitus. Retinopathy was graded from fundus photographs using a modification of the Early Treatment Retinopathy Study (ETDRS) adaptation of the modified Airlie House classification of diabetic retinopathy (DR). Results:  Any retinopathy was found in 34.6% in the type 2 diabetes cohort and in 8.8% in the control group without diabetes. Among the diabetic patients, any retinopathy was significantly associated with duration of diabetes (p = 0.0001), HbA1c (p = 0.0056), systolic blood pressure (p = 0.0091) and lower serum cholesterol (p = 0.0197) in multivariate logistic regression analyses. Having retinopathy in the control group was associated only with systolic blood pressure (p = 0.0014) in logistic regression analysis. Conclusions:  The prevalence of retinopathy among patients with type 2 diabetes in Laxå, Sweden, was similar or somewhat lower compared with other studies in the Nordic countries. The prevalence of retinopathy in a control group without diabetes equalled numbers from population studies worldwide. Our study indicates that the retinopathy that can be attributed to hyperglycaemia in the diabetic state is less common than is usually accounted for. A considerable fraction of retinopathy in subjects with diabetes may instead be due to other factors such as hypertension and should thus be treated correspondingly.     

The association of the PON1 Q192R polymorphism with complications and outcomes of pregnancy: findings from the British Women's Heart and Health cohort study

It has been hypothesised that paraoxonase genes would be related to adverse pregnancy outcomes, via a maternal or fetal effect on placental hypoperfusion and thrombosis. To date only two studies have assessed this possibility. In this study we assessed the associations of the PON1 Q192R polymorphism with self-report of having pregnancy-induced hypertension, gestational hyperglycaemia and a preterm offspring birth. The associations were assessed in 3266 white women who were randomly selected from 23 British towns. There was no association between PON1 Q192R and either self-report of pregnancy-induced hypertension or gestational hyperglycaemia but the prevalence of reporting having a preterm birth increased with each R allele: per allele odds ratio 1.20 [95% confidence interval (CI) 1.03, 1.41]. When our results were pooled with the one previous study of the association of this polymorphism with preterm birth, the pooled per allele odds ratio was 1.19 [95% CI 1.02, 1.39]. Our findings provide some further evidence to suggest that PON1 Q192R is associated with preterm birth; they invite further investigation of both maternal and fetal genotype for PON1 Q192R in relation to preterm birth.     

Characterization of the mechanisms of the increase in PPARδ expression induced by digoxin in the heart using the H9c2 cell line

BACKGROUND AND PURPOSE

Digoxin has been used as an inotropic agent in heart failure for a long time. Troponin I (TnI) phosphorylation is related to cardiac contractility, and the genes are regulated by peroxisome proliferator-activated receptors (PPARs). Our previous studies indicated that cardiac abnormality related to the depressed expression of PPARδ in the hearts of STZ rats is reversed by digoxin. However, the cellular mechanisms for this effect of digoxin have not been elucidated. The aim of the present study was to investigate possible mechanisms for this effect of digoxin using the H9c2 cell line cultured in high glucose (HG) conditions.

METHODS

The effects of digoxin on PPARδ expression, intracellular calcium and TnI phosphorylation were investigated in cultured H9c2 cells, maintained in a HG medium, by using Western blot analysis.

RESULTS

Digoxin increased PPARδ expression in H9c2 cells subjected to HG conditions, and increase the intracellular calcium concentration. This effect of digoxin was blocked by BAPTA-AM at concentrations sufficient to chelate calcium ions. In addition, the calcineurin inhibitor cyclosporine A and KN93, an inhibitor of calcium/calmodulin-dependent protein kinase, inhibited this action. Digoxin also increased TnI phosphorylation and this was inhibited when PPARδ was silenced by the addition of RNAi to the cells. Similar changes were observed on the contraction of H9c2 cells.

CONCLUSION

The results suggest that digoxin appears, through calcium-triggered signals, to reverse the reduced expression of PPARδ in H9c2 cells caused by HG treatment.     

Increased availability of angiotensin AT 1 receptors leads to sustained arterial constriction to angiotensin II in diabetes - role for Rho-kinase activation

BACKGROUND AND PURPOSE

Antagonists of angiotensin AT₁ receptors elicit beneficial vascular effects in diabetes mellitus. We hypothesized that diabetes induces sustained availability of AT₁ receptors, causing enhanced arterial constriction to angiotensin II.

EXPERIMENTAL APPROACH

To assess functional availability of AT₁ receptors, constrictions to successive applications of angiotensin II were measured in isolated skeletal muscle resistance arteries (∼150 µm) of Zucker diabetic fatty (ZDF) rats and of their controls (+/Fa), exposed acutely to high glucose concentrations (HG, 25 mM, 1 h). AT₁ receptors on cell membrane surface were measured by immunofluorescence.

KEY RESULTS

Angiotensin II-induced constrictions to first applications were greater in arteries of ZDF rats (maximum: 82 ± 3% original diameter) than in those from +/Fa rats (61 ± 5%). Constrictions to repeated angiotensin II administration were decreased in +/Fa arteries (20 ± 6%), but were maintained in ZDF arteries (67 ± 4%) and in +/Fa arteries vessels exposed to HG (65 ± 6%). In ZDF arteries and in HG-exposed +/Fa arteries, Rho-kinase activities were enhanced. The Rho-kinase inhibitor, Y27632 inhibited sustained constrictions to angiotensin II in ZDF arteries and in +/Fa arteries exposed to HG. Levels of surface AT₁ receptors on cultured vascular smooth muscle cells (VSMCs) were decreased by angiotensin II but were maintained in VSMCs exposed to HG. In VSMCs exposed to HG and treated with Y27632, angiotensin II decreased surface AT₁ receptors.

CONCLUSIONS AND IMPLICATIONS

In diabetes, elevated glucose concentrations activate Rho-kinase which inhibits internalization or facilitates recycling of AT₁ receptors, leading to increased functional availability of AT₁ receptors and sustained angiotensin II-induced arterial constriction.