Many physicians delay HAART in patients presenting with TB because of pill burden, drug/drug interactions and toxicity. Although the use of HAART led to significant reductions in viral load, ADI and mortality, co-infected patients commonly experienced AE leading to interruptions in TB/HIV therapy. We therefore recommend starting HAART early for patients with advanced HIV disease (CD4 < 100 x 106 cells/l) and deferring HAART until the continuation phase of TB therapy (i.e. after 2 months) for patients who are clinically stable (CD4 > 100 x 106 cells/l).
Objectives
The aims of the study were to describe the clinical presentation and renal and bone abnormalities in a case series of HIV‐infected patients receiving treatment with tenofovir (TDF), and to recommend appropriate screening for toxicity related to TDF.
Methods
Patients were identified from referrals to a specialist HIV renal clinic. Patients were included if treatment with TDF was assessed as the primary cause of the renal function impairment and clinical data were available prior to and following discontinuation of TDF treatment. Data were collected from case note review and clinic databases.
Results
Twenty‐two patients (1.6% of all those who received TDF) were identified with TDF‐associated renal toxicity. All had normal serum creatinine prior to TDF therapy. All presented with proteinuria. On stopping TDF, renal function improved. Eight patients had confirmed Fanconi syndrome. Twelve patients presented with bone pain and osteomalacia was confirmed on an isotope bone scan in seven of these patients. The findings (in those patients tested) of tubular proteinuria, reduced tubular transport maximum of phosphate (TmP), and glycosuria were all consistent with the proximal tubule being the site of toxicity.
Conclusion
Renal toxicity remains a concern in patients treated with TDF. Clinical presentation may be with renal dysfunction, Fanconi syndrome or osteomalacia. Our investigations suggest proximal tubular toxicity as a common pathogenic mechanism.
Mortality risk factors for PCP were identifiable at or soon after hospitalization. The trend towards improved outcome after June 1996 occurred in the absence of highly active antiretroviral therapy.
Two years of field sampling aimed to establish the predominance and association among the fungal pathogens causing Fusarium ear blight (FEB) in four European countries (Hungary, Ireland, Italy and the UK). A PCR-based method was used to detect four Fusarium species and two varieties of Microdochium nivale present in the samples. The prevalence of FEB pathogens differed significantly between countries. Overall, all pathogens were commonly detected in Ireland and to a lesser extent in the UK. In contrast, only two species, F. graminearum and F. poae, were regularly detected in Italy and Hungary. Fusarium culmorum was rarely detected except in Ireland. Log-linear models were used to determine whether there is the independence of the six FEB pathogens at each sampling site. Significant two-pathogen interactions were frequently observed, particularly in harvest samples; all these significant two-pathogen interactions were of the synergistic type, except between F. poae and F. culmorum, and were generally consistent over the 2 years and four countries. Fusarium graminearum and F. poae were least frequently involved in two pathogen interactions but were involved in most of the nine significant three-pathogen interactions. However, only the interaction between F. graminearum, F. avenaceum and F. poae was significant in both years. Potential implications of the present results in FEB management are discussed.
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