Eosinophilic bronchitis presents with chronic cough and sputum eosinophilia, but without the abnormalities of airway function seen in asthma. It is important to know how commonly eosinophilic bronchitis causes cough, since in contrast to cough in patients without sputum eosinophilia, the cough responds to inhaled corticosteroids. We investigated patients referred over a 2-yr period with chronic cough, using a well-established protocol with the addition of induced sputum in selected cases. Eosinophilic bronchitis was diagnosed if patients had no symptoms suggesting variable airflow obstruction, and had normal spirometric values, normal peak expiratory flow variability, no airway hyperresponsiveness (provocative concentration of methacholine producing a 20% decrease in FEV(1) ([PC(20)] > 8 mg/ml), and sputum eosinophilia (> 3%). Ninety-one patients with chronic cough were identified among 856 referrals. The primary diagnosis was eosinophilic bronchitis in 12 patients, rhinitis in 20, asthma in 16, post-viral-infection status in 12, and gastroesophageal reflux in seven. In a further 18 patients a diagnosis was established. The cause of chronic cough remained unexplained in six patients. In all 12 patients with eosinophilic bronchitis, the cough improved after treatment with inhaled budesonide 400 micrograms twice daily, and in eight of these patients who had a follow-up sputum analysis, the eosinophil count decreased significantly, from 16.8% to 1.6%. We conclude that eosinophilic bronchitis is a common cause of chronic cough, and that sputum induction is important in the investigation of cough.
Diabetic angiopathy is a major cause of morbidity and mortality in Type 2 diabetes mellitus (DM). The pathogenesis of vascular complications in this condition appears to be complex, with distinct differences being observed between Type 1 and Type 2 DM. This review outlines the evidence for these differences and identifies endothelial dysfunction as an important associate and antecedent of Type 2DM, which predisposes to characteristic vascular complications and may also have implications for fetal development.
OBJECTIVE -Low birth weight has been linked to an increased risk of type 2 diabetes and cardiovascular disease in adult life. The fetal insulin hypothesis proposed that a genetic predisposition to insulin resistance may also influence vascular development. Therefore, impaired vascular function may be an intrinsic abnormality in low-birth weight infants that antedates clinical features of the insulin resistance syndrome.RESEARCH DESIGN AND METHODS -Two groups of 3-month-old term infants were included in the study: 17 infants of lowest quartile birth weight (LQBW) and 21 infants of highest quartile birth weight (HQBW). Three aspects of skin microvascular function were examined; response to local heating, response to acetylcholine iontophoresis, and capillary density.RESULTS -Median (interquartile ranges) birth weights of the LQBW and HQBW infants were 3,140 g (2,738 -3,254) and 3,920 g (3,750 -4,020), respectively. Skin maximal hyperemic response to local heating was 2.14 V (1.68 -2.30) in the LQBW group vs. 2.44 V (1.96 -2.90) in the HQBW group (P ϭ 0.020), and the endothelium-dependent vasodilatory response was 1.03 V (0.62-1.32) in the LQBW group vs. 0.78 V (0.45-1.32) in the HQBW group (P ϭ 0.297). Capillary density in the LQBW and HQBW groups were 46.3 mm Ϫ2 (40.1-53.7) and 44.1 mm Ϫ2 (41.7-56.0), respectively (P ϭ 0.736).CONCLUSIONS -Skin maximal hyperemic response was lower in LQBW infants, although no reduction in capillary density or defect in endothelium-dependent vasodilatation was observed. Such a lower maximal hyperemic response in early life in LQBW subjects who are at risk for type 2 diabetes and cardiovascular disease supports the hypothesis that impaired microvascular function is an early antecedent to diabetes in later life. Diabetes Care 24:1102-1107, 2001R etrospective studies in the U.K. have shown that low birth weight is associated with the development of type 2 diabetes, hypertension, and increased cardiovascular mortality in adult life, which are clinical features of insulin resistance syndrome (1). This association is independent of social class and adult BMI and has been confirmed in studies conducted in other populations (2) and countries (3,4). Barker (5) proposed the fetal programming hypothesis to explain the association, stipulating that undernutrition in utero leads to impaired fetal growth, which may permanently program the structure and function of the pancreas, thus predisposing later development of type 2 diabetes. An alternative or complementary explanation is the fetal insulin hypothesis, which states that the same polygenic factors that increase insulin resistance in utero and in adult life produce two phenotypic expressions: an infant of low birth weight and an adult with an increased risk for diabetes and hypertension (6).In parallel with these observations has been the understanding that endothelial dysfunction is a crucial biological determinant of cardiovascular disease (7). Furthermore, impaired endotheliumdependent vasodilatation has been linked to key components of i...
Cardiovascular mortality and morbidity are increased in patients with type 2 diabetes. However, there are few data from clinical trials comparing cardiovascular effects of alternative oral anti-diabetic agents. Major cardiovascular outcomes during four one-year, double-blind trials in over 3700 patients with type 2 diabetes randomised to either a thiazolidinedione, pioglitazone, metformin or a sulphonylurea, gliclazide treatment have been combined. Mean blood pressure was slightly reduced by all treatments, with pioglitazone treatment resulting in the largest falls (approximately 1.5 mmHg). Hospitalisations for cardiac or cerebrovascular events were similar with the different treatments. Overall mortality was seven of 1857 for pioglitazone and 10 of 1856 for non-pioglitazone treatments, of which three and six were cardiac deaths, respectively. The incidence of congestive cardiac failure was similar with pioglitazone (12/1857) and non-pioglitazone (10/1856) treatments. The results show similar cardiovascular outcome for the three different treatments over a one-year period, but demonstrate interesting differences, which will require longer-term formal outcome studies to determine their significance.
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