The aim of the study was to characterize patients at risk of asthma exacerbation during spring thunderstorms and identify potential measures to ameliorate the impact of those events.A case-control study was conducted among patients aged 7±60 yrs, who attended Wagga Hospital (NSW, Australia) for asthma during the period of 1 June 1997 to 31 October 1997. One hundred and eighty-three patients who attended on 30 and 31 October 1997 were the cases and the remaining 121 patients were the controls. Questionnaire data were obtained from 148 (81%) cases and 91 (75%) controls.One hundred and thirty-eight (95%) cases who attended during the thunderstorm gave a history of hayfever prior to the event compared to 66 (74%) controls who attended at other times (odds ratio (OR) 6.01, 95% confidence interval (CI) 2.55± 14.15); 111 (96%) cases were allergic to rye grass pollen compared to 47 (64%) controls (OR 23.6, 95% CI 6.6±84.3). Among subjects with a prior diagnosis of asthma (64% cases and 82% controls), controls (56%) were more likely to be taking inhaled steroids at time of the thunderstorm than cases (27%, OR 0.3, 95% CI 0.16±0.57).History of hayfever and allergy to rye grass are strong predictors for asthma exacerbation during thunderstorms in spring. The lower rate of inhaled steroid use in thunderstorm cases suggests that this treatment may be effective in preventing severe attacks during thunderstorms. Eur Respir J 2000; 16: 3±8.

We studied the adhesion of erythrocytes from 30 diabetic patients and 25 controls to human endothelial cells. Washed erythrocytes were labeled with 51Cr and added to confluent endothelial cells cultured from umbilical veins. After incubation at 37 degrees C, the nonadherent erythrocytes were removed by sequential washings. The percentage of erythrocytes adhering to cultured endothelium after each wash was significantly higher when erythrocytes were from diabetics than when they were from controls (P less than 0.005). After the fifth wash, the mean adhesion ratio (percentage of adhering diabetic red cells: percentage of adhering control red cells) was 2.33 (range, 0.8 to 5.2). Increased adhesion was related to the extent of vascular complications in the diabetics, as assessed by a vascular score. With the same technique, fewer erythrocytes adhered to plastic and to cultured human fibroblasts than to endothelial cells, although the adhesion of the diabetic red cells to these surfaces was higher than that of the controls. These results suggest that in diabetes there is an intrinsic erythrocyte abnormality that is related to vascular disease.

Mutations in several subgenomic regions of hepatitis C virus (HCV) have been implicated in influencing the response to interferon (IFN) therapy. Sequences within HCV NS5A (PKR binding domain [PKRBD], IFN sensitivity-determining region [ISDR], and variable region 3 [V3]) were analyzed for the pretreatment serum samples of 60 HCV genotype 1-infected patients treated with pegylated IFN plus ribavirin (1b, n ‫؍‬ 47; 1a, n ‫؍‬ 13) but with different treatment outcomes, those with sustained virologic responses (SVR; n ‫؍‬ 36) or nonresponders (NR; n ‫؍‬ 24). Additionally, the sequence of the PKR/eIF-2␣ phosphorylation homology domain (E2-PePHD) region was determined for 23 patients (11 SVR and 12 NR). The presence of >4 mutations in the PKRBD region was associated with SVR (P ‫؍‬ 0.001) and early virologic responses (EVR; 12 weeks) (P ‫؍‬ 0.037) but not rapid virologic responses (4 weeks). In the ISDR, the difference was almost statistically significant (68% of SVR patients with mutations versus 45% without mutations; P ‫؍‬ 0.07). The V3 region had a very high genetic variability, but this was not related to SVR. Finally, the E2-PePHD (n ‫؍‬ 23) region was well conserved. The presence of >4 mutations in the PKRBD region (odds ratio [OR] ‫؍‬ 9.9; P ‫؍‬ 0.006) and an age of <40 years (OR ‫؍‬ 3.2; P ‫؍‬ 0.056) were selected in a multivariate analysis as predictive factors of SVR. NS5A sequences from serum samples taken after 1 month of treatment and posttreatment were examined for 3 SVR and 15 NR patients to select treatment-resistant viral subpopulations, and it was found that in the V3 and flanking regions, the mutations increased significantly in posttreatment sera (P ‫؍‬ 0.05). The genetic variability in the PKRBD (>4 mutations) is a predictive factor of SVR and EVR in HCV genotype 1 patients treated with pegylated IFN and ribavirin.

Diabetic coma is frequently associated with thromboembolic complications. A prospective study was undertaken of the haemostatic changes occurring in 15 patients (12 with ketoacidosis, three with the hyperosmolar syndrome) during diabetic coma. When compared with the results after stabilization of the diabetes, ketoacidosis was associated with significantly higher levels of factor VIII coagulant activity, factor VIII-related antigen and fibrin degradation products, a shorter partial thromboplastin time and reduced concentrations of antithrombin III. These results suggest that in uncomplicated ketoacidosis, haematological changes occur which may reflect vascular endothelial damage and intravascular fibrin deposition. Out of three deaths, two patients (both with the hyperosmolar syndrome) had evidence of disseminated intravascular coagulation. To reduce further the mortality and morbidity from diabetic coma, controlled clinical trials of anticoagulant and antiplatelet drugs may be indicated.

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