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Acute Respiratory Distress Syndrome (ARDS) is a complex and progressive lung injury that results in respiratory failure, often caused by pulmonary or systemic disorders. We present a 32-year-old male who developed ARDS following intranasal inhalation of cocaine. Diagnosis was established thorough clinical evaluation, identification of characteristic ultrasonographic patterns, and careful exclusion of other potential causes. The patient was managed with conservative medical therapy, including non-invasive ventilation, bronchodilators, antibiotic therapy, and comprehensive supportive care. Despite initial concerns about the severity of his condition, the patient's outcome was favourable, reflecting the diverse presentations and potential reversibility of ARDS. This case highlights two main aspects: i) the critical role of emergency physicians in recognizing and managing ARDS, even when the underlying cause is not immediately apparent; and ii) the importance of considering illicit drug use as a potential trigger during the initial assessment of respiratory complications.

Takotsubo syndrome (TS) is a transient cardiac condition characterized by regional systolic dysfunction, often precipitated by emotional or physical stressors. The pathophysiology of TS is not fully understood, but evidence suggests that it may be influenced by multiple factors. We present a case of TS following a traumatic left humerus fracture in an 82-year-old male patient with hypertension. Diagnosis was confirmed through comprehensive clinical evaluation, identification of ECG abnormalities, echocardiographic findings, and exclusion of other diseases. The patient’s management consisted of β-blockers, aspirin, and supportive care. Despite initial concerns, the patient's clinical course was uneventful, illustrating the various presentations of TS. This case emphasizes that TS can occur as a result of a traumatic event, particularly among older individuals with comorbidities. Early recognition and appropriate management are essential for optimizing outcomes.

Upper Gastro-Intestinal Bleeding (UGIB) spans from minor bleeding to life-threatening events. Identification of early signs of shock, proper management of hemodynamically unstable patients, and correct risk stratification are essential for an appropriate diagnostic workup and therapy. This case reports a young man admitted to the emergency department with haematemesis. His medical history was unremarkable, without any risk factors for gastrointestinal bleeding. A few hours after admission, further episodes of haematemesis occurred, and the patient's condition rapidly deteriorated to irreversible shock. A contrast-enhanced computed tomography (CECT) revealed morphological features of chronic liver disease and oesophagal varices. The patient underwent upper gastrointestinal endoscopy, confirming oesophagal varices with massive bleeding. Although promptly applied, endoscopic hemostasis was ineffective, and the patient died twenty-four hours after admission. Based on this case, we reviewed the diagnostic and therapeutic approaches for patients with massive UGIB and provided a practical approach to this life-threatening emergency.

The enteric nervous system (ENS) is the third division of the autonomic autonomic nervous system and the largest collection of neurons outside the central nervous system (CNS). The ENS has been referred to as “the brain in the gut” or “the second brain of the human body” because of its highly integrated neural circuits controlling a vast repertoire of gut functions, including absorption/secretion, splanchnic blood vessels, some immunological aspects, intestinal epithelial barrier, and gastrointestinal (GI) motility. The latter function is the result of the ENS fine-tuning over smooth musculature, along with the contribution of other key cells, such as enteric glia (astrocyte like cells supporting and contributing to neuronal activity), interstitial cells of Cajal (the pacemaker cells of the GI tract involved in neuromuscular transmission), and enteroendocrine cells (releasing bioactive substances, which affect gut physiology). Any noxa insult perturbing the ENS complexity may determine a neuropathy with variable degree of neuro-muscular dysfunction. In this review, we aim to cover the most recent update on genetic mechanisms leading to enteric neuropathies ranging from Hirschsprung’s disease (characterized by lack of any enteric neurons in the gut wall) up to more generalized form of dysmotility such as chronic intestinal pseudo-obstruction (CIPO) with a significant reduction of enteric neurons. In this line, we will discuss the role of the RAD21 mutation, which we have demonstrated in a family whose affected members exhibited severe gut dysmotility. Other genes contributing to gut motility abnormalities will also be presented. In conclusion, the knowledge on the molecular mechanisms involved in enteric neuropathy may unveil strategies to better manage patients with neurogenic gut dysmotility and pave the way to targeted therapies.

Non-celiac gluten sensitivity is still an undefined syndrome with several unsettled issues despite the increasing awareness of its existence. Gluten is likely responsible for the clinical picture in a subset of patients, whereas in other cases it concurs to this syndrome together with fermentable mono-oligo-disaccharides and polyols and wheat proteins (e.g., amylase trypsin inhibitors). Innate immunity plays a pivotal role in the development of this syndrome, which is characterized by gut inflammation without villous atrophy and likely changes of intestinal barrier function. Data on its epidemiology are still undefined and largely variable. In the USA its prevalence varies from 0.6% to 6% in primary or tertiary care, respectively. Clinically, patients complain of gastrointestinal and extra-intestinal symptoms triggered by the ingestion of gluten without evidence of celiac disease and wheat allergy. Intestinal symptoms resemble those of irritable bowel syndrome, whereas neurological signs are quite common among extra-intestinal manifestations. So far, there are no biomarkers for non-celiac gluten sensitivity, but about half of patients shows anti-gliadin antibodies of immunoglobulin G class. Although not specific for non-celiac gluten sensitivity, the detection of such antibodies can support the diagnosis in patients with gluten-related symptoms. In the absence of diagnostic biomarkers a double-blind, placebo-controlled food challenge is currently the best way for confirming non-celiac gluten sensitivity. Studies aimed at clarifying the pathophysiological, clinical and laboratory features of non-celiac gluten sensitivity will help a better management of patients with this novel and intriguing clinical entity.