Patients with severe acute pancreatitis (SAP) present complications and organ failure, which require treatment in critical care units. These extrapancreatic complications determine the clinical outcome of the disease. Intra-abdominal hypertension (IAH) deteriorates the prognosis of SAP. In this paper, relevant recent literature was reviewed, as well as the authors’ own experiences, concerning the clinical importance of IAH and its treatment in SAP. The principal observations confirmed that IAH is a frequent consequence of SAP but is practically absent in mild disease. Common manifestations of AP such as pain, abdominal distension, and paralytic ileus contribute to increased abdominal pressure, as well as fluid loss in third space and aggressive fluid replacement therapy. A severe increase in IAP can evolve to abdominal compartment syndrome and new onset organ failure. Conservative measures are useful, but invasive interventions are necessary in several cases. Percutaneous drainage of major collections is preferred when possible, but open decompressive laparotomy is the final possibility in some cases in order to definitively reduce abdominal pressure. Intra-abdominal pressure should be measured in all SAP cases that worsen despite adequate treatment in critical care units. Conservative measures must be introduced to treat IAH, including negative fluid balance, digestive decompression by gastric–rectal tube, and prokinetics, including neostigmine. In the case of insufficient responses to these measures, minimally invasive interventions should be preferred.

Localized acute necrohemorrhagic pancreatitis was induced in rats by multiple trypsin injections. Morphological alterations were monitored by light and electron microscopy until complete recovery. In the acute phase, typical pictures of focal acute necrohemorrhagic pancreatitis were observed. In the postacute phase, fibrosis and tubular complexes are characteristic of damaged areas. Tubular complexes appear from the dedifferentiation of acinar cells. They are characterized by duct-like cells bordering wide, empty luminae. In the recovery phase, cellular proliferation was accompanied by differentiation, with progressive acquisition of the morphological characteristics of acinar cells at the periphery of the tubular complexes. In that instance, cellular proliferation was concomitant with the development of collagen septa in tubular complexes. In these structures both duct-like and acinar-like cells presented mitoses. Cell division persisted in the dedifferentiated cells until tubular complexes disappeared. A very similar process was observed in the embryonic pancreas, where organized parenchyma originated from proliferation and differentiation of protodifferentiated cells. We concluded that pancreatic repair following necrohemorrhagic pancreatitis involves proliferation of cells from intact acini and from tubular complexes, at variance with edematous pancreatitis, where regeneration is exclusively due to acinar cell proliferation.

The effect of 3-week CCK-OP treatment on test meal stimulated pancreatic secretion was investigated in chronic pancreatitis patients. One drop of a 1 mg/ml CCK-OP solution applied intranasally, three times daily during 3 weeks resulted in a significant increase in volume, trypsin, lipase and amylase secretion in response to the Lundh test meal. Augmentation of trypsin secretion was the most pronounced. Functional capacity of pancreatic enzyme secretion remained elevated for 3 months after treatment. Nearly all patients became symptom free during and for some time after treatment. The results were attributed to a trophic effect of CCK-OP on human pancreas.

The RAS/RAF/MEK/ERK pathway regulates certain cellular functions, including cell proliferation, differentiation, survival, and apoptosis. Dysregulation of this pathway leads to the occurrence and progression of cancers mainly by somatic mutations. This study aimed to assess if polymorphisms of the RAS/RAF/MEK/ERK pathway are associated with gastric cancer. A case-control study of 242 gastric cancer patients and 242 controls was performed to assess the association of 27 single nucleotide polymorphisms (SNPs) in the RAS/RAF/MEK/ERK pathway genes with gastric cancer. Analyses performed under the additive model (allele) showed four significantly associated SNPs: RAF1 rs3729931 (Odds ratio (OR) = 1.54, 95%, confidence interval (CI): 1.20–1.98, p-value = 7.95 × 10−4), HRAS rs45604736 (OR = 1.60, 95% CI: 1.16–2.22, p-value = 4.68 × 10−3), MAPK1 rs2283792 (OR = 1.45, 95% CI: 1.12–1.87, p-value = 4.91 × 10−3), and MAPK1 rs9610417 (OR = 0.60, 95% CI: 0.42–0.87, p-value = 6.64 × 10−3). Functional annotation suggested that those variants or their proxy variants may have a functional effect. In conclusion, this study suggests that RAF1 rs3729931, HRAS rs45604736, MAPK1 rs2283792, and MAPK1 rs9610417 are associated with gastric cancer.