Artemisia absinthium L. is one of the plants which has been used in folk medicine for many diseases over many centuries. This study aims to analyze the chemical composition of the Artemisia absinthium ethyl acetate and its aqueous extracts and to evaluate their effect on the pancreatic alpha-amylase enzyme and the intestinal alpha-glucosidase enzyme. In this study, the total contents of phenolic compounds, flavonoids, and condensed tannins in ethyl acetate and the aqueous extracts of Artemisia absinthium leaves were determined by using spectrophotometric techniques, then the antioxidant capacity of these extracts was examined using three methods, namely, the DPPH (2, 2-diphenyl-1picrylhydrazyl) free radical scavenging method, the iron reduction method FRAP, and the beta-carotene bleaching method. The determination of the chemical composition of the extracts was carried out using high-performance liquid chromatography-the photodiode array detector (HPLC-DAD). These extracts were also evaluated for their ability to inhibit the activity of the pancreatic alpha-amylase enzyme, as well as the intestinal alpha-glucosidase enzyme, in vitro and in vivo, thus causing the reduction of blood glucose. The results of this study showed that high polyphenol and flavonoid contents were obtained in ethyl acetate extract with values of 60.34 +/- 0.43 mg GAE/g and 25.842 +/- 0.241 mg QE/g, respectively, compared to the aqueous extract. The results indicated that the aqueous extract had a higher condensed tannin content (3.070 +/- 0.022 mg EC/g) than the ethyl acetate extract (0.987 +/- 0.078 mg EC/g). Ethyl acetate extract showed good DPPH radical scavenging and iron reduction FRAP activity, with an IC50 of 0.167 +/- 0.004 mg/mL and 0.923 +/- 0.0283 mg/mL, respectively. The beta-carotene test indicated that the aqueous and ethyl acetate extracts were able to delay the decoloration of beta-carotene with an inhibition of 48.7% and 48.3%, respectively, which may mean that the extracts have antioxidant activity. HPLC analysis revealed the presence of naringenin and caffeic acid as major products in AQE and EAE, respectively. Indeed, this study showed that the aqueous and ethyl acetate extracts significantly inhibited the pancreatic alpha-amylase and intestinal alpha-glucosidase, in vitro. To confirm this result, the inhibitory effect of these plant extracts on the enzymes has been evaluated in vivo. Oral intake of the aqueous extract significantly attenuated starch- and sucrose-induced hyperglycemia in normal rats, and evidently, in STZ-diabetic rats as well. The ethyl acetate extract had no inhibitory activity against the intestinal alpha-glucosidase enzyme in vivo. The antioxidant and the enzyme inhibitory effects may be related to the presence of naringenin and caffeic acid or their synergistic effect with the other compounds in the extracts.

Background-Hyperglycemia may be associated with worse outcome after intracerebral hemorrhage (ICH). We assessed the association of early glycemic trajectory on ICH mortality and edema growth. Methods and Results-We included patients from the Helsinki ICH study with glucose measurements at least once between both 0 to 24 and 24 to 72 hours from onset. Hyperglycemia was defined as blood glucose >= 8 mmol/L (144 mg/dL) based on the local threshold for treatment. Glycemic trajectory was defined on maximum values 0 to 24 and 24 to 72 hours after ICH: (1) persistent normoglycemia in both epochs; (2) late hyperglycemia (only between 24 and 72 hours); (3) early hyperglycemia (only before 24 hours); and (4) persistent hyperglycemia in both epochs. Logistic regression with known predictors of outcome estimated the association of glycemic trajectory and 6-month mortality. A generalized linear model assessed the association of glycemic trajectory and interpolated 72-hour edema extension distance. A total of 576 patients met eligibility criteria, of whom 214 (37.2%) had persistent normoglycemia, 44 (7.6%) late hyperglycemia, 151 (26.2%) early hyperglycemia, and 167 (29.0%) persistent hyperglycemia. Six-month mortality was higher in the persistent (51.1%) and early (26.3%) hyperglycemia groups than the normoglycemia (19.0%) and late hyperglycemia (3.6%) groups. Persistent hyperglycemia was associated with 6-month mortality (odds ratio 3.675, 95% CI 1.989-6.792; P <0.001). Both univariate (P=0.426) and multivariable (P=0.493) generalized linear model analyses showed no association between glycemic trajectory and 72-hour edema extension distance. Conclusion-Early hyperglycemia after ICH is harmful if it is persistent. Strategies to achieve glycemic control after ICH may influence patient outcome and need to be assessed in clinical trials.

Puumala hantavirus (PUUV) causes a hemorrhagic fever with renal syndrome characterized by thrombocytopenia, increased capillary leakage, and acute kidney injury (AKI). As glucosuria at hospital admission predicts the severity of PUUV infection, we explored how plasma glucose concentration associates with disease severity. Plasma glucose values were measured during hospital care in 185 patients with PUUV infection. They were divided into two groups according to maximum plasma glucose concentration: P-Gluc < 7.8 mmol/L (n = 134) and P-Gluc >= 7.8 mmol/L (n = 51). The determinants of disease severity were analyzed across groups. Patients with P-Gluc >= 7.8 mmol/L had higher hematocrit (0.46 vs. 0.43; p < 0.001) and lower plasma albumin concentration (24 vs. 29 g/L; p < 0.001) than patients with P-Gluc < 7.8 mmol/L. They presented with higher prevalence of pulmonary infiltrations and pleural effusion in chest radiograph, higher prevalence of shock and greater weight change during hospitalization. Patients with P-Gluc >= 7.8 mmol/L were characterized by lower platelet count (50 vs. 66 x 10(9)/L; p = 0.001), more severe AKI (plasma creatinine 272 vs. 151 mu mol/L; p = 0.001), and longer hospital treatment (8 vs. 6 days; p < 0.001) than patients with P-Gluc < 7.8 mmol/L. Plasma glucose level is associated with the severity of capillary leakage, thrombocytopenia, inflammation, and AKI in patients with acute PUUV infection.