Plasma cytokine levels imbalance in cirrhotic patients with impaired glucose tolerance and diabetes mellitus. A prospective study.

AIMS: To define if there is an imbalance in plasma levels of proinflammatory, fibrogenic and antifibrogenic cytokines in patients with liver cirrhosis (LC) and impaired glucose tolerance (IGT) or diabetes mellitus (DM). MATERIAL AND METHODS: We randomly selected 54 out of 100 patients with LC who had normal fasting plasma glucose (FPG) levels. Three groups were formed based on an oral glucose tolerance test (OGTT) results: 18 patients were normal, 18 had IGT, and 18 had DM. Plasma levels of cytokines were measured: TNF- α, soluble tumor necrosis factor receptor 1 (sTNF-R1), leptin, TGF-ß1, and hepatocyte growth factor (HGF). Also, fasting plasma insulin (FPI) levels were determined and HOMA2-IR was calculated. Results were compared with those of a control group of 18 patients without liver disease nor DM. Intergroup comparison was performed using non parametric tests. RESULTS: Significantly higher sTNF-R1 and lower TGF-ß1 were found in patients with IGT and DM compared to controls. Leptin, HGF, and TNF-α levels showed no significant differences. According to Child-Pugh classification all cytokines levels were impaired in groups B or C as compared to group A. Positive correlations between sTNF-R1 and HOMA2-IR and between leptin and HOMA2-IR were found. CONCLUSIONS: IGT and DM were associated with abnormalities of sTNF-R1 and TGF-ß1 compared to non cirrhotic controls. Among cirrhotic patients impairment of all cytokines were more marked in advanced liver disease. Finally, sTNF-R1 and leptin correlated with IR. These findings suggest that IGT and DM may be causally implicated with liver inflammation process.

La diabetes en la cirrosis hepática / Diabetes in liver cirrhosis

La prevalencia de la diabetes mellitus (DM) clínica en la cirrosis hepática es del 30%, sin embargo en pacientes con glucemia en ayuno normal puede haber intolerancia a la glucosa y DM en el 90% de los casos después de una carga oral de glucosa. La DM tipo 2 puede producir una cirrosis, sin embargo, la cirrosis puede complicarse con una DM. A esta última forma de diabetes se la conoce como diabetes hepatógena. Se ha demostrado que la DM clínica o subclínica se asocia a un incremento de las complicaciones hepáticas y de la mortalidad. El tratamiento de la diabetes del cirrótico tiene muchas dificultades propias de la enfermedad hepática. Se desconoce cuál es el tratamiento más adecuado, ya que no existen guías de tratamiento. Además, no se sabe cómo impacta el manejo adecuado de este trastorno en la historia natural de la cirrosis hepática (AU)

The prevalence of overt diabetes mellitus (DM) in liver cirrhosis is about 30%. However, DM or impaired glucose tolerance can be observed in 90% after an oral glucose tolerance test in patients with normal fasting plasma glucose. Type 2 DM may produce cirrhosis, whereas DM may be a complication of cirrhosis. The latter is known as «hepatogenous diabetes». Overt and subclinical DM is associated with liver complications and death in cirrhotic patients. Treating diabetes is difficult in cirrhotic patients because of the metabolic impairments due to liver disease and because the most appropriate pharmacologic treatment has not been defined. It is also unknown if glycemic control with hypoglycemic agents has any impact on the course of the liver disease (AU)

[Diabetes in liver cirrhosis]. / La diabetes en la cirrosis hepática.

The prevalence of overt diabetes mellitus (DM) in liver cirrhosis is about 30%. However, DM or impaired glucose tolerance can be observed in 90% after an oral glucose tolerance test in patients with normal fasting plasma glucose. Type 2 DM may produce cirrhosis, whereas DM may be a complication of cirrhosis. The latter is known as «hepatogenous diabetes¼. Overt and subclinical DM is associated with liver complications and death in cirrhotic patients. Treating diabetes is difficult in cirrhotic patients because of the metabolic impairments due to liver disease and because the most appropriate pharmacologic treatment has not been defined. It is also unknown if glycemic control with hypoglycemic agents has any impact on the course of the liver disease.

Diabetic myonecrosis in a patient with hepatic cirrhosis: a case report and review of the literature.

INTRODUCTION: Diabetic myonecrosis was first reported by Angervall and Stener in 1965. In its classical clinical expression, it affects type 1 diabetes mellitus patients with long-standing poor metabolic control and advanced chronic microvascular complications. A sudden-onset of severe pain in the region of the involved muscle, usually the quadriceps, is the typical clinical manifestation. Magnetic resonance imaging (MRI) confirms the clinical diagnosis; in some cases of diagnostic uncertainty, a muscle biopsy may be required. CASE PRESENTATION: We present the case of a 38 year-old Hispanic male from Mexico, with alcohol-induced hepatic cirrhosis (Child-Pugh C/MELD 45) and type 2 diabetes mellitus admitted to the emergency room due to hepatic encephalopathy with intense pain and an increase in volume of the left thigh. MRI showed edema and inflammatory changes of the quadriceps muscle with a hyperintense signal on T2-weighted images; in addition, there was a subacute hematoma. CONCLUSION: To the best of our knowledge, this is the first case of diabetic myonecrosis associated with and complicated by advanced hepatic cirrhosis reported in the literature.

[Gastropathy caused by non-steroidal anti-inflammatory agents and its association with Helicobacter pylori]. / Gastropatía por antiinflamatorios no esteroideos y su asociación con Helicobacter pylori.

BACKGROUND: Upper gastrointestinal bleeding that is related with older patients and NSAIDs use. The frequency of peptic ulcer bleeding varies of 15% to 30% of cases. OBJECTIVE: To determine the gastropathy features of patients who receive nonsteroidal anti-inflammatory drug, and its relation with Helicobacter pylori (Hp). METHODS: Men and women with GU or DU with or without haemorrhage, were included into two groups, NSAIDs users and non users. We determined the incidence rate of peptic ulcer and the frequencies of risk factors as tobacco use, previous peptic ulcer or haemorrhage, concomitant disease presence and its association with Hp infection. RESULTS: We included 434 (67.5%) patients that used NSAIDs and 209 (32.5%) non NSAIDs users control subjects. The average was 62.5 +/- 17.2 years and 49.5 +/- 19.4 years respectively. The annual incidence rate of peptic ulcer in NSAIDs users was 17.5%. Gastrointestinal bleeding was more frequent in NSAIDs users and its relations with Hp infection (23.5%) was smaller than patients without NSAIDs user (47.7%) (OR 0.39 p = 0.0000). CONCLUSIONS: The GU was highly frequent in the older people who using NSAIDs. The Hp infection shows lower incidence of gastrointestinal bleeding NSAIDs users.