Introduction Pegylated-interferon (PEG-IFN) and ribavirin (RBV), current standard treatment for hepatitis C virus (HCV) infection, is frequently associated with neutropenia and anemia, leading to high treatment discontinuation rates in HIV/HCV coinfected patients. Our objective was to compare the effectiveness of intervening with hematologic growth factors versus dose reductions of standard HCV therapy for the management of treatment-induced hematologic disorders. Methods Ninety-two HIV/HCV coinfected, therapy-naive subjects received PEG-IFN alfa-2b 1.5 μg/kg/wk and RBV 13 ± 2 mg/kg/day for up to 48 weeks. Before treatment initiation, subjects were randomized to subsequently receive growth factors, recombinant human erythropoietin (rHuEPO) and/or granulocyte-colony stimulating factor (G-CSF), or dose reduction (RBV and/or PEG-IFN) for anemia and neutropenia management, respectively. We analyzed the ability of each management strategy to control anemia and neutropenia and the percentage of subjects who achieved a successful treatment outcome among subjects according to the different management strategies. Results During treatment, 43 subjects developed anemia (HuEPO, n=24; dose reduction, n=19) while 25 subjects developed neutropenia (G-CSF, n=10; dose reduction, n=15). Following the intervention, the increase in both hemoglobin and absolute neutrophil counts also did not differ between the two side effect management strategies. Sustained response percentages were similar comparing anemic and neutropenic subjects regardless of management strategy (anemia: rHuEPO, 29% versus dose reduction, 21%, p=0.92; neutropenia: G-CSF, 40% versus dose reduction, 20%, p=0.46). Conclusions Growth factor supplementation and dose reduction do not appear to differ as management strategies for anemia and neutropenia in HIV/HCV co-infected individuals treated with PEG-IFN/RBV.

Summary:Stage IV hidradenitis suppurativa in the axilla is a chronic disease in which the removal of the affected area and a reconstruction with disease free skin is the definitive treatment; however there is some controversy about the technique to be used in this reconstruction. Studies show superiority in wide resections, and coverage with flaps rather than grafts. The use of pedicle flaps of lateral thoracic artery perforators and thoracodorsal artery perforators has demonstrated superior performance to other techniques in postsurgical follow-up. This article describes the cases of 2 patients with chronic HS in which lesions were resected with disease-free margins and the reconstruction of the defect is carried out with lateral thoracic wall perforator flaps and the subsequent improvement in their life quality after surgery.

Cystic fibrosis patients display multi-organ system dysfunction (e.g. pancreas, gastrointestinal tract, and lung) with pathogenesis linked to a failure of Cl− secretion from the epithelial surfaces of these organs. If unmanaged, organ dysfunction starts early and patients experience chronic respiratory infection with reduced lung function and a failure to thrive due to gastrointestinal malabsorption. Early mortality is typically caused by respiratory failure. In the past 40 years of newborn screening and improved disease management have driven the median survival up from the mid-teens to 43–53, with most of that improvement coming from earlier and more aggressive management of the symptoms. In the last decade, promising pharmacotherapies have been developed for the correction of the underlying epithelial dysfunction, namely, Cl− secretion. A new generation of systemic drugs target the mutated Cl− channels in cystic fibrosis patients and allow trafficking of the immature mutated protein to the cell membrane (correctors), restore function to the channel once in situ (potentiators), or increase protein levels in the cells (amplifiers). Restoration of channel function prior to symptom development has the potential to significantly change the trajectory of disease progression and their evidence suggests that a modest restoration of Cl− secretion may delay disease progression by decades. In this article, we review epithelial vectorial ion and fluid transport, its quantification and measurement as a marker for cystic fibrosis ion transport dysfunction, and highlight some of the recent therapies targeted at the dysfunctional ion transport of cystic fibrosis.

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