ABSTRACT
Objective@#Cortical iron deposition has recently been shown to occur in Alzheimer’s disease (AD). In this study, we aimed to evaluate how cortical gray matter iron, measured using quantitative susceptibility mapping (QSM), differs in the clinical cognitive impairment spectrum. @*Materials and Methods@#This retrospective study evaluated 73 participants (mean age ± standard deviation, 66.7 ± 7.6 years;52 females and 21 males) with normal cognition (NC), 158 patients with mild cognitive impairment (MCI), and 48 patients with AD dementia. The participants underwent brain magnetic resonance imaging using a three-dimensional multi-dynamic multi-echo sequence on a 3-T scanner. We employed a deep neural network (QSMnet+) and used automatic segmentation software based on FreeSurfer v6.0 to extract anatomical labels and volumes of interest in the cortex. We used analysis of covariance to investigate the differences in susceptibility among the clinical diagnostic groups in each brain region.Multivariable linear regression analysis was performed to study the association between susceptibility values and cognitive scores including the Mini-Mental State Examination (MMSE). @*Results@#Among the three groups, the frontal (P < 0.001), temporal (P = 0.004), parietal (P = 0.001), occipital (P < 0.001), and cingulate cortices (P < 0.001) showed a higher mean susceptibility in patients with MCI and AD than in NC subjects. In the combined MCI and AD group, the mean susceptibility in the cingulate cortex (β = -216.21, P = 0.019) and insular cortex (β = -276.65, P = 0.001) were significant independent predictors of MMSE scores after correcting for age, sex, education, regional volume, and APOE4 carrier status. @*Conclusion@#Iron deposition in the cortex, as measured by QSMnet+, was higher in patients with AD and MCI than in NC participants. Iron deposition in the cingulate and insular cortices may be an early imaging marker of cognitive impairment related neurodegeneration.
ABSTRACT
Acute generalized exanthematous pustulosis (AGEP) is a severe and rare disease usually related to drug eruption. AGEP is induced by drugs in over 90% of cases with antibiotics being the most common. It is characterized by a fever and a pustular eruption on erythematous skin with acute onset and without follicular localization. Acetaminophen is commonly used as an antipyretic and analgesic. Acetaminophen has been reported to be an uncommon cause of AGEP. We report a 79-year-old woman presenting with fever and erythematous maculopapular eruptions on the trunk with sterile pustules arising upon the use of acetaminophen for back pain. Leukocytosis and elevated C-reactive protein levels were noted on the laboratory examination. The histopathological examination of the skin biopsy specimen showed intraepidermal pustule formation with superficial perivascular lymphocytic infiltration, including eosinophils, and extensive red blood cell extravasation. The lesions were resolved with discontinuation of acetaminophen and use of systemic corticosteroid. We report a case of AGEP probably caused by acetaminophen.