Migrants born in hepatitis B virus (HBV) and hepatitis C virus (HCV) endemic countries are at increased risk of being infected with these viruses. The first symptoms may arise when liver damage has already occurred. The challenge is to identify these infections early, since effective treatment has become available. In 2011 we conducted a screening project in first-generation migrants (FGMs) born in Afghanistan, Iran, Iraq, the former Soviet Republics, and Vietnam and living in Arnhem and Rheden. All participants were offered free blood screening for HBV and HCV. In total 959 participants were tested, with the country of origin known for 927, equating to 28·7% of all registered FGMs from the chosen countries. Nineteen percent (n = 176) had serological signs of past or chronic HBV infection and 2·2% (n = 21) had chronic HBV infection. The highest prevalence of chronic HBV infection was found in the Vietnamese population (9·5%, n = 12). Chronic HCV was found in two persons from the former Soviet Republics and one from Vietnam. Twenty-four percent (n = 5) of the newly identified patients with chronic HBV and one of the three patients with chronic HCV received treatment. Three of the patients, two with HCV and one with HBV, already had liver cirrhosis. The highest (9·5%) HBV prevalence was found in FGMs from Vietnam, indicating a high need for focusing on that particular immigrant population in order to identify more people with silent HBV infection. The fact that three patients already had liver cirrhosis underlines the necessity of early identification of HBV and HCV infection in risk groups.

Treatment of calcium or vitamin D deficiency in HIV+ patients on ART including TDF has favorable effects on bone density, but it does not improve serum phosphate levels. Renal phosphate wasting in these patients is not caused by excess PTH, PTH-rp, or FGF-23 nor by vitamin D or calcium deficiency.

Objectives Hypophosphataemia is common in HIV‐positive patients, in particular in those using tenofovir disoproxil fumarate (TDF). Its pathogenesis is not well understood. The importance of fibroblast growth factor 23 (FGF‐23), the most potent phosphaturic hormone known today, has not been studied in these patients. The aim of the study was to investigate whether FGF‐23 might be involved in the aetiology of hypophosphataemia in HIV‐positive patients on tenofovir. Methods Calcium and phosphate metabolism was studied in 36 HIV‐positive patients on TDF. Hypophosphataemia was defined as a serum phosphate level < 0.75 mmol/L. Results Fifteen patients (42%) had hypophosphataemia (group 1), and 21 had a normal serum phosphate level (group 2). The renal phosphate reabsorption threshold [tubular maximum phosphate reabsorption per glomerular filtration rate (TmP/gfr)] was significantly lower in group 1 than in group 2 (0.58 ± 0.04 vs. 0.91 ± 0.03 mmol/L, respectively; P < 0.0001). The serum phosphate concentration was strongly correlated with TmP/gfr (R = 0.71; P < 0.0001). Both groups had normal serum FGF‐23 levels, and serum phosphate and TmP/gfr were not related to serum parathyroid hormone (PTH) or FGF‐23 levels. Conclusion FGF‐23 is not involved in the pathogenesis of hypophosphataemia in HIV‐positive patients on TDF. The data suggest that a PTH‐like factor may be involved.

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