title: Fasting hyperglycaemia following trans-catheter arterial chemo-embolization for hepatocellular carcinoma in cirrhosis.
abstract: OBJECTIVE
  Following a hyperosmolar diabetic coma in a cirrhotic patient with hepatocellular carcinoma undergoing transcatheter arterial chemo-embolization, we assessed the prevalence, severity, causes and prognostic impact of impaired glucose metabolism following transcatheter arterial chemo-embolization.
  
  
  METHODS
  Plasma glucose, pancreatic and thyroid hormones, cortisol, growth hormone, ACTH and TSH concentrations were determined before and after transcatheter arterial chemo-embolization in 98 patients (70 with a normal fasting glucose, 7 with mild fasting hyperglycaemia and 21 diabetics) undergoing 226 transcatheter arterial chemo-embolization procedures. Child status, body temperature, serum ALT and amylase levels, tumour size, gelfoam embolization and disease aetiology were recorded. Liver function was assessed before and after transcatheter arterial chemo-embolization by measuring monoethylglycinexylidide formation after i.v. lidocaine.
  
  
  RESULTS
  A significant rise in glucose levels (p < 0.0001) was observed in 30/98 patients. Hyperglycaemia was more frequent in diabetics (67%) and patients with mild fasting hyperglycaemia (71%). Glucose concentrations doubled in 12 patients; 4 required long-term insulin. Fever, a previously altered carbohydrate metabolism and raised ALT levels were prognostic factors for hyperglycaemia (p < 0.01). Plasma C-peptide, glucose/insulin and glucose/C-peptide ratios, were increased after transcatheter arterial chemo-embolization (p < 0.05). Transcatheter arterial chemo-embolization was followed by a reduction in the monoethylglycinexylidide formation capacity (p < 0.05), particularly in hyperglycaemia patients (p < 0.02).
  
  
  CONCLUSIONS
  Transcatheter arterial chemo-embolization is frequently followed by a derangement in glucose metabolism which is potentially severe, associated with preceding glucose imbalance, fever and a transient deterioration in liver function.
authors.affiliation: Department of Gastroenterology, Padua University, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Farinati
authors.forename: M
authors.initials: M
authors.lastname: Rinaldi
authors.forename: S
authors.initials: S
authors.lastname: Del Prato
authors.forename: S
authors.initials: S
authors.lastname: Lana
authors.forename: N
authors.initials: N
authors.lastname: De Maria
authors.forename: D
authors.initials: D
authors.lastname: Paleari
authors.forename: C
authors.initials: C
authors.lastname: Marafin
authors.forename: R
authors.initials: R
authors.lastname: Naccarato
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002096:C-Peptide / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000097:blood / Q000150:complications / Q000628:therapy*; D016461:Chemoembolization, Therapeutic / Q000009:adverse effects*; D005215:Fasting; D005260:Female; D006728:Hormones / Q000097:blood; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology*; D007328:Insulin / Q000097:blood; D008103:Liver Cirrhosis / Q000150:complications*; D008113:Liver Neoplasms / Q000097:blood / Q000150:complications / Q000628:therapy*; D008297:Male; D008875:Middle Aged
chemical_list: D002096:C-Peptide; D006728:Hormones; D007328:Insulin