We revealed the therapy effect of the stable gastric pentadecapeptide BPC 157 (10 μg/kg, 10 ng/kg ig or po) with specific activation of the collateral rescuing pathways, the azygos vein, on bile duct ligation in particular, and acute pancreatitis as local disturbances (i.e., improved gross and microscopy presentation, decreased amylase level). Additionally, we revealed the therapy’s effect on the acute pancreatitis as vascular failure and multiorgan failure, both peripherally and centrally following “occlusion-like” syndrome, major intoxication (alcohol, lithium), maintained severe intra-abdominal hypertension, and myocardial infarction, or occlusion syndrome, and major vessel occlusion. The application-sacrifice periods were ligation times of 0–30 min, 0–5 h, 0–24 h (cured periods, early regimen) and 4.30 h–5 h, 5 h–24 h (cured periods, delayed regimen). Otherwise, bile duct-ligated rats commonly presented intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, gross brain swelling, hemorrhage and lesions, heart dysfunction, lung lesions, liver and kidney failure, gastrointestinal lesions, and severe arterial and venous thrombosis, peripherally and centrally. Unless antagonized with the key effect of BPC 157 regimens, reversal of the inferior caval and superior mesenteric vein congestion and reversal of the failed azygos vein activated azygos vein-recruited direct delivery to rescue the inferior-superior caval vein pathway; these were all antecedent to acute pancreatitis major lesions (i.e., acinar, fat necrosis, hemorrhage). These lesions appeared in the later period, but were markedly attenuated/eliminated (i.e., hemorrhage) in BPC 157-treated rats. To summarize, while the innate vicious cycle may be peripheral (bile duct ligation), or central (rapidly developed brain disturbances), or peripheral and central, BPC 157 resolved acute pancreatitis and its adjacent syndrome.

Background/Objectives: Acute necrotizing pancreatitis (ANP) with secondary infection of necrotic tissue is associated with a high rate of complications and mortality. The optimal approach is still debatable, but the minimally invasive modality has gained great attention in the last decade as it follows the principle of applying minimal surgical trauma to achieve a satisfying therapeutic objective. We compared clinical outcomes between the step-up approach (SUA) and open necrosectomy (ON) in the treatment of acute necrotizing pancreatitis. Methods: A prospective cohort study over the period of 2011–2021 in a university teaching hospital was performed. Results of 99 consecutive patients with ANP who required surgical/radiological intervention were collected. A case match analysis (2:1) was performed, and the final groups comprised 40 patients in the OA group and 20 patients in the SUA group. Demographic, clinicopathologic, and treatment data were reviewed. Results: Baseline characteristics and disease severity were comparable between the two groups. The patients from the SUA group had a significantly lower morbidity rate and rate of pancreatic insufficiency. Death occurred in 4 of 20 patients (20%) in the SUA group and in 11 of 40 patients (27.5%) in the ON group (risk ratio with the step-up approach, 0.72; 95% confidence interval, 0.26 to 1.99; p = 0.53). Conclusions: A minimally invasive step-up approach provides comparable outcomes to open necrosectomy in the treatment of ANP with infected pancreatic necrosis. While mortality and hospital stay were comparable between the groups, morbidity and pancreatic insufficiency were significantly lower in the SUA group. Further studies on a larger number of patients are required to define the place of SUA in the modern treatment of ANP.

INTRODUCTION Psychogenic nonepileptic seizure (PNES) is a sudden change in a person's behavior, perception, thinking, or feeling that is usually time limited and resembles, or is mistaken for, epilepsy but does not have the characteristic electroencephalographic (EEG) changes that accompanies a true epileptic seizure [1]. It is considered that PNES is a somatic manifestation of mental distress, in response to a psychological conflict or other Stressors [2]. A wide spectrum of clinical presentation includes syncope, generalized tonic-clonic seizure, simple and complex partial seizure, myoclonic seizure, frontal lobe seizures and status epilepticus [3]. Coexistence of epilepsy and PNES is seen in approximately 9% of cases [5]. Between 25-30% of patients referred to tertiary centers and initially diagnosed as refractory epilepsy were on further examination diagnosed as PNES [6,7]. In DSM-IV [12] PNES are usually categorized under conversion disorder with seizures or convulsions. However, psychiatric basis of PNES may be anxiousness (panic attack), somatization or factitious disorder, simulation, dissociative disorders and psychosis [1]. AIM The aim of the study was to establish clinical phenomenology and EEG characteristics as well as basic psychiatric disorder in patients with PNES. METHOD In a retrospective study covering the period from January 1st 1999 till April 31 st 2003, 24 patients (22 female, 2 male) treated at the Institute of Neurology in Belgrade were analyzed. PNES were defined as sudden change in behavior incoherent with epileptiform activity registered on EEG. Possible PNES were determined on the basis of history data and clinical examination during the attack but definitive confirmation was established only by the finding of no ictal EEG changes during typical seizure of each patient. Patients with coexisting epilepsy were included in the study, too. At least two standard EEG (range 2-6, median 4) were performed at the beginning of diagnostic evaluation. Demographic data, clinical presentation (apparent loss of consciousness, type of convulsion and associated clinical signs) and placebo-induced seizures (administration of saline near the cubital vein) with EEG or video-EEG monitoring were analyzed. Basic psychiatric disorder was classified according to DSM IV classification criteria. RESULTS Duration of PNES was 4.7 years (range from 2 months to 30 years). The time from onset to the diagnosis of PNES was 4.5 years. Epilepsy comorbidity was diagnosed in 9 patients (37.5%). The average time of use of antiepileptic drugs (AED) in the group of isolated PNES was 2.4 years and 20% of patients were treated with two or more AED. The vast majority of patients presented with bilateral convulsions (54.16%) with apparent loss of consciousness found in 91.6% of cases. Ictal iwury (16.7%), tongue bite (4.2%) and premonition of the seizure (17.4%) were uncommon. Variability in clinical presentation of seizures was found in over half of patients (57%). Psychological trigger could be determined in over 60% of patients. EEG findings in a group with isolated PNES suggesting the existence of epileptiform activity was found in one case. EEG monitoring of placebo-induced seizure was performed in 20 patients, of whom 19 (95%) showed typical habitual attack with no electroclinical correlate. In 70% of cases conversion disorder DSM-IV criteria were fulfilled. Somatization disorder and undifferentiated somatoform disorder were found in 3 patients. The diagnosis of factitious disorder was made in one case and only two patients were undiagnosed according to DSM-IV. DISCUSSION Average delay from onset to diagnosis of PNES in larger studies was estimated to be approximately 7 years [8]. Even though diagnostic delay in our study was shorter, organizational reasons for this could not be found. Longer duration of a typical attack (compared to the epileptic seizure), apparent loss of consciousness, bilateral convulsion behavior and significant clinical variability in absence of typical epileptic elements such as tongue bite and ictal iwury could be the main clinical manifestation of PNES. We found rare interictal abnormalities (6.7%) in the group with isolated PNES and significant percentage (77.7%) in patients with coexisting epilepsy which is coherent with other reports [8]. The latest could lead to prolonged delay in appropriate diagnosis and suitable treatment. Clear psychological trigger wasn't noted in whole group of patients (61 %). This, however, is not unusual since PNES represents a chronic disorder with repeated triggering that could lead to less significant role of the same psychological trigger in developed PNES. Even insufficiently resolved in ethical terms, placebo-induced procedure was of huge sensitivity. In clinical practice conversion disorder is hard to differ from malingering or implementation of secondary gain. One could make the conclusion only on the basis of detailed and careful estimation of the symptoms developing context Conversion disorder is more prevalent among women (from 2:1 to 10:1) [4, 13] but modest percentage of affected men could be explained only by limited sample in this study. CONCLUSION PNES is often replaced with epilepsy and in number of cases clinical differentiation is not easy. One should be acquainted with clinical presentation of PNES as well as its psychiatric origin in order to adequately recognize and treat the disorder.

Liver transplantation represents the only curative method for end-stage liver disorders and certain liver malignancies. Over the last three decades, advancements in immunosuppression, surgical technique, and intensive care measures have resulted in improved patient and graft survival outcomes, but a deficit of donor organs is constantly the major issue that limits our ability to reduce the mortality on the liver transplant waiting list. To address this, marginal grafts and those from donors after cardiac death are increasingly employed, but these strategies necessitated novel methods to improve the preservation and quality of liver grafts and the most promising one is liver machine perfusion (LMP). LMP evolved significantly in the past 10 years, and consequently, it is gradually establishing itself as a standard protocol at many transplant centers. However, many unresolved questions remain concerning the indications, types, and protocols associated with LMP. Therefore, continuous research is necessary to determine optimal guidelines and recommendations for its clinical application. This review aims to analyze the development of liver machine perfusion, including its different modalities underlying mechanisms of operation, and provide an overview of its historical evolution, current status, and future prospects.

Portopulmonary hypertension (PoPH) and hepatopulmonary syndrome (HPS) present two vascular complications of portal hypertension, which make opposite extremes occur against the same pathophysiological background. In PoPH, vasoconstriction predominates, along with gradual remodeling of pulmonary arteries, while HPS develops due to pathological vasodilation and creation of intrapulmonary shunts. Even though they come about by different mechanisms, both disorders significantly affect quality of life, survival, and the possibility of liver transplant. In the early phases, in clinical practice, symptoms are mainly mild and nonspecific, and overlapping with symptoms of advanced liver disease often delays forming a diagnosis. In PoPH, elevated pressures in pulmonary arteries and increased vascular resistance are observed, while HPS exhibits arterial hypoxemia with normal or lowered pulmonary pressure. Standard diagnostic workup includes echocardiography, right-heart catheterization, and analysis of the arterial gases. In patients with severe PoPH, pronounced pulmonary hypertension can represent absolute contraindication for liver transplantation due to risk of acute right heart failure during operation. Conversely, HPS usually resolves itself after a successful transplant, which confirms that the transplant is an indication of being potentially curative. Therapeutic possibilities for both states are still limited. In PoPH, specific vasodilators and supportive measures are applied, while HPS treatment is mostly supportive, directed at maintaining oxygenation until the transplant. Future research should be focused on the development of targeted therapies that address vascular remodeling, angiogenesis, and oxidative stress, as well as on the standardization of diagnostic criteria and multicentric cooperation. This approach would facilitate earlier recognition, a precise assessment of transplantability, and a better long-term outcome for patients with portal hypertension and lung vascular complications. Key Points: Portopulmonary hypertension (PoPH) and hepatopulmonary syndrome (HPS) represent two opposite vascular complications of portal hypertension, posing distinct challenges for liver transplantation. This review summarizes their pathophysiology, diagnostic pathways, and therapeutic strategies, emphasizing the importance of hemodynamic profiling and multidisciplinary management to optimize transplant outcomes.

Intramural duodenal hematoma (IDH) is a rare entity and is generally associated with trauma. Spontaneous (nontraumatic) intramural duodenal hematoma is associated with bleeding disorders, anticoagulation therapy, alcoholism, pancreatitis, tumours and duodenal ulcers. We report two cases of spontaneous intramural duodenal hematoma in middle-aged men who subsequently developed pancreatitis. The underlying pathophysiology is still unclear. In the cases described, it is not clear whether the intramural duodenal hematoma contributed to the development of pancreatitis or pancreatitis has contributed to the development of IDH.