Cutaneous T-cell lymphomas (CTCLs) are a subgroup of non-Hodgkin lymphomas (NHLs) that include Sézary syndrome (SS) and mycosis fungoides (MF). In CTCLs, there is a proinflammatory environment that supports the malignant transformation of the body’s own T cells. Part of this environment includes a dysregulated JAK/STAT pathway that can lead to disease progression.1
As CTCL progresses, the patient’s immune system becomes significantly impaired, which predisposes patients to infectious complications that can contribute to both morbidity and mortality. Malignant T cells predispose patients to skin breakdown and subsequent infections, especially those with Staphylococcus aureus.2 It has also been proposed that in addition to causing infectious complications, S. aureus could also support a promalignant environment through its enterotoxins, which are thought to stimulate malignant T-cell transformation.3
Recently, a study group in Denmark led by Lindahl and colleagues aimed to further investigate this potential pathogenic link between S. aureus and CTCL by evaluating the effect of short-term, “aggressive” antibiotic therapy in patients with CTCL with skin lesions that were colonized with S. aureus.
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The small study was conducted prospectively at a single center in Denmark and enrolled 8 patients. Patients who were enrolled in the trial were those with advanced CTCL (stage IIB or higher) who did not respond to prior topical or systemic therapy. Blood work, skin biopsies, and swabs were collected at 4 time points (day 0, day 10, month 1, month 2) and sent for DNA and RNA analysis. Two patients were followed for an extended interval for up to 8 months.
