Risk factors for new-onset diabetes after incipient acute pancreatitis / 临床肝胆病杂志

ObjectiveTo investigate the risk factors for new-onset diabetes after incipient acute pancreatitis (AP). MethodsA retrospective analysis was performed for 95 patients with post-acute pancreatitis diabetes mellitus (PPDM-A) after incipient AP who were admitted to The Affiliated Hospital of Southwest Medical University from June 2013 to January 2020 (PPDM-A group), and 190 patients without diabetes after incipient AP during the same period of time were selected at a ratio of 2∶1 and were enrolled as non-PPDM-A group. Baseline data and clinical data were collected. The t-test or the U test was used for comparison of continuous data, and the chi-square test or the Fisher’s exact test was used for comparison of categorical data; a logistic regression analysis was used for multivariate analysis. Results There were significant differences between the two groups in body mass index (BMI), body weight, and proportion of patients with a drinking history, hyperuricemia, or fatty liver disease (all P＜0.05), while there were no significant differences between the two groups in age, male sex, and proportion of patients with a smoking history, a family history of diabetes, or hypertension (all P＞0.05). There were also significant differences in etiologies (biliary, hyperlipidemic, and alcoholic AP) between the two groups (P＜0.05). Compared with the non-PPDM-A group, the PPDM-A group had significantly higher triglyceride, blood glucose, white blood cell count (WBC), C-reactive protein, and proportion of patients with blood glucose ＞11.1 mmol/L on admission (all P＜0.05), while there were no significant differences in Ca2+, blood amylase, and blood lipase between the two groups (all P＞0.05). Compared with the non-PPDM-A group, the PPDM-A group had significantly higher incidence rates of acute peripancreatic necrotic collections and acute peripancreatic fluid collections, proportion of patients with multiple onset of AP, and proportion of patients with CTSI score ＞4 (all P＜0.05), while there were no significant differences in the proportion of patients with systemic inflammatory response syndrome and disease severity between the two groups (both P＞0.05). The multivariate analysis showed that the outcome of PPDM-A in alcoholic AP patients was 5.868 times that in biliary AP patients (95% confidence interval ［CI］: 1.607-21.418, P=0.007), and the outcome of PPDM-A in hyperlipidemic AP patients was 3.312 time that in biliary AP patients (95%CI: 1.593-6.887, P=0.001). The outcome of PPDM-A in overweight patients was 3.694 times that in patients with normal BMI (95%CI: 1.575-8.667, P=0.003), and the outcome of PPDM-A in obese patients was 5.964 times that in patients with normal BMI (95%CI: 2.516-14.139, P＜0.001). Multiple onset of AP (OR=4.522,95%CI: 2.298-8.900, P＜0.001), blood glucose on admission ＞11.1 mmol/L (OR=6.749,95% CI: 3.381-13.469, P＜0.001), CTSI score ＞4 (OR=1.176,95%CI: 1008-1.371, P=0.039), and WBC (OR=1.082,95%CI: 1.009-1.160, P=0.026) were independent risk factors for PPDM-A. ConclusionMultiple onset of AP, alcoholic AP, hyperlipidemic AP, blood glucose on admission ＞11.1 mmol/L, overweight or obesity, CTSI score ＞4, and WBC are independent risk factors for PPDM-A, which can provide a reference for formulating strategies to prevent or reduce the onset of PPDM-A.

Heterogeneity in the aetiology of diabetes mellitus in young adults: A prospective study from north India

Background & objectives: In contrast to Caucasians of European origin, the aetiology of diabetes mellitus (DM) in young adults in other ethnic groups, including Indians is likely to be heterogeneous and difficult to determine. This study was undertaken to determine the aetiology of diabetes in young Indian adults using a protocol-based set of simple clinical and investigation tools. Methods: In this prospective study, 105 Indian young adults with diabetes (age at onset 18-35 yr; duration <2 yr) were studied for a period of 1-3 years. Pancreatic imaging, fasting C-peptide, islet antibodies (against glutamic acid decarboxylase, tyrosine phosphatase and zinc transporter-8) and mitochondrial A3243G mutational analysis were performed in all patients. Four patients were screened for maturity-onset diabetes of the young (MODY) using next-generation sequencing. Results: Type 1 and type 2 diabetes mellitus (T1DM and T2DM) were equally frequent (40% each), followed by fibrocalculous pancreatic diabetes (FCPD, 15%). Less common aetiologies included MODY (2%), mitochondrial diabetes (1%) and Flatbush diabetes (2%). There was considerable phenotypic overlap between the main aetiological subtypes. Elevated islet antibodies were noted in 62 per cent of T1DM patients [positive predictive value (PPV) 84%; negative predictive value (NPV) 78%] while low plasma C-peptide (<250 pmol/l) was present in 56 per cent of T1DM patients [PPV 96% (after excluding FCPD), NPV 72%]. Using these tests and observing the clinical course over one year, a final diagnosis was made in 103 (99%) patients, while the diagnosis at recruitment changed in 23 per cent of patients. Interpretation & conclusions: The aetiology of diabetes in young adults was heterogeneous, with T1DM and T2DM being equally common. FCPD was also frequent, warranting its screening in Indian patients. Testing for islet antibodies and C-peptide in this age group had good PPV for diagnosis of T1DM.

FCPD: An unusual cause of abdominal pain; reminder of important clinical lesson

Fibrocalculous pancreatic diabetes (FCPD) is a type of chronic calcific non-alcoholic pancreatitis. This type is reported mostly in the developing tropical and subtropical countries. Definite diagnosis of FCPD requires younger age of onset, history of malnutrition, and presence of diabetes mellitus along with extensive pancreatic calcification and ductal calculi. Pain abdomen is one of the classical clinical triad of the disease with steatorrhoea and diabetes. In this case report we are presenting a case of 17 years old girl with past history of recurrent pain abdomen for last two years. She came to casualty with complaints of generalized weakness along with pain abdomen. She was diagnosed as case of FCPD with uncontrolled hyperglycemia on subsequent investigations. Importance of this case is that patient has multiple episode of abdominal pain over two years and she consulted several practitioners for the same and she was treated symptomatically without proper work-up. However, FCPD is a rare entity but should be considered in case of recurrent abdominal pain in young patient.

A rare form of pancreatic diabetes complicated by portal venous thrombosis: A 25-year follow-up.

Fibrocalculous pancreatic diabetes (FCPD) is an uncommon type of diabetes mellitus, so called tropical diabetes, due to chronic calcific non-alcoholic pancreatitis. This type of diabetes is associated to several particularities based on glycemic control and the occurrence of degenerative and metabolic complications, in addition to chronic pancreatitis complications such us venous thrombosis. We report here a rare case of a young North-African patient with long standing FCPD followed for 25 years and complicated by portal venous thrombosis. This case presentation highlights how important is to suspect fibrocalculous pancreatic diabetes especially in the presence of chronic abdominal pain. The follow-up of such patients should be focused not only on the clinical and biological markers of diabetes, but also on pancreatitis complications.

Metastatic adenocarcinoma arising from fibrocalcific pancreatic diabetes / Journal of the ASEAN Federation of Endocrine Societies

@#Fibrocalcific pancreatic diabetes (FCPD) is a rare form of ketosis-resistant diabetes in the young (15 to 40 years old) of unknown etiology. It has been observed in tropical and subtropical countries with highest incidence in south India, and is believed to have some association with tropical chronic pancreatitis, malnutrition, toxin exposure (e.g., cassava) and SPINK1 mutation. It is associated with a hundredfold increased risk of pancreatic cancer compared to the general population.

Pancreatic diabetes.

Pancreatic endocrine insufficiency secondary to destruction of acinar cells is a well known complication of chronic pancreatitis (CP). Of all patients with diabetes mellitus, 0.5-1% is secondary to CP. The frequency of occurrence of diabetes in CP is about 40-60%. This figure varies according to the aetiology, extent of calcification, and duration of the disease. Pancreatic diabetes is more commonly associated with alcoholic and tropical calcific pancreatitis of long duration. The pathophysiology of pancreatic diabetes is related to beta cell failure and reduced insulin secretory capacity. The development of pancreatic diabetes calls for careful evaluation and management to prevent long term complications. Pancreatic cancer is a known complication of chronic pancreatitis and sometimes manifests with new onset diabetes. As destruction of pancreatic tissue in CP leads to depletion of both insulin and glucagonproducing cells of the islets of Langherhans, pancreatic diabetics are usually not prone to ketoacidosis. A trial of oral hypoglycemic agents followed by insulin therapy when the need arises has been the line of management thus far in these patients. This review focuses on the prevalence, unique pathophysiological aspects, clinical features and special issues in the management of diabetes secondary to chronic pancreatitis.

Genotype–phenotype correlation in 9 patients with tropical pancreatitis and identifi ed gene mutations.

The etiopathogenesis of tropical chronic pancreatitis (TCP) remains unclear. Malnutrition, dietary toxins like cyanogens in cassava and micronutrient deficiency are proposed factors. The description and characterization of genetic factors in TCP has added a new dimension to the understanding of pathogenesis of the disease. However, there is sparse data on the association of TCP with cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations. We report 8 patients of TCP with CFTR gene mutations, including one with a novel mutation, and describe the clinical profile of these patients. Further prospective genetic studies on the association of CFTR gene mutations are essential in order to unravel the genetic basis of TCP.