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Background: Hashimoto's encephalopathy (HE) is a controversial immunological neuropsychiatric disease, with a poorly understood pathogenesis. It is characterized by symptoms of acute or subacute encephalopathy which usually occur in the presence of elevated levels of antithyroid antibodies. Even though it is also known as steroid responsive encephalopathy associated with autoimmune thyroiditis (SREAT), some cases appear to be steroid-resistant. This review examined whether treatment of Hashimoto's encephalopathy with intravenous immunoglobulin (IVIG) is associated with better clinical outcomes than the standard therapy. Additionally, we presented a case of a 59-year-old man who presented with severe neurological manifestations and was successfully treated with intravenous immunoglobulin., Methods: The online databases PubMed and EMBASE were searched., Results: A total of 1,365 articles were identified. After the deletion of 112 duplicates, 1,253 studies were screened by evaluating the title and abstract, focusing on Hashimoto's encephalopathy cases where IVIG were used. 846 studies were excluded because they were not relevant to the topic or included pediatric population. Therefore, 407 full-text articles were assessed for eligibility. The final analysis included 14 eligible articles after 393 were excluded (irrelevant texts, not written in English, full-text not available). In the majority of the selected case-reports, IVIG was associated with a good outcome, sometimes even with dramatic improvements in patient's status., Conclusion: In last years, intravenous immunoglobulin therapy proved its utility in Hashimoto's encephalopathy's treatment, being a well tolerated therapy associated with remarkable improvement in patient's status. Further research is still needed in order to define the optimal treatment protocol for Hashimoto's encephalopathy and to establish if intravenous immunoglobulin can also be used as a first-line therapy, alone or in combination with steroids., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Şorodoc, Constantin, Asaftei, Lionte, Ceasovschih, Sîrbu, Haliga and Şorodoc.)

Thromboembolic (TE) risk scores used for atrial fibrillation (AF) patients do not include mitral annular calcification (MAC) as a potential indicator of vascular disease. This research evaluated the correlation between MAC and TE risk scores (CHADS 2 and CHA 2 DS 2 -VASc). We compared TE risk score values and clinical and echocardiographic data in patients with and without MAC. We included, prospectively, 103 patients: 40.8% with AF, 83.5% with hypertension, 30.1% with type II diabetes mellitus, 79.6% with chronic heart failure, and 7.8% with a history of stroke. We identified MAC in 50.5% of patients. The mean CHADS 2 and CHA 2 DS 2 -VASc scores were 2.56 ± 1.135 and 4.57 ± 1.61, respectively. In MAC patients, both scores tended to increase significantly compared with the control (2.88 ± 1.114 versus 2.24 ± 1.06, p = 0.005, and 5.21 ± 1.51 versus 3.92 ± 1.46, p < 0.001, respectively). The left ventricular ejection fraction negatively correlated with the presence of MAC (r = -0.254, p = 0.01). The presence of MAC was a risk factor for vascular disease (OR = 2.47, χ 2 = 34.32, p < 0001). Conclusions: The presence of MAC is associated with greater TE risk scores and a higher risk of vascular disease. It appears that adding MAC as a vascular disease parameter to TE risk scores may have benefits for patients by improving their predictive value.

Despite being one of the most debilitating conditions encountered in the field of toxicology, there is a lack of neutralization measures for the toxins involved in acute corrosive poisoning, and this promotes progressive contact injury of deep tissues after poisoning has occurred. Multiple controversies still surround management strategies during the acute phase of poisoning and the long-term follow-up of the patient. Here, we report a severe case of intentional poisoning with nitric acid complicated by extensive injury of the upper digestive tract, multiple stricture formation, and complete dysphagia. Serial endoscopic dilation and insertion of a jejunostomy feeding tube were necessary, and underlying psychiatric illness negatively affected the outcome of the patient. We conclude that an interdisciplinary approach is necessary to properly reduce the extent of lesions and sequelae induced by corrosion. Early endoscopic mapping of injuries is of major importance to better predict the evolution and possible complications of poisoning. Interventional and reconstructive surgical procedures may significantly improve the life expectancy and quality of life of patients following intoxication with corrosive substances.

Hyponatremia is commonly encountered in the setting of heart failure, especially in decompensated, fluid-overloaded patients. The pathophysiology of hyponatremia in patients with heart failure is complex, including numerous mechanisms: increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, high levels of arginine vasopressin and diuretic use. Symptoms are usually mild but hyponatremic encephalopathy can occur if there is an acute decrease in serum sodium levels. It is crucial to differentiate between dilutional hyponatremia, where free water excretion should be promoted, and depletional hyponatremia, where administration of saline is needed. An inappropriate correction of hyponatremia may lead to osmotic demyelination syndrome which can cause severe neurological symptoms. Treatment options for hyponatremia in heart failure, such as water restriction or the use of hypertonic saline with loop diuretics, have limited efficacy. The aim of this review is to summarize the principal mechanisms involved in the occurrence of hyponatremia, to present the main guidelines for the treatment of hyponatremia, and to collect and analyze data from studies which target new treatment options, such as vaptans.

Objective: This study was performed to determine whether a dual-biomarker approach using N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and galectin-3 optimizes the diagnosis and risk stratification of acute cardiac dyspnea. Atypical clinical manifestations and overlapping pathologies require objective and effective diagnostic methods to avoid treatment delays., Methods: This prospective observational study included 208 patients who presented to the emergency department for acute dyspnea. NT-proBNP and galectin-3 were measured upon admission. The patients were divided into two groups according to the etiology of their clinical manifestations: cardiac and non-cardiac dyspnea. The patients' New York Heart Association functional class, left ventricular ejection fraction, and discharge status were assessed., Results: Diagnostic criteria for acute heart failure were fulfilled in 61.1% of the patients. NT-proBNP and galectin-3 were strongly and significantly correlated. Receiver operating characteristic analysis revealed similar areas under the curve for both markers in the entire group of patients as well as in the high-risk subsets of patients., Conclusions: The diagnostic performance of NT-proBNP and galectin-3 is comparable for both the total population and high-risk subsets. Galectin-3 adds diagnostic value to the conventional NT-proBNP in patients with acute cardiac dyspnea, and its utility is of major interest in uncertain clinical situations.