Acute pancreatitis (AP) is an inflammatory disorder with a high mortality rate. Cilostazol is a selective phosphodiesterase-3 inhibitor drug that is commonly used as an antiplatelet, antithrombotic, and vasodilator drug. It exhibits antioxidant, anti-inflammatory, and anti-apoptotic activities, but its effect on AP has not been fully elucidated yet. The present study aimed to investigate the effects of cilostazol on L-arginine-induced AP and the possible protective mechanisms. A rat model of AP was established by a single i.p. injection of 3-g/kg L-arginine on day 13 of the experiment. The treated groups received a single daily oral dose of either 100 or 300 mg/kg/day for 14 consecutive days. Rats with AP showed histopathological changes of pancreatic tissue injury together with increased serum amylase enzyme activity and decreased serum insulin, pancreatic adiponectin, and cGMP levels. Moreover, AP rats showed increased pancreatic inflammatory biomarker (TNF-α, VCAM-1, and MPO) levels with decreased anti-inflammatory IL-10 levels. In addition, oxidative stress biomarkers (MDA and NO) were increased in AP with decreased antioxidant SOD activity and GSH level. Moreover, HO-1 immunostaining was increased in the AP group. Cilostazol pretreatment reversed the histopathological change; decreased the amylase activity and the levels of TNF-α, VCAM-1, and MPO; and increased the levels of insulin, adiponectin, cGMP, cAMP, and IL-10. Moreover, cilostazol decreased MDA and NO but increased SOD and GSH. Lastly, cilostazol increased the HO-1 immunostaining more than in the AP group. These data suggest that cilostazol protects against L-arginine-induced AP, which may be related to an increase in cGMP, cAMP, and upregulation of HO-1 with subsequent anti-inflammatory and antioxidant properties.

Acute pancreatitis (AP) is a common gastrointestinal disease and the leading cause of hospital admission and healthcare burden among gastrointestinal disorders in many countries. Patients can present with varying degrees of inflammation and disease severity, ranging from self-limiting mild AP to devastating and fatal severe AP. Many factors contribute to malnutrition in AP, especially abnormal metabolism and catabolism related to inflammation. The concept of "pancreatic rest" is not evidence-based. There is however, emerging evidence that supports the use of oral or enteral nutrition to improve nutrition status and to reduce local and systemic inflammation, complications, and death. In mild disease, patients are generally able to initiate solid oral diet and do not require specialized nutrition care such as enteral or parenteral nutrition. In contrast, nutrition interventions are imperative in moderately severe and severe AP. The current article aims to review the latest evidence and suggest practical nutrition interventions in patients with AP, including nutrition requirements, routes of nutrition treatment, types of formula, and the role of nutritional supplements, such as glutamine, probiotics, omega-3 fatty acids, and antioxidants.

Diabetic crises occur most often in patients with type 1 diabetes and occasionally in type 2 diabetes, especially under stressful conditions. However, a diabetic crisis occurring directly from prediabetes is an unusual phenomenon.

A 45-year-old woman presented with postprandial left upper quadrant abdominal pain, nausea, and vomiting. She had a past medical history of prediabetes with impaired fasting glucose and HbA1c 6.4%. On admission, routine laboratory tests showed high anion gap metabolic acidosis (pH 6.92), anion gap 41 mmol/L, blood glucose 931 mg/dL, beta-hydroxybutyrate 28 mmol/L, and calculated effective osmolarity 322 mOsm/kg; she was diagnosed with diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS), and DKA-related abdominal pain. Later, the patient was found to have elevated lipase and amylase, and diagnosed with acute pancreatitis. Since DKA can induce abdominal pain and nonspecific lipase elevation, both of which are characteristics of acute pancreatitis, while acute pancreatitis can conversely trigger DKA, there exists a "chicken and egg" paradigm. Therefore, the differential diagnosis is discussed.

It is important to differentiate DKA from concomitant causes of abdominal pain to avoid missing the underlying etiology, which can be the trigger for DKA. During diabetic crises, treating the underlying trigger is just as important as managing metabolic derangements in order to achieve favorable outcomes; meanwhile, managing acute pancreatitis-associated hyperglycemia can promote recovery. Additionally, diabetic crisis that directly evolves from prediabetes illustrates an atypical form of diabetes called ketosis-prone diabetes; we briefly discuss its clinical characteristics, classification, and follow-up.

It is considered natural that glucose tolerance worsens after pancreatectomy. However, diabetes mellitus (DM) resolves after metabolic bypass surgery and anatomic changes after PD resemble those after metabolic surgery. This study assessed the incidence of DM resolution after pancreatectomy and differences in metabolic parameters following pancreatoduodenectomy (PD) and distal pancreatectomy (DP).

Between 2007 and 2013, 218 consecutive patients with pancreatic diseases underwent PD (n = 112) or DP (n = 106) at Seoul National University Hospital. Factors associated with changes in glucose homeostasis were evaluated by assaying serum glucose concentrations in prospectively collected samples.

Of the 218 patients, 88 (40.4%) had preoperative DM, with 27 (30.7%) of the latter showing postoperative resolution of DM, a rate significantly higher in patients who had undergone PD than DP (40.4% vs. 12.9%, p = 0.008). Fasting blood glucose (p = 0.001), PP2 (p < 0.001), and HOMA-IR (p = 0.005) significantly decreased after PD but not after DP. Multivariate analysis revealed that PD was independently associated with DM resolution (odds ratio 7.790, p = 0.003). PD was associated with a significantly higher DM resolution rate than DP among the 37 pancreatic cancer patients with preoperative DM (34.6% vs. 0%, p = 0.036). DM resolution rates were similar in pancreatic cancer and other pancreatic diseases (p = 0.419).

More than 40% of patients with preoperative DM show resolution after PD. Decreased insulin resistance and suspected enhanced glucose stimulated insulin secretion decreasing PP2 seem to contribute improved glucose homeostasis after PD. BMI was unrelated to DM resolution, indicating that PD-associated physio-anatomical changes may help resolve DM independent of weight.

The pathophysiology of acute pancreatitis represents a diverse mix of congenital, hereditary, and acquired problems associated with or causing acute pancreatic inflammation. Acute pancreatitis is characterized by acinar cell injury that may involve regional and systemic inflammatory responses. The systemic manifestations of acute pancreatitis are responsible for the majority of pancreatitis-associated morbidity and are due to the actions of specific inflammatory cytokines. This report summarizes this pancreatic injury, the role of cytokines in the pathogenesis of acute pancreatitis, and the pancreatic healing response that follows.

A comprehensive literature review of experimental pancreatitis as well as reports of cytokine involvement and healing response during clinical pancreatitis was performed.

Histamine release, bradykinin generation, and cytokine release play a significant role during acute pancreatic inflammation. Following an experimental insult, there is rapid expression of tumor necrosis factor-alpha, interleukin-6, interleukin-1, and chemokines by pancreatic acinar cells and/or transmigrated leukocytes. Preventing the action of these mediators has a profound beneficial effect in experimental animals. Pancreatic fibrosis is a central histologic response after pancreatitis. Transient collagen deposition with acinar necrosis occurs in acute pancreatitis; in chronic pancreatitis, permanent and disorganized pancreatic fibrosis and parenchymal cell atrophy occur.

Inflammatory mediators are responsible for the systemic manifestations of acute pancreatitis and the associated distant organ dysfunction. After the acute injury, regeneration or pancreatic repair is characterized by decreased release of proinflammatory mediators and decreased infiltrating inflammatory cells. Differentiation and proliferation of pancreatic myofibroblasts or "stellate" cells may be responsible for increased extracellular matrix production. The predictable nature in which the inflammation and fibrosis are produced may stimulate novel approaches to disease treatment.

In order to recognize acute pancreatitis in the setting of the acute abdomen, the surgeon must be thoroughly familiar with the numerous etiologies of the disease. No specific test is available to diagnose acute pancreatitis. CT scanning is arguably the most useful single tool, but surgical judgment is critical. Most cases of acute pancreatitis resolve spontaneously without sequelae, but the spectrum of the disease also includes highly lethal forms associated with a variety of systemic complications. Operative intervention is indicated when other, more rapidly fatal, abdominal processes cannot be reliably excluded and when local complications develop.

RBC insulin binding was examined in Reye's survivors and families of affected patients to determine whether their previously reported hyperinsulinemic responses to oral glucose are accompanied by alterations in insulin binding and could contribute to the hypercatabolism seen in this disorder. The mean (125I)-insulin binding to 3 X 10(9) RBC's was 5.7 +/- SEM 0.4 percent in survivors compared to 6.6 +/- 0.3 in siblings (p less than .05) and 6.6 +/- 0.4 in control children (p = .05). Sex and maturity differences were found with higher binding values in men than women as well as higher values in men than boys. Receptor numbers in survivors were comparable to control values. Average affinities varied widely. Plasma insulin levels were low in the fathers (9 +/- SEM 1.4 uU/ml compared to 18.3 +/- 1.8 for control men and 20 +/- 4.5 for mothers of affected patients). The acute syndrome is accompanied by hypercatabolism in the presence of increased plasma insulin levels and familial clustering of cases and recurrences are known to occur. Reduction in insulin binding may play a role in the acute disease if such is shared by more traditionally hormone-responsive cells.