Histological evidence of pancreatitis is commonly found in necropsy studies in cats. A clinical diagnosis of pancreatitis is challenging due to nonspecific clinical signs, a lack of diagnostic lipase cutoffs, and frequent presence of multiple diseases. It is still unknown how often pancreatitis alone is found in sick cats and how often clinicopathological evidence of pancreatitis in sick cats does not lead to a clinical diagnosis of pancreatitis. Our aims were to evaluate the extent of comorbidities in cats with suspected pancreatitis, evaluate how often sick cats with hyperlipasemia are diagnosed only with non-pancreatic diseases, and compare their clinical findings. Medical records of 563 client-owned hospitalized cats with available lipase activity measurement (LIPC Roche) > 30 U/L (RI, 6-26) were searched and medical diagnoses recorded and grouped by organ system. Clinicopathological findings were compared between cats with pancreatitis alone (PA), pancreatitis with concurrent disease (PD), and no suspected pancreatitis (NP). We found that PA was present in 33 (6%) cats, 159 cats (28%) were in the PD group, and 371 cats (66%) had no suspected pancreatitis (NP). Clinical, laboratory, and ultrasonographic findings did not differ between PA and PD cats. Lipase activities did not differ between the three groups. The most common disease categories in PD and NP cats were gastrointestinal, hepatobiliary, renal/urinary, and endocrine, and renal/urinary, gastrointestinal, cardiac, and musculoskeletal, respectively. We conclude that cats are rarely hospitalized because of suspected pancreatitis alone, and PA cats did not differ clinically from PD cats. Hyperlipasemia in sick cats without a diagnosis of pancreatitis may be due to a reactive pancreatopathy or preexisting chronic pancreatitis.

Type 1 diabetes (T1D) is one of the most frequent chronic autoimmune diseases in humans, characterized by the lack of insulin production resulting in high blood glucose levels and lifelong requirement of exogenous insulin administration for survival. It is now recognized that the autoimmune process begins years before the clinical onset, in a stage called pre-symptomatic T1D, in which the presence of β-cell-specific autoantibodies is detectable. Our aim is to review evidence for T1D as a \"whole-pancreas disease,\" featured by both endocrine and exocrine pancreas alterations already at early disease stages.
In this review, we discuss a series of recent observations indicating that in genetically predisposed individuals, structural and functional abnormalities as well as immune cell infiltration of the exocrine pancreas are already present in the pre-symptomatic stages of the disease. Despite T1D being considered a β-cell-specific disease, numerous reports point to the presence of exocrine pancreas subclinical abnormalities occurring during disease development. These observations challenge the long-standing idea that T1D exocrine damage exists as a mere consequence of disease progression and provide further explanation of mechanisms underlying T1D pathogenesis.

BACKGROUND: Limited data exists concerning the coincidence of chronic pancreatitis (CP) and liver cirrhosis with respect to the patient outcome after liver transplantation (LT). The aim of the study was to identify risk factors for graft loss after liver transplantation and to evaluate the impact of CP on graft survival.
METHODS: We analyzed the data of 421 cirrhotic patients who underwent evaluation for primary liver transplantation from January 2007 to January 2014. Diagnosis of CP based on morphologic findings which were graded according to the Cambridge and Manchester classification. (Graft) survival after LT was analyzed by Cox regression analysis. Recipient- and donor-related risk factors for graft loss were evaluated using univariate and multivariate analysis.
RESULTS: 40/421 cirrhotic patients suffered from CP (9.5%). 250/421 (59.4%) patients underwent LT between January 2007 and January 2014. In total, 89 patients died or were in need of a re-transplantation during follow-up until August 2017. Patients with CP (N = 26) were at increased risk for graft loss after LT (hazard ratio = 2.183; 95% confidence interval = 1.232-3.868). CP (P = 0.001), a MELD score ≥24 (P = 0.021), absence of esophageal or gastrical varices (P = 0.018), the age of the donor (P = 0.008) and infections after transplantation (P = 0.030) were independent risk factors for organ loss after transplantation in the multivariate Cox regression analysis.
CONCLUSIONS: Patients with chronic pancreatitis are at increased risk for graft loss after LT. A high MELD score, the absence of esophageal or gastrical varices, an advanced donor age and post-transplant infections negatively affect graft survival, too.