Sabato 27 ottobre 2012 - Pacini Editore

PoStER
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Bile duct lesions in diabetic hepatosclerosis could
explain raised ALP and GGT in diabetic patients
T. Celiento1 , E. Nazzari2 , F. Pitto1 , S. Bruno1 , M.P. Brisigotti1 ,
M. Bruzzone1 , L. Mastracci1 , F. Grillo1 University of Genoa 1 Histopathology (DISC); 2 Endocrinology (DIMI)
Azienda Ospedaliera e Universitaria San Martino-IRCCS-IST, Genoa
Introduction. Diabetes mellitus (DM) is a complex chronic
metabolic disease characterized by hyperglycaemia. Many of the
severe complication of DM, such as diabetic nephropathy, retinopathy,
peripheral neuropathy and skin ulceration, are the result
of microangiopathy. High levels of blood glucose may damage
the sinusoidal endothelial cells via diverse mechanisms. The
hallmark is thickening of capillary basement membranes in the
vascular beds of the respective organs and tissue.
Liver disease associated with DM is common and usually takes
the form of simple steatosis/non-alcoholic fatty liver disease
(NAFDL), non-alcoholic steatohepatitis (NASH) 1 or rarely glycogenic
hepatopathy 2 .
The liver however may also be a target organ for microvascular
disease and this finding has been called diabetic hepatosclerosis
(DH) 3 . Only few reports and case series regarding this rare form
are found in the Literature 4-6 . The aim of this report is to describe
a further case of DH and describe bile duct lesions as a new histological
feature.
Methods and materials. The patient was male, aged 37 years
and had a long history of type 1 DM. He had a severe complications
of diabetes such as retinopathy, nephropathy, peripheral
neuropathy and systemic hypertension. At the time of hospitalization
he was oliguric with anasarca.
Liver function tests were characterized by elevated serum alkaline
phosphatase and bilirubin with clinical evidence of cholestasis.
After initial stabilization the patient showed a progressive worsening
of his general conditions with evidence of acute renal failure
for which he required dialysis. Septicemia then ensued secondary
to infection of a lower limb ulcer for which he was placed
under antibiotic cover and was consequently amputated. His liver
function tests however were still abnormal (total bilirubin: 14.6
mg/dL; Direct Bilirubin: 12.3 mg/dL; AST: 9 U/L; ALT: 6 U/L;
ALP: 1063 U/L; GGT: 209 U/L) and the patient became jaun-
369
diced. The clinical differential diagnoses which prompted biopsy
were steatohepatitis, sepsis, drug induced liver injury or chronic
bile duct disease.
Percutaneous liver biopsy (14 mm and 8 mm cores) was performed
and after formalin fixation and paraffin embedding 4
µm sections were cut and stained with haematoxylin and eosin,
Gordon and Sweet’s reticulin stain, Masson’s Trichrome, orcein,
Perl’s stain for iron and periodic acid-Shiff after diastase digestion
(DPAS). Further immunohistochemical stains for cytokeratin
7 for bile duct evaluation and smooth muscle actin (SMA) for
Fig. 1. a) dense concentric hyaline thickening of portal small hepatic
artery branches, highlighted by dpaS; b) dense perisinusoidal fibrosis
mainly in the centrivenular area, demonstrated with trichrome
staining; c) immunohistochemistry for Sma shows the presence of
extracellular matrix producing activated stellate cell.
A
B
C