A retrospective study of pregnant patients with acute pancreatitis.

OBJECTIVE: Acute pancreatitis is a rare disease in pregnant patients. Although it may have serious maternal and fetal consequences, morbidity and mortality rates have decreased recently due to appropriate and rapid treatment with earlier diagnosis. The aim of this study was to evaluate pregnant patients diagnosed with acute pancreatitis. METHODS: The study included pregnant patients diagnosed with acute pancreatitis who were admitted to Adana City Training and Research Hospital in Adana, Turkey, between January 2014 and January 2022. Patients' files were screened. Patients' demographics, acute pancreatitis etiology, severity, complications, and applied treatment, as well as maternal and fetal outcomes were evaluated. RESULTS: The study included 65 pregnant patients with acute pancreatitis. The mean age was 26.6±5 (19-41) years. Acute pancreatitis was observed in the third trimester. The most common cause of acute pancreatitis was gallstones, and its severity was often mild. Only two patients required endoscopic retrograde cholangiopancreatography, and the remaining patients were treated medically. Maternal and infant death developed in a patient with necrotizing acute pancreatitis secondary to hyperlipidemia. CONCLUSION: The most common etiology of acute pancreatitis in pregnancy was gallstones. Acute pancreatitis occurred in the third trimester. Most of the patients had mild acute pancreatitis. Maternal and fetal complications were rare. We think that the reasons for the low mortality rate were mild disease severity and biliary etiology, and most patients were in the third trimester, as well as early diagnosis and no delay in the intervention.

What does the dialysate level of matrix metalloproteinase 2 tell us?

Long-term peritoneal dialysis leads to encapsulating peritoneal sclerosis (EPS), which is a rare but often fatal complication. The pathogenesis of EPS is characterized by increased inflammation, neoangiogenesis, epithelial-mesenchymal transition (EMT), and fibrosis. Matrix metalloproteinase 2 (MMP-2), which degrades type IV collagen, plays an important role in pathogenesis. Clinical trials report that dialysate levels of MMP-2 can be used as an early marker of peritoneal sclerosis. We aimed to determine the association of MMP-2 with peritoneal function, histology, and effluent cytokine levels in an experimental EPS model in rats. We evaluated data for 71 rats from our various studies using an experimental EPS model. Functional assessment was performed using a 1-hour peritoneal equilibration test with peritoneal dialysis fluid containing 3.86% glucose. Specimens of parietal peritoneum were examined with light microscopy for histologic evaluation. Parietal peritoneum thickness and submesothelial area were measured. Fibrosis, number of vessels, neovascularization, and cellular infiltration were evaluated by one pathologist. The relationships between MMP-2 and other parameters were analyzed using Pearson correlation analysis. Dialysate levels of MMP-2 reflect both functional and histologic change in peritoneum. Levels of MMP-2 were negatively correlated with net ultrafiltration, effluent protein levels, and end (1-hour)-to-initial dialysate concentration ratio of glucose. Cytokines such as vascular endothelial growth factor transforming growth factor beta, monocyte chemotactic protein 1, and osteopontin-which are known to play important roles in neovascularization, inflammation, and EMT leading to fibrosis-were correlated with MMP-2. In peritoneal dialysis patients, MMP-2 levels may be an early marker of EPS and EMT

Can N-acetylcysteine preserve peritoneal function and morphology in encapsulating peritoneal sclerosis?

Long-term use of the peritoneum as a dialysis membrane results in progressive irreversible dysfunction, described as peritoneal fibrosis. Oxidative stress during peritoneal dialysis has been established in many studies. Generation of reactive oxygen species (ROS) by conventional peritoneal dialysis solutions, regardless of whether produced by high glucose, angiotensin II, or glucose degradation products may be responsible for progressive membrane dysfunction. The well-known antioxidant molecule N-acetylcysteine (NAC) is capable of direct scavenging of ROS. The aim of the present study was to investigate the effect of NAC therapy on both progression and regression of encapsulating peritoneal sclerosis (EPS). We divided 49 nonuremic Wistar albino rats into four groups: Control group-2 mL isotonic saline intraperitoneally (IP) daily for 3 weeks; CG group-2 mL/200 g 0.1% chlorhexidine gluconate (CG) and 15% ethanol dissolved in saline injected IP daily for a total of 3 weeks; Resting group-CG (weeks 1 - 3), plus peritoneal resting (weeks 4 - 6); NAC-R group-CG (weeks 1 - 3), plus 2 g/L NAC (weeks 4 - 6). At the end of the experiment, all rats underwent a 1-hour peritoneal equilibration test with 25 mL 3.86% PD solution. Dialysate-to-plasma ratio (D/P) urea, dialysate white blood cell count (per cubic milliliter), ultrafiltration (UF) volume, and morphology changes of parietal peritoneum were examined. The CG group progressed to encapsulating peritoneal sclerosis, characterized by loss of UF, increased peritoneal thickness, inflammation, and ultimately, development of fibrosis. Resting produced advantages only in dialysate cell count; with regard to vascularity and dialysate cell count, NAC was more effective than was peritoneal rest. Interestingly, we observed no beneficial effects of NAC on fibrosis. That finding may be a result of our experimental severe peritoneal injury model. However, decreased inflammation and vascularity with NAC therapy were promising results in regard to membrane protection.

The effects of renin-angiotensin system inhibition on regression of encapsulating peritoneal sclerosis.

BACKGROUND: Encapsulating peritoneal sclerosis (EPS) is a clinical syndrome associated with symptoms of ileus and irreversible sclerosis of both visceral and parietal peritoneum. Peritoneal dialysis (PD) patients rarely develop EPS, a severe life-threatening condition of unknown pathogenesis. Angiotensin II is known to promote fibrosis and inflammation in various tissues. Renin-angiotensin system (RAS) blockade provides advantages in the course of diseases such as hypertension, chronic kidney disease, and proteinuria. We have also previously shown that RAS blockade has beneficial effects on hypertonic (3.86%) PD solution-induced peritoneal alterations. Because it shares the same characteristics as other fibrotic processes, peritoneal fibrosis can benefit from RAS blockade. OBJECTIVE: To determine the advantages of RAS blockade in regression of EPS. METHODS: We divided 56 nonuremic albino Wistar rats into 6 groups: control group (n = 10), daily intraperitoneal (IP) injection of 2 mL isotonic saline for 3 weeks; CG group (n = 10), daily IP injection of 2 mL/200 g chlorhexidine gluconate (CG) for 3 weeks; resting group (n = 10), daily IP injection of CG (0 - 3 weeks) plus peritoneal rest (4 - 6 weeks). After 3 weeks of being injected with CG (0 - 3 weeks), a fourth group (n = 9) was treated with 100 mg/L enalapril (ENA group); a fifth group (n = 10) was treated with 80 mg/L valsartan (VAL group), and a sixth group (n = 7) was treated with 100 mg/L enalapril + 80 mg/L valsartan (ENA+VAL group) in drinking water for an additional 3 weeks (4 - 6 weeks). At the end, a 1-hour peritoneal equilibration test was performed with 25 mL 3.86% PD solution. Dialysate-to-plasma ratio of urea (D/P urea), dialysate WBC count, ultrafiltration volume (UF), and morphological changes of parietal peritoneum were examined. RESULTS: Exposure to CG for 3 weeks resulted in alterations in peritoneal transport (increased D/P urea, decreased UF volume; p < 0.05) and morphology (increased inflammation, neovascularization, fibrosis, and peritoneal thickness; p < 0.05). Peritoneal rest had some beneficial effect only on UF failure and dialysate cell count (p < 0.05). However, RAS blockade was more effective than peritoneal rest with respect to UF volume, vascularity (p < 0.05), and peritoneal thickness (p > 0.05). Dual blockade of RAS had no additional beneficial effects. CONCLUSION: We suggest that RAS blockade either with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be a more effective option than resting in the management of EPS.