A Rare Case of Drug-Induced Sweet Syndrome After Pembrolizumab Therapy.

Sweet syndrome is an uncommon inflammatory disorder characterized by the abrupt appearance of painful, erythematous papules, plaques, or nodules on the skin. Fever and leukocytosis frequently accompany the cutaneous lesions. In addition, involvement of the eyes, musculoskeletal system, and internal organs may occur. Sweet syndrome has been associated with a broad range of disorders. There are three subtypes: classical Sweet syndrome, malignancy-associated Sweet syndrome, and drug-induced Sweet syndrome. Classical Sweet syndrome is not associated with malignancy or drugs. It is essentially associated with an upper respiratory infection, gastrointestinal infection, inflammatory bowel disease, and pregnancy. Malignancy-associated Sweet syndrome is associated with hematologic malignancy more than solid malignancy, most commonly with acute myeloid leukemia. Drug-induced Sweet syndrome usually develops approximately two weeks after drug exposure, in patients who lack a prior history of exposure to the inciting drug. Here we are discussing our patient, a 68-year-old male who presented eight weeks after starting chemotherapy with pemetrexed, carboplatin, and pembrolizumab for left lung adenocarcinoma with macular rash. On further investigation with biopsy was found to have neutrophilic dermatitis, hence being diagnosed with drug-induced Sweet syndrome. Histopathology revealed a dermis with infiltration of neutrophils with lekocytoclasia.

Reevaluating the imaging definition of tumor progression: perfusion MRI quantifies recurrent glioblastoma tumor fraction, pseudoprogression, and radiation necrosis to predict survival.

INTRODUCTION: Contrast-enhanced MRI (CE-MRI) represents the current mainstay for monitoring treatment response in glioblastoma multiforme (GBM), based on the premise that enlarging lesions reflect increasing tumor burden, treatment failure, and poor prognosis. Unfortunately, irradiating such tumors can induce changes in CE-MRI that mimic tumor recurrence, so called post treatment radiation effect (PTRE), and in fact, both PTRE and tumor re-growth can occur together. Because PTRE represents treatment success, the relative histologic fraction of tumor growth versus PTRE affects survival. Studies suggest that Perfusion MRI (pMRI)-based measures of relative cerebral blood volume (rCBV) can noninvasively estimate histologic tumor fraction to predict clinical outcome. There are several proposed pMRI-based analytic methods, although none have been correlated with overall survival (OS). This study compares how well histologic tumor fraction and OS correlate with several pMRI-based metrics. METHODS: We recruited previously treated patients with GBM undergoing surgical re-resection for suspected tumor recurrence and calculated preoperative pMRI-based metrics within CE-MRI enhancing lesions: rCBV mean, mode, maximum, width, and a new thresholding metric called pMRI-fractional tumor burden (pMRI-FTB). We correlated all pMRI-based metrics with histologic tumor fraction and OS. RESULTS: Among 25 recurrent patients with GBM, histologic tumor fraction correlated most strongly with pMRI-FTB (r = 0.82; P < .0001), which was the only imaging metric that correlated with OS (P<.02). CONCLUSION: The pMRI-FTB metric reliably estimates histologic tumor fraction (i.e., tumor burden) and correlates with OS in the context of recurrent GBM. This technique may offer a promising biomarker of tumor progression and clinical outcome for future clinical trials.

Localizing sadness activation within the subgenual cingulate in individuals: a novel functional MRI paradigm for detecting individual differences in the neural circuitry underlying depression.

Variations in frontal lobe (FL) functional anatomy, especially the subgenual cingulate gyrus (SGC) suggest that mapping on an individual rather than group level may give greater insight regarding dysregulation of the neural circuitry involved in depression, as well as potentially provide more specific or individualized treatment plans for depressed patients. We designed a functional MRI task capable of imaging FL activity in individuals, including the SGC region, using a transient sadness paradigm. We sought to develop a method that may better detect individual differences of FL subregions related to sadness, since this region has been implicated to show dysregulation in depression. The task was based on a block design that also accommodates individual differences in responsivity to a sadness induction paradigm. Individual differences from nine non-depressed healthy volunteers were analyzed. We also performed functional connectivity analyses to further characterize our findings to the networks associated with the SGC in each individual. The study was designed to account for individual variation rather than using a true experimental design; therefore, no control group was necessary. As expected, due to inter-individual variability, the specific site of SGC activation during sadness varied across individuals. Activation was also observed in other brain regions consistent with other studies of induced sadness and depression. Patterns of functional connectivity to the SGC also highlighted neural circuits known to subserve sadness and depression. This task promises to more precisely localize a given individual's functional organization of the brain circuitry underlying sadness, and potentially depression, in an efficient, standardized way. This task could potentially aid in providing individualized targets in the treatment of depression.

Brain retraction and thickness of cerebral neocortex: an automated technique for detecting retraction-induced anatomic changes using magnetic resonance imaging.

BACKGROUND: Treating deep-seated cerebral lesions often requires retracting the brain. Retraction, however, causes clinically significant postoperative neurological deficits in 3% to 9% of intracranial cases. OBJECTIVE: This pilot study used automated analysis of postoperative magnetic resonance images (MRIs) to determine whether brain retraction caused local anatomic changes to the cerebral neocortex and whether such changes represented sensitive markers for detecting brain retraction injury. METHODS: Pre- and postoperative maps of whole-brain cortical thickness were generated from 3-dimensional MRIs of 6 patients who underwent selective amygdalohippocampectomy for temporal lobe epilepsy (5 left hemispheres, 1 right hemisphere). Mean cortical thickness was determined in the inferior temporal gyrus (ITG test), where a retractor was placed during surgery, and in 2 control gyri-the posterior portion of the inferior temporal gyrus (ITG control) and motor cortex control. Regions of cortical thinning were also compared with signs of retraction injury on early postoperative MRIs. RESULTS: Postoperative maps of cortical thickness showed thinning in the inferior temporal gyrus where the retractor was placed in 5 patients. Postoperatively, mean cortical thickness declined from 4.1 +/- 0.4 mm to 2.9 +/- 0.9 mm in ITG test (P = .03) and was unchanged in the control regions. Anatomically, the region of neocortical thinning correlated with postoperative edema on MRIs obtained within 48 hours of surgery. CONCLUSION: Postoperative MRIs can be successfully interrogated for information on cortical thickness. Brain retraction is associated with chronic local thinning of the neocortex. This automated technique may be sensitive enough to detect regions at risk for functional impairment during craniotomy that cannot be easily detected on postoperative structural imaging.