The relative balance between Th1 and Th2 cytokines appears crucial, since the role of cytokines has been evaluated in several studies by comparison of clinically heterogeneous groups of patients. The aim of this study is to determine the role of proinflammatory Th1 cytokines, interleukin-12 (IL-12) and gamma interferon (IFN-␥), and anti-inflammatory Th2 cytokines, IL-4 and IL-10, in a homogeneous group of patients with uncomplicated Plasmodium falciparum malaria. Levels of IL-12, IFN-␥, Il-4, and IL-10 in serum for 20 adult patients and 15 healthy control subjects were determined by an immunoenzymatic assay. Serum levels of Th1 cytokines, IL-12 (8.6 ؎ 2.8 pg/ml; controls, 3.2 ؎ 0.7 pg/ml) and IFN-␥ (39.2 ؎ 67.6 pg/ml; controls, 8.4 ؎ 6.3 pg/ml), were significantly increased at admission; 3 days later, levels of IL-12 in serum remained significantly high (8.8 ؎ 2.6 pg/ml), whereas IFN-␥ levels returned to control values. The anti-inflammatory response of Th2 cytokines (IL-10 and IL-4) was distinct. Levels of IL-10 in serum were not significantly increased at day 0 and day 3 (306.6 ؎ 200.4 pg/ml and 56.6 ؎ 38.4 pg/ml, respectively; controls, 17.4 ؎ 9.0 pg/ml). In contrast, levels of IL-4 in serum were not increased on admission (3.4 ؎ 1.2 pg/ml; controls, 2.4 ؎ 0.8 pg/ml), but at day 3 a moderate and significant increase of IL-4 levels was observed (4.5 ؎ 1.7 pg/ml). In conclusion, the increase of Th1 cytokine IL-12 and IFN-␥ levels during the acute phase of uncomplicated P. falciparum malaria may reflect an early and effective immune response regulated by proinflammatory Th1 cytokines, and in particular IFN-␥ may play a role in limiting progression from uncomplicated malaria to severe and life-threatening complications.

Serum levels of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in patients with acute viral hepatitis were investigated. Twelve patients suffering from acute viral hepatitis were studied; 8 patients presented with acute hepatitis B, 2 patients with acute hepatitis A, and 2 patients with acute hepatitis C. Serum levels of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha were significantly increased in all patients with acute viral hepatitis. Decreased serum levels of all cytokines were noted in four patients with acute hepatitis B during the recovery phase of infection. In addition, IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha were undetectable at the end of a follow-up period of 6 months. Our study shows that increased levels of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha are probably related to hepatitis activity and thus may have some role in hepatocytic injury.

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Objectives: To determine if lopinavir/ritonavir +/-hydroxychloroquine will reduce the proportion of participants who survive without requiring ventilatory support, 15 days after enrolment, in adult participants with non-critically ill SARS-CoV-2 infection. Trial design: ASCOT is an investigator-initiated, multi-centre, open-label, randomised controlled trial. Participants will have been hospitalised with confirmed COVID-19, and will be randomised 1:1:1:1 to receive lopinavir /ritonavir, hydroxychloroquine, both or neither drug in addition to standard of care management. Participants: Participants will be recruited from >80 hospitals across Australia and New Zealand, representing metropolitan and regional centres in both public and private sectors. Admitted patients will be eligible if aged ≥ 18 years, have confirmed SARS-CoV-2 by nucleic acid testing in the past 12 days and are expected to remain an inpatient for at least 48 hours from the time of randomisation. Potentially eligible participants will be excluded if admitted to intensive care or requiring high level respiratory support, are currently receiving study drugs or their use is contraindicated due to allergy, drug interaction or comorbidities (including baseline QTc prolongation of 470ms for women or 480ms for men), or death is anticipated imminently.

Thromboembolic complications in HIV-infected patients have been reported. To our knowledge, no case-control studies have compared the prevalence of thromboembolic events between HIV-positive and HIV-negative individuals. One hundred and sixty-nine HIV-infected patients and 180 randomly selected blood donors were enrolled. Selected patients completed a specific questionnaire and were subsequently interviewed. Information was collected on family and personal history of cardiovascular disorders and the presence of personal risk factors for venous and arterial thrombosis. All reported events were adjudicated only if adequate documentation of objective tests was available. Mean age and sex were similar in the two groups. A vascular event was documented in six HIV-infected patients (3.55%) and in none of the controls (P=0.0108). Family history of cardiovascular disorders, cigarette smoking and hypertriglyceridemia were more prevalent in HIV patients than in controls. In multivariate analysis, neither family traditional cardiovascular risk factors nor HIV infection were independently associated with the presence of thromboembolic events. The results confirm the hypothesis that HIV-positive patients have an increased risk of thromboembolic disorders. Whether this increased risk has been provoked by HIV infection itself or by other associated risk factors for cardiovascular events, such as cigarette smoking and hypertriglyceridemia, remain to be clarified.

The high cardiovascular risk of HIV infected (HIV þ ) patients is still partly unexplained. We aimed to evaluate if HIV infection and highly active antiretroviral therapy (HAART) are linked per se to left ventricular (LV) remodelling, independently of blood pressure (BP) values. We enrolled 4 groups of patients matched by gender, age, body mass index and smoking habit: 30 HIV þ hypertensives, 30 HIV þ normotensives, 30 notinfected (HIVÀ) hypertensives and 30 HIVÀ normotensives. HIV þ patients were on chronic HAART. Hypertension was newly diagnosed (p6 months) and never treated. Each patient underwent blood tests, 24-h BP monitoring and LV echocardiogram. The 4 groups had similar fasting glucose and cholesterol; triglycerides, HOMA index and prevalence of metabolic syndrome were higher in the HIV þ groups. Despite similar 24-h BP values, HIV þ hypertensives had greater LV mass and higher prevalence of preclinical diastolic dysfunction than HIVÀ hypertensives. Compared to HIVÀ normotensives, HIV þ normotensives had similar 24-h BP values, but greater LV mass and lower LV diastolic indices, similar to HIVÀ hypertensives, whose 24-h BP values were higher. Asymptomatic HIV infection and chronic HAART are associated with myocardial hypertrophy and preclinical diastolic dysfunction, independently of BP values.

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