Chronic pancreatitis is an inflammatory disease that causes irreversible anatomical changes including infiltration of inflammatory cells, fibrosis and pancreatic calcification with destruction of the structure of the gland, leading to abdominal pain, endocrine and exocrine dysfunction. Pancreatic exocrine insufficiency (PEI) prevalence in chronic pancreatitis varies between 40 and 94%. PEI is diagnosed by direct and indirect tests. Nutritional status is assessed by anthropometric indicators; laboratory tests—hemoglobin, plasma proteins (albumin, prealbumin, retinol-binding protein, transferrin), fat-soluble vitamins A, D, E, K; micronutrients. Pancreatic enzyme replacement therapy (PERT) is a fundamental part of PEI treatment. An optimal PERT could prevent serious PEI complications such as metabolic bone disease, adverse cardiovascular events, cachexia, poor quality of life and mortality. A periodic screening for PEI complications with a respect to their primary and secondary prophylaxis is mandatory. Diabetes mellitus secondary to pancreatic disease is defined as pancreatogenic diabetes or type 3c diabetes mellitus. Patients with chronic pancreatitis are at increased risk for pancreatic cancer influenced by smoking, alcohol abuse, chronic inflammation and pancreatic stellate cells over-proliferation. However, chronic pancreatitis could be further complicated with splenic vein thrombosis, pseudocysts, duodenal or biliary obstruction, pseudoaneurysm and pancreatic duct stones which might require endoscopic or surgical treatment.

Lecithinized superoxide dismutase (PC-SOD) was found to have a significantly improved half-life in the bloodstream and better pharmacological effects compared with unmodified SOD. However, there is no direct evidence that parenterally administered PC-SOD decreases superoxide levels in blood and tissues in vivo. In the present study, we investigated the ability of PC-SOD versus unmodified SOD as a superoxide scavenger in mice subjected to oxidative stress. Experiments were performed on a lipopolysaccharide (LPS) mouse model of acute inflammation known to be accompanied by the overproduction of superoxide in the blood. The mice were divided into four groups: untreated (healthy; n = 6), LPS-treated (n = 7), LPS/SOD-treated (n = 6), and LPS/PC-SOD-treated (n = 7) mice. SOD and PC-SOD were injected intravenously. Blood samples were collected at four time intervals and analyzed by electron paramagnetic resonance (EPR) spectroscopy using a nitroxide probe, 3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (CMP). The following effects were observed: (i) In the blood of healthy mice, the EPR signal was significantly lower compared with the control (p < 0.001) and LPS-treated mice (p < 0.01); (ii) in the blood of LPS-treated mice, the EPR signal was identical to that of the control; and (iii) in the blood of LPS/SOD-treated mice collected immediately after enzyme injection, the EPR signal was significantly lower compared with the control (p < 0.01) and LPS-treated mice (p < 0.05). However, the effect disappeared in the samples collected 30 min and 1 h after enzyme injection. (iv) In LPS/PC-SOD-treated mice, the EPR signal was significantly lower compared with the control (p < 0.01) and LPS-treated mice (p < 0.05), even in the blood samples collected within 1 h after enzyme injection. The data indicate that the blood of healthy mice was characterized by a high reducing capacity, while the blood of LPS-treated mice was characterized by a high oxidative capacity. SOD decreased superoxide production immediately after enzyme injection. However, the effect was short-lived and disappeared within 30 min. PC-SOD effectively decreased superoxide production in the bloodstream of LPS-treated mice and restored the redox balance to the control level even two hours after enzyme injection. The effects of PC-SOD were more pronounced and long-lasting compared with those of SOD. The possible reason is the longer half-life of PC-SOD in the bloodstream, its better stability, and its slower clearance from the circulation due to the increased hydrophobicity of the enzyme and its interaction with plasma proteins. The data are discussed in the context of recent clinical trials showing that PC-SOD is a promising pharmaceutical product for adjuvant therapy of a variety of pathologies accompanied by inflammation, redox imbalance, and oxidative stress.

Background: Vitamin D (VD) insufficiency is present in chronic pancreatitis (CP), leading to increased cardiovascular risk, bone complications, impaired quality of life, and increased mortality. This study aimed to determine the prevalence of VD deficiency in patients with CP and to assess its relationship to CP progression and associated cardiovascular complications. Methods: Seventy patients were enrolled and evaluated for pancreatic exocrine insufficiency by fecal elastase-1, CP severity by M-ANNHEIM classification, cardiovascular risk by 10-year risk mortality scores (SCORE and FRS), and for arterial stiffness using pulse wave velocity (PWV) at a. carotis and a. femoralis. Determination of 25-hydroxyvitamin D was performed by an LC-MS/MS method. Resting energy expenditure was calculated using the Harris–Benedict formula. Results: Mean VD levels were 37.86 ± 24.36 nmol/L (range 3.854–99.874 nmol/L); only five patients were in sufficiency status. VD levels correlated significantly with body mass index (BMI) and resting energy expenditure. In patients with severe structural changes, we observed lower VD levels regardless of etiology (p < 0.01). VD levels were lower in patients with pancreatic exocrine insufficiency (PEI), p < 0.05. Patients with mild CP by M-ANNHEIM had lower levels of VD compared to moderate and advanced CP, p < 0.05. At a cut-off of VD 11.95 nmol/L, we verified pancreatic lithiasis with 89.4% sensitivity, 83.3% specificity, and AUC of 0.826 ± 0.113 (95% CI, 0.61–1). VD status worsened with the increase in the 10-year risk mortality by both SCORE and FRS and PWV, p < 0.05. Conclusions: Most of our patients with CP were VD insufficient. Monitoring of nutritional status in patients with CP is mandatory to prevent the development of malnutrition complications and the associated morbidity and mortality.

Background: Extrinsic compression of the left atrium (LA) is a rare and underrecognized condition that may result in significant hemodynamic compromise and atrial arrhythmias. The available evidence has been largely limited to isolated case reports and small case series, and clinical awareness has remained low. Methods: We performed a structured review of published case reports and case series indexed in PubMed between 2016 and 2026 describing extracardiac LA compression. A predefined and reproducible literature search strategy with explicit eligibility criteria was applied. The structured review included 22 publications reporting 23 individual cases of LA compression; in addition, two institutional cases with distinct etiologies were presented separately. Demographic characteristics, presenting symptoms, diagnostic modalities, complications, management strategies, and outcomes were synthesized descriptively. Results: The structured review identified gastroesophageal disorders, particularly hiatal hernia, as the most frequent etiology, followed by vascular, mediastinal, malignant, and musculoskeletal causes. Dyspnea was the most common presenting symptom, while hemodynamic compromise, pulmonary edema, and atrial arrhythmia represented the most frequent complications. Transthoracic echocardiography was the initial diagnostic modality in all reported cases, with computed tomography required for definitive etiological diagnosis. The two institutional cases illustrated both a common cause, hiatal hernia mimicking intracardiac mass, and a rare, aggressive malignant cause with extensive mediastinal involvement. Conclusions: Extrinsic LA compression arises from diverse extracardiac pathologies and may be clinically severe. Transthoracic echocardiography can serve as a pivotal first-line tool for early recognition and differentiation from intracardiac masses, while cross-sectional imaging is essential for etiological clarification. By integrating institutional experience with a structured synthesis of published cases, this review can provide practical insights to support timely diagnosis and management of this potentially life-threatening condition.