We describe a 42-year-old man with AIDS and Hodgkin's lymphoma whose severe and recalcitrant cutaneous warts resolved following treatment with local 1% cidofovir. Clinically significant improvements were observed in a two-week period of therapy. In advanced HIV disease complicated by additional haematological malignancy, cutaneous warts may be difficult to treat and present a challenge for the attending physicians. In similar clinical condition topical anti-human papillomavirus therapy may prove to be safe and curative.

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Infections often complicate the course of hematological diseases and may represent a diagnostic challenge. In particular, visceral leishmaniasis diagnosis may be missed in lymphoma patients, as lymphoma-related immunosuppression can lead to a misleadingly negative Leishmania serology and to atypical clinical manifestations, including the lack of fever, considered a common symptom in leishmaniasis. Herein, we report a case of visceral leishmaniasis in a patient with a long history of B-cell chronic lymphocytic leukemia presenting with increasing fatigue and diarrhea, in the absence of fever. Leishmania serology was negative. Bone marrow biopsy performed with the clinical suspicion of transformation to high-grade lymphoma disclosed intracytoplasmic inclusion bodies resembling Leishmania amastigotes within the cytoplasm of macrophages, and CD1a immunohistochemical expression helped to confirm the diagnosis of leishmaniasis. Liposomal amphotericin B was administered with complete symptom resolution. The correct identification of Leishmania is critical as visceral leishmaniasis represents a severe disease with an often fatal outcome, particularly in frail patients, unless promptly recognized and adequately treated. A review of the literature of visceral leishmaniasis cases occurring in B-cell chronic lymphocytic leukemia patients is performed.

Introduction Miliary TBC represents a complex disease, quite rare at our latitudes. We present a case with severe pericardial involvement. Case report a 25-year-old Pakistani male, recently come in Italy, presented for fever and orthopnea. Anamnesis was difficult because of linguistic barrier. Echocardiogram revealed a large pericardial effusion with signs of tamponade, so a pericardiocentesis was promptly performed and exudative fluid was drained out and sent to laboratory. Blood tests showed anemia, mild hyponatremia, VES elevation and several vitamin deficiencies. Few days after the procedure the patient developed fever with chills, so blood samples for cultural tests were taken, but resulted negative. To better understand the etiology of pericardial effusion and fever a thoraco-abdominal CT was performed and bared multiple micronodular lesions disseminated to lungs, spleen and lever and pleural and peritoneal effusion. At the same time, the DNA search for Koch's bacillus in the pericardial fluid resulted positive for Mycobacterium TBC complex. So, a diagnosis of miliary TBC with pericardial involvement was done and corticosteroid therapy together with antitubercular drugs were started. Encephalic MRI excluded neurological involvement. Patient was isolated and moved to the infectious disease ward, where therapy was continued until recovery. Discussion Miliary TBC is a disseminated form due to the hematogenous spread of tubercle bacilli resulting in the formation of multiple tuberculous foci. This manifestation is more frequent in countries where TBC is still endemic (Pakistan, India, Philippines). The disease can progress slowly with few symptoms or acutely (typical of younger) and the identification may be challenging due to its rarity in developed countries and the lack of uniform criteria. Diagnosis is mainly based on the isolation mycobacterial from a specimen or molecular methods such as PCR. Treatment is based on standard antitubercular drugs regimen. The role of corticosteroids is still controversial. Conclusions Miliary TBC is a rare disease in developed countries with not well-defined diagnosis criteria and different clinical presentations. However, because of the increase of migration flows, is important to recognize this manifestation, especially when it develops acutely and with life-treating conditions such as pericardial tamponade.

A high prevalence of bone demineralization has been reported in HIV-infected patients, but its aetiology and mechanism are still unknown. Prevalence estimates vary widely and may be influenced by antiretroviral therapy, lipodystrophy, severity of HIV disease, and overlapping bone loss risk factors. We sought to assess bone metabolism and calcium intake in HIV-infected patients, naïve or treated with HAART. MethodsFrom February 1, 2008, 100 consecutive outpatients attending the Department of Infectious Disease, Perugia Hospital, were included in this study. Every patient was screened for serum level of 25 (OH) vitamin D, parathyroid hormone (PTH), bone-specific alkaline phosphatase (BALP), serum crosslaps, calcium and phosphate. A questionnaire on consumption of calcium-containing foods was administered. Data on race, age, BMI, duration of infection and HAART, smoking, alcohol, viral load and CD4+ cells count were collected from our medical records. Summary of resultsOut of 100 patients studied (including 83 Caucasians and 13 Africans) 70 were men; mean age was 45 years (range 27-69); mean BMI was 23.9 (range 15.6-30.9); 54 were active smokers and six had an alcohol intake >30 g/day; 82 patients had been treated with HAART for at least 6 months. Mean CD4 cell count was 603 cells/mcl (range 4-1630) and HIV viremia was undetectable in 59 patients. Lipodystrophy and HBV or HCV co-infection were present in 21 and 27, respectively. Vitamin D deficiency (25(OH) vitamin D level <20 ng/ml) was present in 84 and secondary hyperparathyroidism in 26 patients. Serum crosslaps and BALP results were elevated in 71 and 34, respectively. Serum calcium level was in the normal range while phosphate level results were low in 20 patients. Assessment of calcium consumption showed that 65 patients did not meet calcium recommendations for age, with an average calcium intake deficit of 340 mg/ day (range 10-804). ConclusionThis study shows that the majority of our patients have a deficit of calcium intake associated with low level of vitamin D, elevation of PTH and increase in markers of bone turnover (serum crosslaps and BALP). Because hypovitaminosis D was present in almost all the patients (naïve or treated), we believe that levels of vitamin D should be assessed and routinely corrected in all HIV patients, not only for the well-known action of this hormone on bone metabolism and bone fractures, but also because of its immunomodulatory properties and effects on adipocyte differentiation.