When a Late Metastasis Is Hard to Swallow.

Pseudoachalasia is an uncommon disorder characterised by aperistalsis in the tubular oesophagus and impaired relaxation of the lower oesophageal sphincter (LES). It presents with symptoms and radiologic, endoscopic and manometric findings that mimic idiopathic achalasia. There is a huge spectrum of underlying causes for pseudoachalasia, although malignancy is the most common aetiology. We report the case of a 70-year-old Portuguese female with a history of breast cancer, submitted to tumourectomy, radiotherapy and hormonotherapy, in complete remission for 16 years, who presented in the emergency department with a two-month history of dysphagia, weight loss, heartburn and nausea. Blood work, body computed tomography (CT) scan, mammography, upper endoscopy, colonoscopy and skeletal scintigraphy did not show any alterations, but barium swallow scan and oesophageal manometry suggested achalasia. She was submitted to oesophageal dilatation with partial symptomatic improvement. Six months later, new onset of dysphonia and worsening of initial symptoms was noticed. A new CT scan revealed unilateral pleural effusion, large mediastinal adenopathy and multiple pulmonary nodules highly suggestive of a metastatic malignancy. Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) from mediastinal adenopathies confirmed the tumoural invasion by a carcinoma, and immunohistochemistry suggested a breast origin. She underwent a nasoendoscopy that revealed bilateral vocal cord paralysis. After chemotherapy was started, symptoms of achalasia completely resolved, and tumour markers, which were increased, have normalised. The presented case highlights a pseudoachalasia as the first manifestation of a late breast metastasis. It is essential to always have in mind patients' past history as a key that can help resolve clinical doubts.

Glucose intolerance after chronic stress is related with downregulated PPAR-γ in adipose tissue.

BACKGROUND: Chronic stress is associated with increased risk of glucose intolerance and cardiovascular diseases, albeit through undefined mechanisms. With the aim of gaining insights into the latter, this study examined the metabolic profile of young adult male rats that were exposed to chronic unpredictable stress. METHODS: Young adult male rats were submitted to 4 weeks of chronic unpredictable stress and allowed to recover for 5 weeks. An extensive analysis including of morphologic, biochemical and molecular parameters was carried out both after chronic unpredictable stress and after recovery from stress. RESULTS: After 28 days of chronic unpredictable stress (CUS) the animals submitted to this protocol displayed less weight gain than control animals. After 5 weeks of recovery the weight gain rebounded to similar values of controls. In addition, following CUS, fasting insulin levels were increased and were accompanied by signs of impaired glucose tolerance and elevated serum corticosteroid levels. This biochemical profile persisted into the post-stress recovery period, despite the restoration of baseline corticosteroid levels. The mRNA expression levels of peroxisome proliferator-activated receptor (PPAR)-γ and lipocalin-2 in white adipose tissue were, respectively, down- and up-regulated. CONCLUSIONS: Reduction of PPAR-γ expression and generation of a pro-inflammatory environment by increased lipocalin-2 expression in white adipose tissue may contribute to stress-induced glucose intolerance.