The effects of disclosure of sequential rhinomanometry scores on post-septoplasty subjective scores of nasal obstruction: a randomised controlled trial.

OBJECTIVE: We sought to evaluate the effects of awareness of rhinomanometric results on subjective sensation of nasal breathing in patients after septoplasty. DESIGN: Prospective randomised study. SETTING: Clinical Hospital Rijeka. PARTICIPANTS: A study of 60 patients (45 M, 15 F) who underwent septoplasty was performed at the ENT Clinic, Clinical Hospital Rijeka. The patients were randomised into two groups; group A was shown their rhinomanometry scores at 3 months postoperatively, while group B remained unaware of their rhinomanometry results. MAIN OUTCOME MEASURE: The assumption is that in the same settings patients aware of their rhinomanometric results have better performances of their Nasal Obstruction Symptom Evaluation (NOSE) scale and thereby a better quality of life (QOL) after septoplasty. RESULTS: The differences in rhinomanometric results and NOSE scale prior and after septoplasty were statistically significant (P < 0.001), all patients achieving better results after the operation. There was no statistically significant difference in resistance (F = 0.004; P = 0.948) and improvement of rhinomanometry results in postoperative measurements (F = 0.110; P = 0.896) between groups A and B. The symptoms measured by the NOSE scale were the same in both groups preoperatively and 1 month after septoplasty (F = 2.906; P = 0.094). Three months postoperatively in group A, the NOSE scale score was lower (M = 11.67; sd = 12.34) than in group B (M = 27.50; sd = 18.04). CONCLUSIONS: The results suggest that disclosing information to patients about their post-septoplasty rhinomanometry results may improve subjective nasal breathing, and thus improve their QOL.

A double blind comparison of the effects of amlodipine and enalapril on insulin sensitivity in hypertensive patients.

This study compares the effects of a calcium channel blocker (amlodipine) and an angiotensin converting enzyme inhibitor (enalapril) on in vivo insulin sensitivity in patients with essential hypertension. Forty-six patients with mild and moderate hypertension were studied. After a 2-week single-blind placebo phase, they were randomly assigned to double-blind therapy with either amlodipine (2.5 to 10 mg/day) or enalapril (5 to 40 mg/day) for 16 weeks. Both groups were comparable in terms of demographic characteristics, degree of obesity, metabolic parameters, and arterial blood pressure. Insulin sensitivity was measured at baseline and at week 16 during the active phase using euglycemic hyperinsulinemic clamps. Arterial blood pressure decreased similarly in both groups. Whole body glucose uptake (M-value) increased with amlodipine from 3.63 +/- 0.32 (mean +/- SEM) to 3.97 +/- 0.31 mg/kg/min (P = .02). A similar tendency was observed with enalapril: from 3.59 +/- 0.32 to 3.94 +/- 0.30 mg/kg/min (P = .09). A trend to lower steady-state insulin level during the second clamp (compared to baseline) was observed in both groups. The clamp-derived insulin sensitivity index (that corrects for steady-state insulin levels and glucose levels during the clamp) increased similarly in both groups: from 1.15 +/- 0.11 to 1.39 +/- 0.13 with amlodipine (P = .03) and from 1.25 +/- 0.13 to 1.49 +/- 0.16 with enalapril (P = .01). LDL cholesterol decreased with amlodipine (mean change, -11.3 mg/dL, P = .004). Amlodipine and enalapril were associated with increments in insulin sensitivity. Amlodipine provided an additional benefit with decreased low density lipoprotein cholesterol levels.

Essential hypertension is associated with decreased insulin clearance and insulin resistance.

Essential hypertension is associated with multiple metabolic abnormalities, among them, hyperinsulinemia. This hyperinsulinemia is attributed to the presence of decreased insulin sensitivity (insulin resistance) with consequent compensatory insulin secretion. We tested the hypothesis that decreased insulin clearance is present in hypertensive subjects and contributes to hyperinsulinemia independently of the degree of insulin resistance. Seventy-five subjects were studied (48 hypertensive and 27 normotensive). Both groups were comparable in terms of age, body fat content, waist-to-hip ratio, and sex distribution. A primed continuous insulin infusion at 40 mU/m2 per minute was performed. Glucose was maintained at baseline levels with the euglycemic clamp technique. Hypertensive subjects were characterized by decreased insulin sensitivity (insulin-mediated glucose uptake: 5.14 +/- 0.28 versus 7.26 +/- 0.61 mg glucose/kg fat-free mass per minute, hypertensive versus normotensive, P = .002), increased insulin levels during the insulin infusions (804 +/- 36 versus 510 +/- 38 pmol/L, hypertensive versus normotensive, P < .001), and decreased insulin metabolic clearance rate (328 +/- 15 versus 521 +/- 30 mL/min per meter squared, hypertensive versus normotensive, P < .001). In an ANCOVA (including sex, degree of obesity, waist-to-hip ratio, and insulin sensitivity as covariates) the differences in insulin metabolic clearance rate between normotensive and hypertensive subjects remained highly significant (P < .001). Insulin metabolic clearance rate was significantly associated with fasting insulin levels. We conclude that essential hypertension is independently associated with decreased insulin metabolic clearance rate in addition to insulin resistance. A low insulin metabolic clearance rate may be a contributory factor to the hyperinsulinemia observed in essential hypertension.

Relationship between insulin sensitivity, hyperinsulinemia, and insulin-mediated sympathetic activation in normotensive and hypertensive subjects.

The adrenergic response to high physiological hyperinsulinemia was studied in 39 hypertensive subjects (28 men and 11 women) and 25 normal volunteers (15 men and 10 women), using the euglycemic clamp technique. Control studies using 0.45% saline infusions (sham studies) were also performed. Before and during the clamp procedure, plasma norepinephrine (NE) and epinephrine (E) were measured using a high performance liquid chromatographic method (HPLC). The association between the increment in NE and E levels and insulin sensitivity, steady-state insulin level during the clamps, waist to hip ratio (WHR), baseline NE levels and gender was studied. NE levels increased during the hyperinsulinemic period (mean increase 46 +/- 6 pmol P < .001 upsilon baseline and P < .01 upsilon sham studies). E levels did not differ between the insulin clamps and the sham studies. Insulin sensitivity was not significantly associated with the increment in NE. Hypertensive subjects had a higher NE increase than the normotensive individuals (55 +/- 7 upsilon 30 +/- 10 pmol, P = .03), but also had higher insulin levels during the clamps (839 +/- 43 upsilon 522 +/- 38 pmol, P < .001). Insulin levels accounted for most of the differences in NE increase between the normotensive and hypertensive groups. Gender, adiposity and WHR were also associated with NE increment. We conclude that the insulin mediated sympathetic activation is not affected in the presence of decreased insulin sensitivity for glucose utilization. The greater degree of sympathetic activation observed in hypertensive subjects is a function of the level of insulinemia obtained during the clamps.

Superoxide production and LDL oxidation by diabetic neutrophils.

The mechanism(s) resulting in the premature atherosclerosis of diabetes is unknown. Increased phagocyte release of reactive oxygen species such as superoxide anion (O2.-), resulting in low-density lipoprotein (LDL) oxidation, could be one possible cause. The purpose of the present study was to compare the abilities of polymorphonuclear leukocytes (PMN) from 12 non-insulin-dependent diabetes mellitus (NIDDM) subjects free of vascular disease to produce O2.- anion and oxidize LDL with PMN from age- and gender-matched normoglycemic controls. PMN were activated with phorbol 12-myristate 13-acetate (PMA) to measure O2.- production. In addition, the PMN were activated with PMA and opsonized zymosan (OZ) to assess LDL oxidation over 5 hours. LDL oxidation was measured by conjugated diene formation and apolipoprotein B (apo B) fluorescence. PMN superoxide production stimulated by PMA was similar between groups. LDL oxidation by PMN was also not different between the NIDDM and control groups. The results of this study indicate that PMN O2.- production and LDL oxidation are not enhanced in NIDDM subjects without vascular disease. Other factors, such as reduced antioxidant concentrations and non-enzymatic glycation of LDL, may play a greater role in the premature atherosclerosis of diabetes.

Insulin requirements in lipodystrophic diabetes.

A ten-fold increase in daily insulin requirements during the administration of total parenteral nutrition (TPN) is described in a patient with congenital generalized lipodystrophy, insulin-requiring diabetes mellitus, and acanthosis nigricans during an episode of acute pancreatitis secondary to hypertriglyceridaemia. After a period of 13 days on TPN, insulin requirements increased dramatically to an average of 1428 units per day for a period of 12 days, to achieve a mean blood glucose level of 10.9 mmol l-1. When the patient resumed feeding and the TPN was discontinued, the average daily insulin requirement was 104 units with a mean 24 h blood glucose of 11.8 mmol l-1. Parenteral administration of energy substrates in a rare case of diabetes mellitus and congenital lipodystrophy complicated by acute pancreatitis resulted in a severe insulin insensitive state due to the combination of the hypermetabolism conferred by the pancreatitis plus transient impairments of the glucose disposal mechanism by the energy substrates provided.

[New results on ageing of connective tissue (author's transl)]. / Neue Befunde zur Bindegewebsalterung.

Some new results on ageing of connective tissue are demonstrated, regarding not only mesenchymal, but also parenchymal organs of human and rat (both sexes). These results show that ageing of connective tissue is more a dynamic process (with measurable metabolic parameters of the several connective tissue cells and their products) than a passive or so-called degenerative connective tissue process. The bradytrophy concept of connective tissue cannot be accepted any longer. Then connective tissue cells can produce metabolic rates of the same level like parenchymal cells. The different organs possess partly common basic processes partly differences in connective tissue ageing, dependent on the composition and patterns of proteoglycans resp. of GAG and collagen types, furthermore dependent on localisation, structure and function. The results on ageing of connective tissue are useful for better understanding of ageing processes of parenchymal organs. Then their ageing is influenced essentially by the ageing of the own connective tissues. The turnover, more than the number of mesenchymal and parenchymal cells, decreases with ageing. More old than young cells seem to exist in old tissues and organs. The performance of ageing connective tissue cells can be constant or increase or decrease. Many mesenchymal and parenchymal organs develop a so-called "ageing-fibrosis".