Although there is reasonable agreement about the frequent association between osteopenia/osteoporosis and HIV infection, opinions on the aetiopathogenesis of osteopenia and osteoporosis during HIV infection are widely divergent. Some authors suggest that bone dysmetabolism is related to the HIV infection itself. The loss of bone mineral density (BMD) occurs in two-thirds of HIV-1-seropositive individuals naive to antiretroviral therapy (ART), and improves during the follow-up of patients receiving ART, irrespective of the drug class used. Moreover, reduced BMD has also been associated with both ART-induced lipodystrophy and mitochondrial toxicity. An association between HAART and osteoporosis has been broadly observed; however, methodological bias, particularly the lack of control groups, could have obscured the data. Today, the role of HAART on bone metabolism and on BMD in HIV-seropositive patients is still controversial. The available data on BMD studies after the introduction of HAART are much more contradictory than those from before this era. The variety and complexity of changes in bone metabolism in patients with HIV infection and the different pathomechanisms leading to changes in bone mass, as well as the different stages of disease at the time of clinical investigation, may contribute to the contradictory data on BMD measurements in HIV-infected patients after HAART.

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HIV-infected patients may undergo renal damage related to the HIV infection itself, to the presence of co-infections, arterial hypertension, diabetes or to the exposure to nephrotoxic drugs. Tenofovir has been associated with the development of acute renal failure with Fanconi syndrome and acute tubular necrosis and, albeit rarely, with chronic liver disease. Patients with low CD4 cell count, low body weight and with concomitant diseases such as arterial hypertension and diabetes or co-infections with HCV, HBV or Treponema pallidum seem at higher risk of tenofovir-related nephrotoxicity. Other risk factors include previous exposure to nephrotoxic drugs and the association of tenofovir with boosted protease inhibitors or with didanosine. However, from the analysis of published papers the incidence of tenofovir-related renal toxicity seems low, as confirmed also by our personal casuistry (SCOLTA Project). Thus, a careful selection of patients including the evaluation of existent renal disease before starting an antiretroviral regimen including tenofovir is necessary to prevent renal damage. Furthermore, frequent monitoring of renal function in patients at higher risk of renal damage is strongly recommended, as well as a tenofovir dose adjustment if an alteration of renal function is detected.

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Auxological and endocrinological complications frequently occur in children with connatal HIV infection. These complications seem to be related both to the infection itself and the antiretroviral therapy. Many children consequently show height-weight and pubertal retardation without any evidence of hormonal deficit. We studied 10 children with connatal HIV infection who were enrolled in this analysis and followed up for 7 years in order to evaluate their height-weight growth, pubertal maturation, bone age progression and hormonal pattern (basal Growth hormone (GH) and GH after Clonidine or Insulin stimulation, Insulin-like Growth Factor 1 (IGF-1), Insulin-like Growth Factor Binding Protein 3 (IGFBP-3), FSH, LH, ACTH and Cortisol, TSH, fT4, T4, T3, Ab-TGO, Leptin). Three children showed a height < 3rd centile during the first two years of their life and in prepubertal age, with recurring improvement in their growth rate. Weight growth was very compromised in one girl, remaining firmly <3rd centile during the follow-up. Three children presented a weight <3rd centile until they were two years old. However, a height growth rate >10th centile was found in nine children throughout the follow-up, while it was pathological in five children. The blood level of Leptin was higher at the beginning of the study: 0.82 – 11.68 ng/l (M ± DS: 3.29 ± 4.15) than at its conclusion: 0.2 – 3 ng/l (M ± DS: 1.65 ± 1.01). There was a statistically significant correlation between leptinemia and the CD4/CD8 count (p: 0.010; r: 0.916) and the CDC classification (p: 0.006; r: 0.937), indicating a strong relationship with the degree of virological and immunological impairment. The authors stress the importance of a careful height-weight growth rate control in HIV-infected children, as it reflects the clinical and virological course of the disease. Adequate control of the infection allows physiological growth in most patients. Moreover, we emphasize the utility of IGFBP-3 and IGF-1 measurements, since they represent growth markers which are more exact and better capable of reproduction than GH.

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The aim of our study was to assess the efficacy and tolerability of lamivudine alone versus lamivudine plus alpha-interferon for treatment of chronic active hepatitis B, anti-HBe positive. In all, 59 patients were randomly divided into 3 groups: A) 21 patients received lamivudine at 100 mg/daily orally for 52 weeks; B) 20 patients received lamivudine at 100 mg/die plus alpha-interferon at 6 MU subcutaneously three times weekly for 52 weeks; C) 18 patients received the same combination therapy for 40 weeks after pre-treatment with lamivudine for 12 weeks. The complete sustained response in the three groups was 33.3% vs 35.0% vs 33.3%, respectively. Our study demonstrates that in anti-HBe positive chronic hepatitis B a 12-month course of lamivudine plus alpha-interferon combination therapy is as beneficial as lamivudine monotherapy. Moreover, the combination therapy for 40 weeks after pre-treatment with lamivudine for 12 weeks did not increase the sustained response. The aim of our study was to assess the efficacy and tolerability of lamivudine alone versus lamivudine plus alpha-interferon for treatment of chronic active hepatitis B, anti-HBe positive. In all, 59 patients were randomly divided into 3 groups: A) 21 patients received lamivudine at 100 mg/daily orally for 52 weeks; B) 20 patients received lamivudine at 100 mg/die plus alpha-interferon at 6 MU subcutaneously three times weekly for 52 weeks; C) 18 patients received the same combination therapy for 40 weeks after pre-treatment with lamivudine for 12 weeks. The complete sustained response in the three groups was 33.3% vs 35.0% vs 33.3%, respectively. Our study demonstrates that in anti-HBe positive chronic hepatitis B a 12-month course of lamivudine plus alpha-interferon combination therapy is as beneficial as lamivudine monotherapy. Moreover, the combination therapy for 40 weeks after pre-treatment with lamivudine for 12 weeks did not increase the sustained response.

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We describe an unusual case of disseminated peritoneal hydatidosis in a 64-year-old woman, with previous surgery for liver hydatidosis (22 years before) and show the radiological features in question. Serological tests and radiological imaging allow diagnosis of hydatid disease and are useful in assessing response to therapy. In this case no changes in size, number and density of lesions and clinical features are present after albendazole therapy.

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We present an intriguing case report of a septicemic post-elective surgical staphylococcal knee arthritis and cellulitis which did not respond to long-term courses of associated rifampicin and teicoplanin or vancomycin despite apparently favourable in vitro susceptibility assays, but rapidly resolved after i.v. followed by oral administration of linezolid. The lack of response to a two-week course of glycopeptides cannot be explained by the in vitro mimimum inhibitory concentrations (MIC90) of involved organisms, which showed full susceptibility of Staphylococcus aureus to vancomycin and teicoplanin, and sensitivity of an accompanying Staphylococcus epidermidis isolated from blood cultures to vancomycin and rifampicin, with borderline “intermediate” values found for teicoplanin. Since neither abscess formation nor bone involvement were of concern, effective glycopeptide and rifampicin penetration into infectious tissue should have been ensured. From a clinical point of view, only the introduction of a two-week i.v. linezolid followed by one more week of oral linezolid obtained a complete clinical and microbiological cure, and an unhoped-for functional success. When managing severe multiresistant gram-positive infections, in vitro activity should be carefully evaluated against expected drug penetration rates into the relevant infectious tissues.

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Since the Classical age, humankind has had to cope with petechial typhus, especially during wars and famine. Epidemics chiefly occurred during sieges and followed the paths of armies, when infected soldiers transmitted the infection to populations with whom they came into contact. Winter exacerbated the disease due to the use of unhygienic woollen clothes that allowed the spread of pediculosis. It was only in the early 18th century that petechial typhus outbreaks diminished thanks to the use of Marseille soap and to the new custom of changing clothing at bedtime. In many military campaigns, deaths from typhus were higher than those due to war wounds: recent studies established that the French defeat during the Napoleonic Russian military campaign has to be attributed more to typhus than to the military superiority of the enemy. Indeed, the contagion is estimated to have affected 80% of the 600,000 troops involved. The role of Pediculus as a vehicle of infection established in 1909 by Charles Nicolle, microbiological isolation performed by Howard Ricketts and Stanislaus von Prowazck, and finally the advent of antibiotic therapy, all laid the basis for controlling the disease in the 20th century.

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