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Amyloidosis is a group of diseases characterized by the extracellular deposition of abnormally folded, insoluble proteins that lead to organ dysfunction. While it commonly affects the cardiovascular system, gastrointestinal (GI) tract involvement is undetermined. Recent research has focused on understanding the pathophysiology, diagnostic challenges, and therapeutic approaches to GI amyloidosis, particularly in systemic amyloid light-chain (AL) and amyloid A (AA) forms. GI manifestations can include motility disorders, bleeding, and, in severe cases, bowel obstruction. This review highlights the importance of the early recognition of digestive symptoms and associated imagistic findings in GI amyloidosis by analyzing the research that included clinical, pathological, and endoscopic approaches to amyloidosis. A systematic search of the PubMed and Scopus databases identified 19 relevant studies. Our findings showed that amyloid deposits commonly affect the entire GI tract, with AL amyloidosis being the most predominant form. Endoscopic evaluations and biopsy remain key diagnostic tools, with Congo Red staining and mass spectrometry being used to confirm amyloid type. Although progress has been made in diagnosis, the absence of targeted therapies and the indistinct nature of GI symptoms continue to be challenging.

Background: Acute pancreatitis is an inflammation of the pancreas with variable outcomes depending on its severity. Multiple systems of prediction have been proposed, each with variable specificity and sensitivity and with uneven clinical use. Ferritin is a versatile protein associated with various acute and chronic conditions. Aims: In our study, we aimed to assess the association of serum ferritin and the ferritin-to-hemoglobin ratio (FHR) with the severity of acute pancreatitis. Methods: A retrospective study was conducted in our hospital from January 2020 to September 2022 and included 116 patients with acute pancreatitis (graded according to the revised Atlanta classification). Serum ferritin and FHR were determined next to established laboratory parameters in the first 24 h following admission (hematological parameters, amylase, lipase, C-reactive protein, D-dimers, lactate dehydrogenase). We performed a receiver operating characteristic curve analysis for potential predictors. Also, we made correlations and conducted univariate and multivariate analyses for all potential severity biomarkers. Results: The median values of serum ferritin and FHR differed significantly between patients with severe acute pancreatitis and mild cases (serum ferritin: 352.40 vs. 197.35 ng/mL, p = 0.011; FHR: 23.73 vs. 13.74, p = 0.002) and between patients with organ failure and those without organ failure (serum ferritin: 613.45 vs. 279.65 ng/mL, p = 0.000; FHR: 48.12 vs. 18.64, p = 0.000). The medians of the serum ferritin and FHR levels were significantly higher in non-survivors compared with survivors (serum ferritin: 717.71 vs. 305.67 ng/mL, p = 0.013; FHR: 52.73 vs. 19.58, p = 0.016). Serum ferritin and FHR were good predictors for organ failure and mortality, next to D-dimers and procalcitonin (AUC > 0.753 for organ failure and AUC > 0.794 for mortality). In univariate regression analysis, serum ferritin and FHR were independent variables for moderate–severe forms of acute pancreatitis. Still, adjusting the multivariate analysis, only FHR remained a significant predictor. The cut-offs for serum ferritin and FHR for predicting organ failure were 437.81 ng/mL (sensitivity, 71%; specificity, 75%) and 45.63 (sensitivity, 61%; specificity, 88%), and those for mortality during hospitalization were 516 ng/mL (sensitivity, 83%; specificity, 74%) and 51.58 (sensitivity, 66%; specificity, 86%). Conclusions: Serum ferritin and the ferritin-to-hemoglobin ratio stood out in this study as valuable and accessible predictors of disease severity in the early assessment of acute pancreatitis, next to established severity serum markers (CRP, fibrinogen, D-dimers).

(1) Background: Currently available guidelines require upper gastrointestinal (GI) endoscopy with biopsy sampling for adult celiac disease (CD) diagnosis. Based on the pediatric experience, there has been a growing interest if serology-based diagnosis would be possible for adult CD also. Our aim was to analyze the associated upper GI tract lesions in newly diagnosed CD patients, to see if significant associated pathology is detected during index endoscopy, which might impact patient management not related to CD. (2) Methods: We performed a retrospective analysis of newly diagnosed CD cases diagnosed over a period of 7 years (2014–2020). Demographic, clinical, laboratory, endoscopy and histopathology data were collected from the patients’ charts. Diagnosis was set according to ACG Guideline 2013. (3) Results: Altogether 79 patients were recruited for this study purpose, 75.9% female, median age 39 years. All patients had positive CD-specific serology and atrophic mucosal injury in duodenal biopsy samples. Besides villous atrophy, associated endoscopic findings were detected in 42/79 (53.16%) of patients. Most of the gastric lesions were minor endoscopic findings—small sliding hiatal hernias, non-specific chronic gastritis, but we also found two cases of peptic ulcers, one case of metaplastic gastritis, six cases of atrophic gastritis and one subepithelial lesion. Only one patient had changes in the duodenum except CD-related findings—an inflammatory polyp in the duodenal bulb. No malignancies were found. (4) Conclusions: In our cohort, there was a significant number of newly diagnosed CD patients who had associated lesions during the index upper GI endoscopy, but most of them were minor endoscopic findings.

The Golgi apparatus plays a central role in protein sorting, modification and trafficking within cells; its dysregulation has been implicated in various cancers including those affecting the GI tract. This review highlights two Golgi target proteins, namely GOLPH3 and GOLGA proteins, from this apparatus as they relate to gastroenterological cancers. GOLPH3—a highly conserved protein of the trans-Golgi network—has become a key player in cancer biology. Abnormal expression of GOLPH3 has been detected in various gastrointestinal cancers including gastric, colorectal and pancreatic cancers. GOLPH3 promotes tumor cell proliferation, survival, migration and invasion via various mechanisms including activating the PI3K/Akt/mTOR signaling pathway as well as altering Golgi morphology and vesicular trafficking. GOLGA family proteins such as GOLGA1 (golgin-97) and GOLGA7 (golgin-84) have also been implicated in gastroenterological cancers. GOLGA1 plays an essential role in protein trafficking within the Golgi apparatus and has been associated with poor patient survival rates and increased invasiveness; GOLGA7 maintains Golgi structure while having been shown to affect protein glycosylation processes. GOLPH3 and GOLGA proteins play a pivotal role in gastroenterological cancer, helping researchers unlock molecular mechanisms and identify therapeutic targets. Their dysregulation affects various cellular processes including signal transduction, vesicular trafficking and protein glycosylation, all contributing to tumor aggressiveness and progression.

Introduction. The concept of underactive bladder is relatively new. Currently there is no generally accepted definition of this pathology. Diagnosis depends on urodynamic findings, and symptoms are usually rare and intricated with the symptoms of other urinary pathology. Matherials and methods. This review examines the current literature on underactive bladder regarding pathology, definition, diagnosis, current guidelines, and any further potential medical developments. Conclusions. Underactive bladder is a poorly understood pathologic condition. Only since 2002 has there been any consensus regarding the definition. The diagnosis relies only on urodynamics; clinical diagnosis is a challenge even for a consultant; and treatment does not seem to alleviate much of the suffering. This disease remains underrecognized and undertreated. More research is needed to identify less invasive diagnosis tools and treatment for this pathology.

Vitamin D deficiency is one of the most common medical conditions, with approximately one billion people having low vitamin D levels. Vitamin D is associated with a pleiotropic effect (immunomodulatory, anti-inflammatory and antiviral), which can be essential for a better immune response. The aim of this research was to evaluate the prevalence of vitamin D deficiency/insufficiency in hospitalized patients focusing on demographic parameters as well as assessing the possibility of its associations with different comorbidities. Of 11,182 Romanian patients evaluated in the study over 2 years, 28.83% had vitamin D deficiency, 32.11% insufficiency and 39.05% had optimal vitamin D levels. The vitamin D deficiency was associated with cardiovascular disorders, malignancies, dysmetabolic disorders and SARS-CoV2 infection, older age and the male sex. Vitamin D deficiency was prevalent and showed pathology association, while insufficiency of vitamin D (20–30 ng/mL) had lower statistical relevance and represents a grey zone in vitamin D status. Guidelines and recommendations are necessary for homogeneity of the monitoring and management of inadequately vitamin D status in the risk categories.

Esophageal stroke, also known as acute esophageal necrosis or Gurvits syndrome, is an entity that has gained more and more recognition in the last two decades. It is also named “black esophagus” because of striking black discoloration of the esophageal mucosa, with an abrupt transition to normal mucosa at the gastroesophageal junction. Its most common clinical presentation is represented by upper gastrointestinal bleeding and esophagogastroduodenoscopy is the main diagnostic tool. Among the etiopathogenetic and multiple predisposing factors described are hypovolemia, shock state, ischemia, congestive heart failure, acute renal failure, infections, trauma, and diabetes mellitus. Current management of this condition consists of treating the underlying pathology, nil per os, and antacid administration in uncomplicated cases. Although most of the cases have favorable prognosis, complications such as pneumomediastinum or esophageal stricture may occur and fatal cases are a consequence of underlying comorbidities.

Background: Secondary thrombotic thrombocytopenic purpura (TTP) due to interferon beta-1a intramuscular (im) treatment is an uncommon adverse effect with only a few cases in multiple sclerosis patients reported worldwide. TTP together with haemolytic uremic syndrome (HUS) are classic forms of thrombotic microangiopathy, characterized by small-vessel platelet micro-thrombi that manifest clinically in a similar manner. Most common signs and symptoms include bruises and ecchymosis, neurologic symptoms and renal impairment. Interferon beta-1a represents one of the first-line therapies for relapsing-remitting multiple sclerosis due to its accessibility and efficacy. Case presentation: A 36-year-old woman who was previously diagnosed with relapsing-remitting multiple sclerosis had received weekly intramuscular injections with beta-interferon-1a (Avonex 30 mcg). After 9 months of treatment, she presented bruises and ecchymosis on her limbs and torso, epistaxis, gingival bleeding aggravated within 48 h and a persistent headache that was non-responsive to common analgesics. Haematology tests revealed typical results for thrombotic microangiopathy, including severe thrombocytopenia (4000/mm3) and microangiopathic haemolytic anaemia with frequent schistocytes on the peripheral blood smear. Once the beta-interferon administration was ceased and upon the initiation of methylprednisolone, the symptoms remitted. Conclusions: In this case study, we portrayed the particular association between the remission phase of multiple sclerosis and the violent onset of interferon-induced thrombotic thrombocytopenic purpura.

Celiac disease (CD) is a systemic autoimmune disease driven by gluten-ingestion in genetically predisposed individuals. Although it primarily affects the small bowel, CD can also involve other organs and manifest as an extraintestinal disease. Among the extraintestinal features of CD, hematologic ones are rather frequent and consist of anemia, thrombocytosis (thrombocytopenia also, but rare), thrombotic or hemorrhagic events, IgA deficiency, hyposplenism, and lymphoma. These hematologic alterations can be the sole manifestation of the disease and should prompt for CD testing in a suggestive clinical scenario. Recognition of these atypical, extraintestinal presentations, including hematologic ones, could represent a great opportunity to increase the diagnostic rate of CD, which is currently one of the most underdiagnosed chronic digestive disorders worldwide. In this review, we summarize recent evidence regarding the hematological manifestations of CD, with focus on practical recommendations for clinicians.

Introduction: Despite being one of the most frequent chronic digestive diseases worldwide, with a prevalence of 1%, celiac disease (CD) remains severely underdiagnosed. Among the instruments used to improve its diagnostic rate, hematologic parameters have been proposed as screening tests to select patients with an increased probability of having CD. Assessment of coagulation is included in routine check-ups, and CD has been reported to be associated with coagulopathy. We aimed to assess if subtle changes in coagulation tests could be used in clinical practice to prompt testing for CD. Methods: We retrospectively recruited all patients with clinical suspicion for CD during a study period of 7 years (between 2015 and 2022), who were tested using IgA tissue transglutaminase (tTG) serology and serum total IgA (IgG tTG in case of IgA deficiency) and who underwent upper gastrointestinal endoscopy with multiple biopsy sampling of the duodenal bulb and distal duodenum. We stratified patients into three groups: newly diagnosed CD, gluten-free diet-treated CD, and non-CD controls. Results: Altogether, there were 133 CD patients (71 newly diagnosed, 62 GFD-treated) and 57 non-CD controls. Mean age and gender distribution were similar among the three groups: 43.3 years for newly diagnosed CD, 41.6 years for non-CD controls, and 44 years for GFD-treated CD patients, with a male gender distribution of 21.1%, 28%, and 24.1%, respectively. Among the included newly diagnosed CD patients, 14% had a prolonged INR. The mean INR was slightly higher in newly diagnosed CD patients, compared to GFD-treated CD patients and non-CD controls: 1.12 ± 0.30, 1.02 ± 0.83, and 1.00 ± 0.08, respectively (p = 0.009). Consequently, prothrombin activity was slightly lower in newly diagnosed CD patients, compared to GFD-treated CD and non-CD controls: 94.9 ± 19.3%, 102.3 ± 12.8%, and 101.9 ± 15.15, respectively. Interestingly, after GFD, the mean INR and prothrombin activity of CD individuals reached a value similar to that of non-CD controls. Conclusions: Subtle changes in INR, defined as a value within the normal range, but closer to the upper limit, could be an indicator of probability for CD.

Anomalies in lipid metabolism involve multifactorial pathogenesis, among other factors, being associated with an inflammatory state and disturbances in vitamin D status. The literature has focused on the binary relationships between inflammation and dyslipidemia, vitamin D and dyslipidemia, or vitamin D and inflammation. Our study aimed to explore the link between all these three factors: 25-OH vitamin D serum levels, the presence of inflammation assessed through serum C-reactive protein (CRP), and serum lipid profile in 2747 hospitalized patients. Our results showed a positive correlation of HDL-C with 25 (OH) vitamin D and a negative correlation of HDL-C with CRP. This relationship had different patterns in the statistical network analysis. The network analysis patterns are preserved for males and females, except for the relationship between CRP and vitamin D, which is present in male cases and absent in females. The same triangular relationship between all three—CRP, vitamin D, and HDL-C was found with different strengths of partial correlation in obese and non-obese patients. This pattern was similar in patients with and without fatty liver. A shifted pattern was found in the network analysis of hypertensive patients. The CRP was negatively correlated with vitamin D and HDL-C, and vitamin D was positively correlated with HDL-C in non-hypertensive patients. Castelli’s Risk indexes I and II were positively associated with CRP, suggesting that increased cardiovascular risk is proportional to an inflammatory state. The triad formed by altered serum lipid levels, inflammation, and vitamin D represents a complex relationship marked by specific dynamics between lipidic fractions such as HDL-C and C-reactive protein and vitamin D.

Background and Objectives: Glucose metabolism alterations are very common in solid pancreatic lesions, particularly in pancreatic cancer. Similarly, diabetes and especially new-onset diabetes (NOD) have been associated with the malignant transformation of pancreatic cysts. We aimed to assess the prevalence and relevant associations of glycemic abnormalities in pancreatic cystic lesions (PCLs) in a retrospective analysis. Materials and Methods: We retrospectively recruited all patients who underwent endoscopic ultrasound for a PCL over a period of 36 months (January 2018 to December 2021). Final diagnosis was set by means of tissue acquisition, surgery, follow-up, or board decision. Demographic and clinical data, laboratory workup, and imaging features were extracted from the patients’ charts according to a predefined protocol. We considered fasting blood glucose (FBG) and HbA1c values and stratified the patients as nondiabetic (FBG ≤ 99 mg/dL, HbA1c ≤ 5.6%, no history of glycemic abnormalities), prediabetic (FBG 100–125 mg/dL, HbA1c 5.7–6.4%), or diabetic (long-lasting diabetes or NOD). Results: Altogether, 81 patients were included, with a median age of 66 years, and 54.3% of them were male. The overall prevalence of fasting hyperglycemia was 54.3%, comprising 34.6% prediabetes and 22.2% diabetes, of which 16.7% had NOD. The mean FBG and HbA1c levels were higher in malignant and premalignant PCLs (intraductal papillary mucinous neoplasm (IPMN), mucinous cystic neoplasm (MCN), cystadenocarcinoma, and cystic neuroendocrine tumor) compared to the benign lesions (pseudocysts, walled-off necrosis, and serous cystadenoma): 117.0 mg/dL vs. 108.3 mg/dL and 6.1% vs. 5.5%, respectively. Conclusions: Hyperglycemia and diabetes are common in PCLs, with a high prevalence in premalignant and malignant cysts. Screening and follow-up for glycemic abnormalities should be routinely conducted for PCLs, as they can contribute to a tailored risk assessment of cysts.

Background: Infective endocarditis (IE) is a pathological condition caused by various microbial agents that can lead to severe complications affecting the heart. Accurate diagnosis is crucial for the effective management of patients with IE. Blood culture is the gold standard for identifying the primary infectious agents, which is a key factor in diagnosing IE using the modified Duke criteria. Objective: The main objective of this study was to investigate the distribution of the etiological agents of IE and the most common secondary diagnoses associated with it. Method: A total of 152 patients aged 23–95 years with a diagnosis of IE and proven etiology (through blood cultures or serological tests) were included in this study. Results: The most common etiological agent identified through blood tests was Enterococcus faecalis, which was detected in 39 patients (23.5%). Staphylococcus aureus was the second most common agent and was identified in 33 patients (19.9%), followed by Staphylococcus epidermidis, which was identified in 12 patients (13.1%). Nine patients (5.8%) had high levels of anti-Coxiella burnetti IgG phase I and II antibodies. Conclusions: IE is a leading cause of death in the Department of Infectious Diseases. Early and accurate diagnosis, along with interdisciplinary treatment, can significantly increase the chances of patient survival. Currently, Enterococcus faecalis and Staphylococcus aureus are the dominant etiological agents of IE, highlighting the need to revise protocols for prophylaxis, diagnosis, and initial treatment of this condition.

Rheumatoid arthritis (RA) is an independent osteoporosis risk factor. Biologic and immunosuppressive treatment, and levels of homocysteine and 25-OH vitamin D may influence the trabecular bone score (TBS) in RA patients. We aimed to compare the effects of biological (b) and conventional synthetic (cs) disease-modifying anti-rheumatic drugs (DMARDs) on TBS in patients with RA and hyperhomocysteinemia (HHcy) or 25-OH vitamin D deficiency. Patients who had tests conducted for trabecular bone score, bone mineral density (BMD), homocysteine (Hcy) and 25-OH vitamin D at an interval of one year and met the inclusion criteria were enrolled in this retrospective study. Sixty-four patients with RA were enrolled and were divided into the following two groups: the first group (34 patients) had received treatment with bDMARDs and the second group (30 patients) had received csDMARDs. BDMARDs and csDMARDs had a positive influence on TBS and BMD. The best results were observed in the Adalimumab group (p = 0.033). Hyperhomocysteinemia and 25-OH vitamin D deficiency led to lower TBS values. Both bDMARDs and csDMARDs positively affected TBS and BMD in RA patients. High homocysteine serum levels or 25-OH vitamin D deficiency had a negative impact on TBS and BMD after 12 months. Our study aims to show the potential benefits of anti-TNF α drugs on TBS. This impact appears to be strongly associated with serum 25-OH vitamin D and homocysteine levels. Anti-TNF drugs may increase bone mineral density and microstructure. As a result, they may minimize the incidence of fractures in RA patients.

Chronic pancreatitis is characterised by progressive and irreversible damage of the pancreatic parenchyma and ductal system, which leads to chronic pain, loss of endocrine and exocrine functions. Clinically, pancreatic exocrine insufficiency becomes apparent only after 90% of the parenchima has been lost. Despite the simple definition, diagnosing chronic pancreatitis remains a challenge, especially for early stage disease. Because pancreatic function tests can be normal until late stages and have significant limitations, there is an incresing interest in the role of imaging techniques for the diagnosis of chronic pancreatitis. In this article we review the utility and accuracy of different imaging methods in the diagnosis of chronic pancreatitis, focusing on the role of advanced imaging (magnetic resonance imaging, endoscopic retrograde cholangiopancreatography and endoscopic ultrasound).

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) impacted the world and caused the 2019 coronavirus disease (COVID-19) pandemic. The clinical manifestations of the virus can vary from patient to patient, depending on their respective immune system and comorbidities. SARS-CoV-2 can affect patients through two mechanisms: directly by targeting specific receptors or by systemic mechanisms. We reviewed data in the latest literature in order to discuss and determine the risk of new-onset liver injuries due to COVID-19 in preexisting hepatic conditions. The particular expression of angiotensin-converting enzyme 2 (ACE2) receptors is an additional risk factor for patients with liver disease. COVID-19 causes more severe forms in patients with non-alcoholic fatty liver disease (NAFLD), increases the risk of cirrhosis decompensation, and doubles the mortality for these patients. The coinfection SARS-CoV-2—viral hepatitis B or C might have different outcomes depending on the stage of the liver disease. Furthermore, the immunosuppressant treatment administered for COVID-19 might reactivate the hepatic virus. The high affinity of SARS-CoV-2 spike proteins for cholangiocytes results in a particular type of secondary sclerosing cholangitis. The impact of COVID-19 infection on chronic liver disease patients is significant, especially in cirrhosis, influencing the prognosis and outcome of these patients.

Introduction. Hepatocellular carcinoma (HCC) is one of the most aggressive neoplasms and a leading cause of cancer-related deaths worldwide with an incidence that continues to increase. Data regarding epidemiology is heterogeneous worldwide. Even if viral hepatitis is known as an important risk factor for HCC development, non-alcoholic fatty liver disease (NAFLD) became a leading cause of HCC in developed countries. Despite the considerable improvements in diagnosis and therapy, the overall outcomes of HCC are still far from satisfactory. Objective. Data regarding epidemiology of HCC in Romanian population is scarce. This study aims to investigate HCC etiology, risk factors, the clinical impact of tumor location, and management of these patients. Materials and Methods. In this retrospective study, we used medical coding data to identify patients with a diagnosis of HCC from Central Military Emergency Hospital Dr. Carol Davila who were hospitalized between March 2020 and February 2023. Statistical analyses were carried out using SPSS 29.0.1.0. Continuous variables were compared using an analysis of variance (ANOVA) while the categorical variables were compared using the Chisquare test. Results. A total of 74 patients with a mean age of 65.29 (SD +/- 8.04) were diagnosed with HCC out of which 67.6% were males. Hepatitis C was the main cause of HCC (28.4%), followed by hepatitis B (25.7%) and alcoholic liver disease associated with hepatitis B (10.8%). Half of the patients found with HCC were known with cirrhosis. Furthermore, at the moment of the diagnosis, 25.7% of the patients were already stage IV, lung metastasis being the most frequent site of dissemination. The most frequent location of the tumor was the right liver lobe (64%). There was no association between the etiology of HCC and the location of the tumor. Hepatocellular carcinoma diagnoses was made at more than 4 months after the initial discovery of the liver lesion. The sensitivity of AFP levels in detecting HCC with a cut-off value of 20 ng/ml was only 56.9%. Conclusions. Our analysis revealed that in Romania viral hepatitis is still a major health problem in comparison with the actual trend. HCC is still diagnosed in advanced stages, despite the screening programs for patients at risk. Difficulty regarding optimal management could have been determined by Covid-19 Pandemic. Data highlights that we should develop better prevention strategies and that we need to implement better monitoring programs for the early diagnosis of HCC. [ABSTRACT FROM AUTHOR]

Introduction. Bariatric surgery represents the most efficient treatment addressing obesity and its related consequences. Even if the medical benefits for patients are huge due to weight loss, and despite technical improvements in bariatric procedures, it is still associated with different types of complications. Most of the complications appear due to nutrient deficiency, as absorption is compromised after surgical anatomy modification, but also secondary to inflammatory and mechanical pathways induced by surgical procedures. The most common deficiencies reported after bariatric surgery are vitamin B deficiency (74%), hypovitaminosis D which is described in 25-70% of patients, and iron deficiency in more than 30% of patients. These deficiencies are associated with a wide spectrum of clinical manifestations. Objective. The aim of this review is to identify neurological complications that occur after bariatric surgery. Methods. We performed a systematic search in two databases, PubMed and Google Scholar, from inception until February 2023, without language restrictions. We included all observational studies that described neurologic manifestations after the bariatric procedure regardless of the surgical technique used. Results. Nutritional impairment after bariatric surgery is common and implies a large spectrum of vitamin and micronutrient deficiencies, fat malabsorption, protein loss, and mineral deficiencies with different clinical manifestations. Neurological complications after bariatric surgery are very diverse with an occurrence within days to years after surgery, most frequently in patients with gastrointestinal or surgical complications. Any segment of the nervous system can be affected with different types of manifestations ranging from peripheral axonal neuropathy, nerve palsy secondary to compartment syndrome, encephalopathy, myelopathy, to psychiatric and demyelinating central nervous system diseases. Identifying patients at risk and systematic screening for nutrients deficiency with proper supplementation is essential for preventing neurological complications and lifelong sequelae. Conclusions. Complications after bariatric surgery have a broad spectrum of manifestations involving both peripheral and central nervous system and should be suspected and diagnosed as soon as possible to prevent long term sequelae. The risk of developing central nervous system demyelination or stroke events after bariatric surgery should be further evaluated in future studies. [ABSTRACT FROM AUTHOR]