Glycogenic Hepatopathy in a Patient with Pancreatogenic Diabetes

Glycogenic hepatopathy is characterized by acute liver injury secondary to reversible accumulation of excess glycogen in hepatocytes. This phenomenon has been described in type 1 diabetes, with few cases reported in patients with type 2 diabetes. Glycogenic hepatopathy in the setting of pancreatogenic (type 3c) diabetes has yet to be reported. A 57-year-old female with a history of insulin-requiring pancreatogenic diabetes mellitus secondary to alcohol-induced chronic pancreatitis status post distal pancreatectomy presented with recurrent admissions for abdominal pain, hyperglycemia, hyperosmolar hyperglycemic state (HHS), and unexplained elevation of liver transaminase levels. Glycemic control remained poor over many years with consistently elevated HbA1c in the setting of labile blood sugars, medication noncompliance, and lifestyle non-adherence. The patient was admitted to the hospital with altered mental status and markedly elevated blood glucose (1,182 mg/dL) concerning for HHS. On admission, her liver function tests (LFTs) revealed elevated alkaline phosphatase (1,011 U/L, n <150 U/L), AST (583 U/L, n <34 U/L), and ALT (517 U/L, n <55 U/L). Direct and total bilirubin were within normal limits. The patient underwent extensive workup including drug and toxin levels, autoimmune evaluation, serology for infectious causes, abdominal computed tomography scanning, right upper quadrant ultrasound, and magnetic resonance cholangiopancreatography (MRCP). All laboratory workup was negative, ultrasound was unremarkable, and MRCP showed no evidence of biliary or common bile duct dilatation. Throughout her hospitalization, LFTs gradually improved with optimization of blood glucose. Less than one week later, the patient returned with blood glucose of 673 mg/dL and LFTs notable for alkaline phosphatase 789 U/L, AST 1,068 U/L, and ALT 299 U/L. Again, all testing was negative for causes of rapid increase in liver enzymes. Similar to previous admissions, her LFTs improved with resolution of hyperglycemia. Review of electronic medical record revealed a similar trend during previous admissions. The patient did not undergo liver biopsy; however, the parallel relationship of LFTs and hyperglycemia, in the absence of radiologic or laboratory evidence of alternate liver pathology, supports the diagnosis of glycogenic hepatopathy. This is the first case of glycogenic hepatopathy reported in a patient with pancreatogenic diabetes. Due to the rarity of this condition and minimal literature of its occurrence in adult non-type-1 diabetics, glycogenic hepatopathy is likely infrequently considered when evaluating patients with recurrent hyperglycemia and elevated LFTs. This case accentuates the need for further research of this condition in non-type 1 diabetics as the prognosis and management differ from other forms of acute liver injury.

Insulinbedarf und Glukosehomöostase bei Menschen nach partieller und totaler Pankreatektomie im Vergleich zu Menschen mit anderen Diabetesformen

Zusammenfassung Einleitung Pankreasresektionen werden bei schwerwiegenden Pankreaserkrankungen durchgeführt. Bei Komplikationen einer chronischen Pankreatitis, teilweise jedoch auch bei Raumforderungen, kann eine Pankreasteilresektion sinnvoll sein. Eine totale Pankreatektomie führt zum absoluten Insulinmangel und der Notwendigkeit einer Insulintherapie. Bei Teilresektionen (partielle Pankreatektomie) werden weniger gravierende Konsequenzen für den Glukosemetabolismus erwartet. Es ist das Ziel der vorliegenden Arbeit, die Insulinregime nach Pankreatektomie mit denen anderer Diabetesformen zu vergleichen. Material und Methodik Es wurden Patientencharakteristika und Details der postoperativen Insulintherapie von pankreasoperierten Patienten einer spezialisierten Universitätsklinik für Viszeralchirurgie ausgewertet. Diese Daten wurden mit Kohorten nicht operierter Patienten mit Typ-1-Diabetes (T1DM; absoluter Insulinmangel) bzw. Typ-2-Diabetes (T2DM; Insulinresistenz und relativer Insulinmangel), jeweils unter Insulintherapie, verglichen. Ergänzt wurde diese Datenanalyse durch eine Literaturrecherche zu den Stichworten „pancreatogenic diabetes“, „type 3c diabetes“ und „pancreatectomy diabetes“. Ergebnisse Daten von 32 (68,8 % Frauenanteil) bzw. 41 (43,9 % Frauenanteil) Patienten nach totaler bzw. partieller Pankreatektomie wurden analysiert. Vor der totalen Pankreatektomie hatten 56,3 % der Patienten einen Diabetes mellitus, postoperativ bestand bei allen Patienten eine Insulinpflichtigkeit. Dabei waren die Insulindosierungen im Vergleich mit Patienten mit T1DM (unter intensivierter Insulintherapie) signifikant niedriger (p < 0,0001). Die Dosierungen von Basal- (48,6 % weniger) und Mahlzeiteninsulin (38,1 % weniger) waren gleichermaßen betroffen. Eine partielle Pankreatektomie führte deutlich seltener zu einem Diabetes mellitus, und eine Insulintherapie war nur bei 26,8 % der Patienten erforderlich. Diskussion Der basale und prandiale Insulinbedarf nach Pankreatektomie ist niedriger als bei einem T1DM und einem T2DM. Dies sollte bei der Blutzuckereinstellung nach Pankreatektomie berücksichtigt werden.

Pancreatogenic Diabetes: Triggering Effects of Alcohol and HIV

Multiorgan failure may not be completely resolved among people living with HIV despite HAART use. Although the chances of organ dysfunction may be relatively low, alcohol may potentiate HIV-induced toxic effects in the organs of alcohol-abusing, HIV-infected individuals. The pancreas is one of the most implicated organs, which is manifested as diabetes mellitus or pancreatic cancer. Both alcohol and HIV may trigger pancreatitis, but the combined effects have not been explored. The aim of this review is to explore the literature for understanding the mechanisms of HIV and alcohol-induced pancreatotoxicity. We found that while premature alcohol-inducing zymogen activation is a known trigger of alcoholic pancreatitis, HIV entry through C-C chemokine receptor type 5 (CCR5) into pancreatic acinar cells may also contribute to pancreatitis in people living with HIV (PLWH). HIV proteins induce oxidative and ER stresses, causing necrosis. Furthermore, infiltrative immune cells induce necrosis on HIV-containing acinar cells. When necrotic products interact with pancreatic stellate cells, they become activated, leading to the release of both inflammatory and profibrotic cytokines and resulting in pancreatitis. Effective therapeutic strategies should block CCR5 and ameliorate alcohol’s effects on acinar cells.

Correction of Metabolic Disorders in Patients with Pancreatic Cancer

Presented the case of complex examination of a patient with pancreatic cancer using a bioimpedance method for assessing the nutritional status before and after surgical treatment. Provided the literature data related to this problem. The presented clinical case demonstrates the features of correction of the nutritional status of a patient with conditionally resectable pancreatic cancer in conditions of cholestasis, severe external pancreatic insufficiency and pancreatogenic diabetes mellitus on the background of constitutional obesity

Transplantation technologies for treatment of carbohydrate metabolism disorders

The review includes results of retrospective and prospective clinical studies (foreign and national) and guidelines on the use of transplantation technologies for treatment of type 1 diabetes and pancreatogenic diabetes in chronic pancreatitis and pancreatic conditions. Modern data on prevalence of diabetes and modern insulin delivery methods are presented. Results of transplantation of pancreas and islets of Langerhans in primary insulin-dependent conditions are considered. Analysis of the technology for isolation and autotransplantation of islets after pancreatectomy in chronic pancreatitis and benign tumor diseases are given.