Spontaneous poisoning by Baccharis vulneraria Backer in cattle

ABSTRACT: Baccharis vulneraria Backer is a sub-shrub frequently found in southern Brazil, which leads to gastrointestinal tract intoxication. The objective of this study is to describe epidemiological, clinical and anatomopathological aspects of two cases of B. vulneraria poisoning in cattle. Two bovines from two different municipalities in the Itajaí Valley, Santa Catarina, Brazil were necropsied and performed the histopathological evaluation and botanical classification of the plant found in the pasture. Bovine 1 had dehydration, ruminal atony, diarrhea, congested mucous membranes and hypothermia for 20 hours, and died during clinical care. At necropsy, there was moderate multifocal detachment and reddening of the forestomachs mucosa. Bovine 2 presented anorexia, dry feces, ruminal atony, vocalization and muscle tremors for ten days, unresponsive to treatments, evolving to death. At necropsy were seen loosening of the mucosa with marked diffuse reddening and transmural edema. The microscopic exam revealed degeneration, necrosis, vesiculation, and detachment of the forestomachs’ mucosa, associated with moderate multifocal neutrophilic infiltrate (Bovine 1); marked diffuse transmural necrosis, edema, hemorrhage, and marked fibrinous exudation (Bovine 2). A large amount of B. vulneraria was found in the pastures, with signs of consumption. In this report, a case of subacute evolution of B. vulneraria poisoning was observed, since the poisoning by this plant is usually acute. More knowledge about poisoning by this plant is necessary for the prevention and control, avoiding new mortality cases.

Sweet Syndrome, Not so Sweet during an Ulcerative Colitis Flare Especially When You Cannot Eat

Sweet syndrome is a rare skin condition characterized by painful papules, nodules, or plaques with dense neutrophilic infiltrate in the upper dermis. It has been observed as idiopathic (classical), malignancy-associated, and drug-induced. The pathogenesis is not completely understood, but it is thought to involve hypersensitivity reactions to specific triggers. In some cases the etiology is unclear or may be multifactorial. We present a case of Sweet syndrome secondary to ulcerative colitis flare versus adalimumab re-induction.

DOP03 Early change in epithelial neutrophilic infiltrate predicts long-term response to biologics in Ulcerative Colitis

Background The prognostic value of histologic scores, grades, and individual histologic sub-components, alone or in combination with endoscopy, for predicting endoscopic improvement (EI) and histo-endoscopic mucosal improvement (HEMI) during maintenance therapy in ulcerative colitis (UC) remains uncertain. Methods Post-hoc analysis of participants from the VARSITY trial (n=734 with histology). Receiver operating characteristic and multi-variate logistic regression analyses were performed to assess whether baseline and/or week 14 assessments for the Robarts Histopathology Index (RHI), Geboes score, or individual histologic sub-components, could predict the achievement of EI and HEMI at week 52. Results RHI and Geboes scores at baseline, and changes in scores at week 14, had fair to poor accuracy for predicting week 52 EI or HEMI (Area Under the Curve [AUC] 0.58–0.67). Among individual sub-components, changes in epithelial neutrophil involvement from baseline to week 14 had the best performance for predicting week 52 EI (AUC 0.83, 95% confidence interval (CI) 0.74–0.91) and HEMI (AUC 0.85, 95% CI 0.76–0.94). On multivariate analyses, improvement of neutrophils in the epithelium was associated with increased odds of week 52 EI (Odds Ratio [OR] 3.63, 95% CI 1.45–9.08, p=0.0059) and HEMI (OR 6.88, 95% CI 3.29–14.36, p<0.0001), and lack of improvement of neutrophils in the epithelium was associated with lack of week 52 EI (OR 0.24, 95% CI 0.12–0.48, p<0.0001) and lack of HEMI (OR 0.03, 95% CI 0.01–0.014, p<0.0001). No other parameters significant on univariate analysis were significant within the multivariate model. Among patients with endoscopic Mayo scores of 2 or 3 at week 14, those who had >50% crypts involved with neutrophils at week 14 were significantly less likely to achieve week 52 EI (18.0%; 31/172 vs. 34.3%; 72/210, p<0.001), HEMI (9.9%; 17/172 vs. 22.4%; 47/210, p=0.001) (Figure 1) and clinical remission (11.0%; 19/172 vs. 23.3%; 49/210, p=0.002). Among patients with endoscopic Mayo scores of 0 or 1 at week 14, those who had >50% crypts involved with neutrophils were significantly less likely to achieve HEMI at week 52 (33%; 4/12 vs. 62.4%; 141/226, p=0.044) (Figure 1). Conclusion Our results on epithelial neutrophilic infiltrate following induction therapy as the only independent predictor for achievement of maintenance EI or HEMI helps clarify the clinical relevance of measuring histologic disease activity in UC. Epithelial neutrophilic infiltrate poses a means to stratify patients according to their likelihood of response to biologic treatment.

An atypical case of eosinophil-Rich Sweet’s syndrome

Sweet’s syndrome is an inflammatory disease that occurs mainly in young adults. Its clinical and histological aspects are usually characteristic. Its diagnostic criteria were proposed by von den Driesch. Two major and at least two minor criteria are required to establish the diagnosis. Sweet’s syndrome is classically associated with neutrophilic infiltrate. A few cases of Sweet’s syndrome with dense eosinophil infiltrate have been described. Here, we report a new case of eosinophil-rich Sweet’s syndrome in a young woman without underlying pathology.

Apixaban as a Rare Cause of Leukocytoclastic Vasculitis

Apixaban is a rare cause of leukocytoclastic vasculitis (LCV). To our knowledge, there is only one other reported case due to apixaban in the literature. We present a case of apixaban-induced leukocytoclastic vasculitis in a 95-year-old male. He had been started on apixaban 12 days prior to presentation and developed worsening palpable purpura of his lower extremities. Possible etiologies of this new rash were excluded, with biopsy showing extensive purpura with superficial perivascular neutrophilic infiltrate and leukocytoclasis. Apixaban was discontinued, and the patient was started on a slow prednisone taper with subsequent resolution of his rash.