Primary liver cancer is more aggressive in HIV-HCV coinfection than in HCV infection. A prospective study (ANRS CO13 Hepavih and CO12 Cirvir)

OBJECTIVE: Since HAART, primary liver cancer has emerged as an increasing cause of morbidity and mortality in patients with HIV infection. Our aim was to compare characteristics and outcome of primary liver cancer according to HIV status in HCV cirrhotic patients submitted to periodic ultrasonographic surveillance. METHODS: All patients with primary liver cancer and cirrhosis were selected from two prospective cohorts (ANRS CO12 Cirvir, viral cirrhosis, n=1081; ANRS CO13 Hepavih, HIV-HCV coinfection, n=1175). Cirrhosis was diagnosed by liver biopsy in monoHCV group and biopsy and/or non-invasive tests in HIV-HCV group. Ultrasonographic surveillance was performed every 6 months. Diagnosis of primary liver cancer was established according to EASL-AASLD guidelines. RESULTS: Primary liver cancer was diagnosed in 32 patients, 16 in each group, and corresponded to hepatocellular carcinoma in all except for two cholangiocarcinomas in HIV-HCV patients. Ultrasonographic follow-up was similar (median time since last ultrasonographic without focal lesion: 237 days in HIV-HCV group (n=12) versus 208 days in HCV group, NS). At primary liver cancer diagnosis HIV-HCV patients were markedly younger (48 vs. 60 yrs, P<0.001), primary liver cancer was more advanced in HIV-HCV patients (single nodule: 43% vs. 75%, P=0.07; mean diameter of main nodule: 24 vs. 16 mm, P=0.006; portal obstruction: 3 vs. 0). Curative treatment was performed in four HIV-HCV patients versus 11 HCV patients (P=0.017). During follow-up, 10 HIV-HCV patients died versus only one HCV patient (P=0.0005). CONCLUSIONS: This result suggests more aggressiveness for tumors in HIV infected patients and, if confirmed, could result in shortening the length between ultrasonographic examinations

Effets toxiques du cadmium et du 3.5-dichlorophenol sur l'activité et la mortalité des bactéries nitrifiantes des boues activées - Effet des basses températures

International audienceBackground, aims, and scope: Sometimes, urban wastewaters convey a more or less significant part of toxic products from industries or the craft industry. Nitrifying activity can be affected by these substances, implying higher ammonia concentrations in the outlet effluent and contributing to toxicity for the aquatic environment. Moreover, the more stringently treated wastewater standards now require a reliable treatment for nitrogen. One of the key issues is the identification of the inhibition behavior of nitrifying bacteria facing a toxic substance. This new understanding could then finally be integrated into models in order to represent and to optimize wastewater treatment plants (WWTP) operation in cases involving 'toxic scenarios'. Materials and methods: The toxic substances studied in this work, cadmium and 3.5-dichlorophenol (3.5-DCP), are representative of chemical substances commonly found in municipal sewage and industrial effluents and symbolize two different contaminant groups. The effects of Cd and 3.5-DCP on nitrification kinetics have been investigated using respirometry techniques. Results: IC50 values determination gives concentrations of 3.1 mg/L for 3.5-DCP and 45.8 mg/L for Cd at 21±1°C. The variation to low temperature seems to have no real effect on IC50 for DCP, but induces a decrease of cadmium IC50 to 27.5 mg/L at 14°C. Finally, specific respirometric tests have been carried out in order to determine the potential effect of these toxic substances on the nitrifying decay rate b a . No significant effect has been noticed for Cd, whereas the presence of 3.5-DCP (at IC50 concentration) induced a dramatic increase of b a at 20°C. The same behavior has been confirmed by experiments performed in winter periods with a sludge temperature around 12°C. Discussion: The target substances have different modes of action on activity and mortality, notably due to the abilities of the contaminant to be precipitated, accumulated, or even to be progressively degraded. Studies realized at low temperature confirmed this assumption, and put in evidence the effect of temperature on toxic substances capable of being biosorbed. However, the change in the sludge sample characteristics can be pointed out as a problem in the investigation of the temperature effect on nitrification inhibition, as biosorption, bioaccumulation, and predation are directly linked to the sludge characteristics (VSS concentration, temperature) and the plant operating conditions (loading rates, sludge age, etc.). Conclusions: This work brings new understandings concerning the action mode of these specific contaminants on nitrifying bacteria and, in particular, on the role of temperature. The experiments lead to the determination of the IC50 values for both toxic substances on biological nitrification. The inhibition mechanisms of Cd and 3.5-DCP on nitrifying activity have been simply represented by a non-competitive inhibition model. Recommendations and perspectives: Other experiments carried out in a continuous lab-scale pilot plant should be done with a proper control of the operating conditions and of the sludge characteristics in order to better understand the mechanisms of nitrification inhibition for each contaminant. Finally, these first results show that toxic substances can have an effect on the growth rate but also on the decay rate, depending on the characteristics of the toxic substance and the sludge. This eventual double effect would imply different strategies of WWTP operation according to the behavior of the contaminant on the bacteria