Reduced Pancreatic Volume and β-Cell Area in Patients With Chronic Pancreatitis

Schrader, Henning; Menge, Bjoern A.; Schneider, Simone; Belyaev, Orlin; Tannapfel, Andrea; Uhl, Waldemar; Schmidt, Wolfgang E.; Meier, Juris J.

doi:10.1053/j.gastro.2008.10.083

Cited by 100 publications

(82 citation statements)

References 35 publications

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“…This was done by necessity, because pancreatic weight cannot be determined in living humans. We have tried to overcome this problem previously by generating a measure of pancreatic volume based on abdominal computed tomography (CT) scans in a controlled subset of patients with CP without any other detectable pancreatic abnormalities [17]. In the present study, the clinical evaluation of the abdominal CT scans had revealed a pancreatic oedema in a considerable group of patients, thereby likely inducing bias with respect to the determination of pancreatic volume.…”

Section: Discussionmentioning

confidence: 88%

“…In type 2 diabetes, hyperglycaemia has been associated with a deficit in beta cell mass of ∼20-65% of normal [5][6][7][8][9][10][11], and studies in rodent models of autoimmune diabetes or in patients with newly onset type 1 diabetes indicate that the extent of beta cell loss amounts to ∼50-70% around the manifestation of type 1 diabetes [12][13][14]. Diabetes is also frequently found in patients with chronic pancreatitis (CP), secondary to the inflammatory process within the pancreas [15][16][17]. Previous studies have shown that beta cell mass is also significantly reduced in patients with CP, even though the islet destruction appears to occur relatively late during the clinical course of the disease [17].…”

Section: Introductionmentioning

confidence: 99%

“…Diabetes is also frequently found in patients with chronic pancreatitis (CP), secondary to the inflammatory process within the pancreas [15][16][17]. Previous studies have shown that beta cell mass is also significantly reduced in patients with CP, even though the islet destruction appears to occur relatively late during the clinical course of the disease [17]. However, conflicting data have been reported with regard to the prevalence of diabetes in patients with CP and its relationship to disease duration [15,16,18].…”

Section: Introductionmentioning

confidence: 99%

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Determinants of glucose control in patients with chronic pancreatitis

et al. 2010

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Aims/hypothesis Diabetes frequently develops in patients with chronic pancreatitis (CP). Partial pancreatectomy has emerged as a treatment option for such patients. We addressed whether the development of diabetes in CP patients is related to pancreatic beta cell area or clinical variables, and which factors predict the diabetes risk after partial pancreatectomy. Methods Fractional beta cell area was determined in pancreatic tissue samples obtained from 114 CP patients undergoing pancreatic surgery and related to measures of glucose control, as well as clinical and anthropometric data. Seventy-four patients without diabetes at the time of surgery were contacted again 2.5±1.0 years after partial pancreatectomy in order to obtain information about the post-operative development of diabetes. Results In the surgical samples in the whole cohort, pancreatic beta cell area was 0.40±0.06% in patients with and 0.64±0.06% in those without previously known diabetes (p=0.039). There was an inverse non-linear relationship between pancreatic beta cell area and fasting glucose concentrations (r=0.29) as well as HbA 1c levels (r=0.36). Nineteen out of 74 previously normoglycaemic patients (26%) developed diabetes over an average period of 2.5 years of follow-up. Pre-operative fasting glucose levels, HbA 1c and BMI were identified as predictors of diabetes after partial pancreatectomy. However, pancreatic beta cell area did not differ in those who subsequently developed diabetes (0.66±0.15%) and those who did not (0.62± 0.08%, p=0.45). Conclusions/interpretation Hyperglycaemia in CP patients is associated with reduced beta cell area. However, reduced beta cell area does not predict the development of diabetes, suggesting that other factors are more important determinants of alterations in glucose metabolism in patients with CP.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Determinants of glucose control in patients with chronic pancreatitis

et al. 2010

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“…In fact, the manifestation of diabetes in lean patients without a typical history of type 2 diabetes has been considered as a clinical indication of pancreatic carcinoma [4]. At present, studies on the pathogenesis of pancreatic diabetes in humans are relatively sparse, but progressive beta cell destruction is held to be the major underlying cause [5,6]. Whether insulin resistance is involved in the development of diabetes in such patients is not known, given the paucity of studies in this area.…”

Section: Introductionmentioning

confidence: 98%

Pancreatic diabetes manifests when beta cell area declines by approximately 65% in humans

et al. 2012

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Aims/hypothesis Diabetes frequently develops in patients with pancreatic disorders. We aimed to determine the lower threshold of beta cell area for diabetes manifestation as well as the impact of insulin sensitivity on glucose homoeostasis in patients with pancreatic diabetes. Methods Eighty-two patients undergoing pancreatic surgery underwent pre-operative oral glucose challenge. Fractional pancreatic beta cell area was determined, and indices of insulin sensitivity and beta cell function were calculated. Results HbA 1c and glucose levels were similar in patients with high and intermediate beta cell area, but were significantly higher in those with the lowest beta cell area (p< 0.0001). Insulin secretion was reduced only in patients with the lowest beta cell area (p<0.001). The relative beta cell deficits at the onset of diabetes and impaired glucose tolerance were 64% and 21%, respectively, based on 2 h glucose levels. Deteriorating insulin sensitivity was associated with a small increase in the incidence of diabetes. Conclusions/interpretation In conclusion, pancreatic diabetes probably develops after a reduction in beta cell area of 65%. Post-challenge glucose excursions are much more closely related to pancreatic beta cell area than to fasting

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“…While such an observation was made after the occurrence of overt hyperglycemia, decreased insulin secretion in patients with long standing CP were documented earlier. 7 Tests for insulin secretion after maximal β-cell stimulation with combined oral administration of glucose, intravenous administration of glucagon, and tolbutamide have demonstrated decreased β-cell secretory capacity even in patients with normal oral glucose tolerance; with progression to diabetes, the β-cell secretory capacity becomes markedly reduced. 8 In addition, decreased glucose stimulated insulin secretion by the islet cells isolated from surgical specimens of chronic pancreatitis patients was recently demonstrated even in non diabetic CP patients.…”

mentioning

confidence: 99%

The Enigma of Type 3c Diabetes in Chronic Pancreatitis

Sasikala¹,

Talukdar²,

Subramanyam³

et al. 2016

Pancreas Open J

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Pancreatogenic or Type 3c diabetes (T3cDM) is relatively a new entry in the complex world of diabetes study. While the general population and physicians are well aware of type 1 and type 2 diabetes mellitus, as evidenced by numerous study groups and the reams of guidelines on diagnosis and treatment of type 1 and type 2 diabetes mellitus, relatively much less is known, considered and documented about diabetes mellitus that occurs secondary to pancreatic diseases. A casual search of Pubmed reveals less than 100 entries on type 3c diabetes. This may be because physicians earlier considered type 3c diabetes to be of rare occurrence and thus a condition rarely considered in everyday practice. Yet, recent data on type 3c diabetes (T3cDM) showed that it might be more common than generally thought. Studies also propose that this clinically important condition might be consistently under and misdiagnosed in routine clinical practice. 1 The World Health Organization (WHO) and American Diabetes Association (ADA) have categorized diabetes occurring as a result of benign and malignant disease to exocrine pancreas, such as chronic pancreatitis, hemochromatosis, cystic fibrosis, fibrocalculous pancreatopathy, pancreatic trauma, pancreatic cancer and pancreatectomy as Pancreaticogenic diabetes (T3cDM). 2,3 It is estimated that about 78.5% of T3cDM patients are with chronic pancreatitis and 8% of T3cDM are suffering from pancreatic cancer. 4 Globally about 10% of the total diabetic population has been diagnosed for Chronic Pancreatitis (CP), which is characterized by progressive fibrosis, irreversible exocrine and early onset endocrine dysfunction of pancreas. Recurrent and intractable abdominal pain is the dominant clinical hallmark that mandates aggressive treatment. An initial population-based study in Kerala (1996), confirmed later by questionnaire based studies in the Asia Pacific region, has recorded the prevalence of CP to be 114-200/100,000 populations in southern India, which is markedly higher than that in western industrialized nations (10-15/100,000). 5 Importantly, patients report initially with diabetes and then diagnosed for CP with the mean age of diagnosing CP being less than 30 years. However, it is noted that about 30% of patients with CP have diabetes and more than 50% of these individuals will develop diabetes before 40 years of age. In comparison to the western countries wherein it takes about 10 years for diabetes to manifest in diagnosed CP patients, it is within 2 years between onset of CP and diagnosis of diabetes in Indian patients, indicating the rapid loss of endocrine functions in these individuals.Although pathogenesis of diabetes in chronic pancreatitis has long been recognized, only recently it is classified as a distinct entity and guidelines have been developed supporting a specified diagnostic and therapeutic algorithm. 6 T3C DM is distinct from Type 1 and Type 2 DM as it arises due to chronic inflammation and has unique clinical and laboratory parameters and is associated with high incidence...

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Reduced Pancreatic Volume and β-Cell Area in Patients With Chronic Pancreatitis

Cited by 100 publications

References 35 publications

Determinants of glucose control in patients with chronic pancreatitis

Determinants of glucose control in patients with chronic pancreatitis

Pancreatic diabetes manifests when beta cell area declines by approximately 65% in humans

The Enigma of Type 3c Diabetes in Chronic Pancreatitis

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