Of course. This is the first step for development of diabetes and liver disease-T2DM associated. In Hepatogenous diabetes IR appears after liver disease has emerged. Nevertheless IR in hepatogenous diabetes is associated with function deterioration and failure, also progresion to HCC. IR has diferent position regarding LC secondary to T2DM and Hepatogenous diabetes.
It could. It turns out that hepatitis, which causes liver cirrhosis and carcinoma, may also make individuals much more likely to develop type 2 diabetes. A recent study from Australia has reported that persons with hepatitis C possess elevated insulin resistance, which is a forerunner to diabetes.
Very true...My own article on Insulin resistance in euglycemic cirrhosis..I have shown IR develops in early stages of liver disease especially NAFLD, HCV, AIH. Insulin resistance progressively increases with rise in MELD/ CTP score. Pancreatic Liver crosstalk results in pancreatic beta cell increase functioning to compensate the insulin resistance. Fall in pancreatic beta cell results in development of hepatogenous diabetes. But over what period the pancreatic beta cell dysfunction occurs is yet to be clarified
Article Insulin resistance in euglycemic cirrhosis
Of course. This is the first step for development of diabetes and liver disease-T2DM associated. In Hepatogenous diabetes IR appears after liver disease has emerged. Nevertheless IR in hepatogenous diabetes is associated with function deterioration and failure, also progresion to HCC. IR has diferent position regarding LC secondary to T2DM and Hepatogenous diabetes.
There appears to be a close link - patients with NAFLD and IR, prediabetes or diabetes have more severe liver injury than those without all other parameter being "equal", at least that is what I see inpatients locally. I think this relates to the way IR affects lipid flow through the liver - easier in and harder out. On the other site patients with advanced cirrhosis of any cause of develop diabetes as a late complication - they usual will need insulin due to SE and risk profile of oral medication for diabetes.
One of the most important question concerning to liver disease and diabetes is related to the clinical implication of this association.
I have to explain: In onse side, It has been observed that hereditary Type 2 Diabetes Mellitus may give rise to liver steatosis, NASH and liver cirrhosis (and finally HCC). In the other side, in cirrhotic patients without history of DM and normal plasma glucose levels, 70% have insulin resistance (IR), glucose intolerance or DM after an oral glucose tolerance test (OGTT). Particularly, those with viral, alcoholic, and metabolic etiology (1). It means that liver cirrhosis must be considered as a diabetogenic condition. Diabetes that appears as a consequence of liver disease is called ¨hepatogenous diabetes¨ (not recognized by the ADA). The following question is : What is the clinical implication of HD? At least 3 prospective studies (1-3) (one from our team) have demonstrated that cirrhotic patients with hepatogenous diabetes (abnormal OGTT) have long term higher mortality than those without. It has been speculated that diabetes may deteriorate liver function and increase fibrosis stimulation and inflammation by means of an impairment of adipocytokines: increase of R1-TNF, soluble TNFα and TGFβ as well as a reduction of adiponectine. These findings have been reported in cirrhotic-diabetic patients. HD has been implicated with hepatic encephalopathy, spontaneous primary peritonitis and renal impairment In base of the above mentioned, Diabetes may be considered as a complication of cirrhosis in the same level as hepatic encephalopathy, ascites, portal hypertension.
Currently it is ironic that the impact of the adequate control of glucose levels on liver complications and survival of these patients have not been established. Furthermore because treatment of diabetes in these patients is quite difficult given toxicity and sensibility of these patients to hypoglycemic drugs and insulin. However it is probable that glucose control may improve prognosis.
Attending for more research regarding therapeutic guidelines for treatment of diabetes in cirrhotics it is highly recommended to control glucose level in these patients. Pioglitazone, metformin and acarbose seem to be safe therapeutic agents. Currently incretin mimetics are being assayed and seem to bw promising. Insulin should to be initiated only in in-hospital patients.
Finally I think that an OGTT should be performed to all patients with liver cirrhosis, with no history of diabetes and with normal glucose plasma levels in order to detect glucose metabolism disorders for evaluating prognosis and adaptations of therapy.
References
1. García-Compeán D, Jáquez-Quintana JO, Lavalle-González FJ, et al. The prevalence and clinical characteristics of glucose metabolism disorders in patients with liver cirrhosis. A prospective study. Ann Hepatol. 2012; 11:240-248.
2. García-Compeán D, Jáquez-Quintana JO, Lavalle-González FJ et al. Subclinical abnormal glucose tolerance is a predictor of death in liver cirrhosis.World J Gastroenterol. 2014 Jun 14;20(22):7011-8
3. Holstein A, Hinze S, Thiessen E et al. Clinical implications of hepatogenous diabetes in liver cirrhosis. J Gastroenterol Hepatol 2002; 17:677-681.
4. Nishida T, Tsuji S, Tsujii M, et al. Oral glucose tolerance test predicts prognosis of patients with liver cirrhosis. Am J Gastroenterol 2006; 101:70-75.
More and more study is needed to establish the diabetes which develops after liver disease. Hepatogenous diabetes should be named as Type 4 DM after the Type 3 DM which develops in pancreatic dysfunction. Lot of work needs to be done before its entity gets established