Hand-foot syndrome (HFS), also called hand-foot skin reaction, palmar-plantar erythrodysesthesia, acral erythema, and Burgdorf reaction, is a dose-limiting cutaneous toxicity of many chemotherapeutic agents. Recently, the multiple tyrosine kinase inhibitor class of novel targeted therapies, including sorafenib and sunitinib, has emerged as an important cause of HFS, with 10–28% of patients treated with sunitinib and 10–62% of patients treated with sorafenib reporting HFS. This review examines the epidemiology, clinical features, histopathology, pathogenesis models, prognostic implications, and management of HFS, with particular attention to HFS induced by sorafenib and sunitinib. The high prevalence of HFS reported by patients treated with these medications underscores the need for greater understanding of the pathogenesis and management of this syndrome.

Inadequate initial antimicrobial therapy is an independent risk factor for mortality in ESBL-EK infections, but only among nonurinary infections. Multidrug resistance was a strong risk factor for IIAT.

The emergence of MDR among ESBL-EK has important implications for the future ability to treat these infections. The strong association between the species of infecting organism and MDR suggests that the epidemiology in K. pneumoniae may be unique. PFGE results suggest that horizontal spread is important in the emergence of MDR ESBL-EK.

The effect of antimicrobial formulary interventions intended to curb emergence of ESBL-EK may differ substantially across institutions, perhaps as a result of differences in patient populations. Variability in the epidemiological profiles of ESBL-EK isolates at different hospitals must be considered when designing interventions to respond to these pathogens.

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BackgroundPrior studies repeatedly showed that cultures of skin lesions diagnosed as "cellulitis" are usually negative. However, lack of a gold standard for diagnosis (against which culture might be judged) and failure to assess the human immune response are important limitations of prior work. In this pilot study, we aimed to develop a criterion standard for research on bacterial cellulitis, to evaluate the sensitivity of procalcitonin for bacterial cellulitis, and to use gene expression analysis to find other candidate diagnostic markers.MethodsWe classified lesions via biopsies, 16s rRNA gene detection, culture, and histopathology. We quantified procalcitonin expression in blood. We also used Nanostring technology to quantify transcription of immunomodulators that may distinguish cases from inflamed controls.ResultsOf 28 participants, 15 had a clinical diagnosis of cellulitis, six had a diagnosis of non-infectious dermatitis, and seven were normal volunteers. Of the “cellulitis” patients, three (20%) had pathogens isolated, and were designated confirmed cases. Procalcitonin was undetectable in all three. HLA-DQA1 was expressed 34-fold more in confirmed cases vs. controls (fold change of geometric mean). Heat maps depicting multiplex gene expression analysis revealed a distinct profile of gene expression in confirmed cases relative to comparators.ConclusionsMost “cellulitis” patients had microbiologically-negative biopsies. Procalcitonin was undetectable, and HLA-DQA1 elevated, in confirmed bacterial cases. Multivariable transcriptomic profiling results supported our algorithm’s ability to identify patients with true bacterial cellulitis. A larger sample may allow discovery of an immunological signature capable of distinguishing bacterial cellulitis from its mimics in clinical practice.

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