Our results indicate that the differences in biological behaviour of malignant mesothelioma in long-term and short-term survivors may be explained in part by differences in tumour growth fraction and that proliferation index could represent an important prognostic parameter for this tumour.

There is a significant treatment need for children with HIV.

Objectives HIV‐related lipodystrophy is a syndrome of adipose tissue redistribution, dyslipidaemia and insulin resistance. Combination antiretroviral therapy (CART) is a key risk factor. We hypothesized that fat redistribution in HIV‐infected children is related to altered endocrine function of adipose tissue, namely leptin secretion. Methods Serum leptin and fat redistribution were measured in 104 HIV‐infected children in a prospective observational study from 2003 to 2004. Fat redistribution was defined by clinical observation. Body fatness was estimated using body mass index and four skinfold measurements. Serum leptin was determined using an enzyme‐linked immunosorbent assay (Quantikine; R&D Systems, Abingdon, UK). Linear analogue models were used to adjust the leptin concentration for body fatness. Results There was no significant difference in serum leptin among children treated with protease inhibitors (PIs), children on non‐PI CART and children not treated with CART (P>0.05). When leptin concentrations were adjusted for body fatness, there was again no difference among PI‐treated, non‐PI‐treated and untreated children. Categorization of CART exposure as never, current or past did not change these results. Conclusions There is no evidence that leptin plays any role in lipodystrophy other than reflecting body fatness.

Background Mannose-binding lectin (MBL; encoded by MBL-2) is a circulating pattern-recognition molecule that recognizes microbial carbohydrate motifs, leading to complement activation and cell lysis. Mutations in the MBL-2 promoter and of the MBL-2 gene exon 1 result in reduced protein levels and increased susceptibility to infection. We have investigated the effect of MBL-2 polymorphisms on susceptibility and progression of HIV-1 infection in children. Patients and methods One-hundred and twenty-eight children, aged 2–16 years were recruited. MBL-2 genotypes were determined by PCR and heteroduplex analyses. Serum MBL levels were measured by ELISA. Comparison of genotypes (A=wild type, 0=variant alleles) and protein levels between groups was performed using χ2, Mann–Whitney U or Kruskal–Wallis tests. Results Children were classified according to the Centers for Disease Control and Prevention clinical classification: A, B or C (mildly symptomatic [ n=39], moderately symptomatic [ n=58] or severely symptomatic AIDS [ n=31]) or immune category 1 ( n=77), 2 ( n=46) or 3 ( n=5). Analysis of MBL-2 genotypes with respect to clinical classification yielded minimal differences. However, patients in immunological categories 2 and 3 (<25% CD4+ T cells) were more likely to have MBL-2 variant alleles ( P=0.01). We further explored MBL status with respect to disease progression. Only 1/10 long-term non-progressors (LTNPs) had an MBL-2 mutation (A/D) with a corresponding protein level of 611 ng/ml. Conclusions MBL deficiency was more frequent in patients with severe disease as assessed by CD4+ T-cell status. MBL-2 variants may be less frequent in children classified as LTNPs. MBL analysis could be useful in identifying children with slow disease progression and, consequently, may not require immediate antiretroviral treatement.

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