Revaluation of clinical and histological criteria for diagnosis of dysmetabolic iron overload syndrome.
OBJECTIVE
To re-evaluate the diagnostic criteria of insulin resistance hepatic iron overload based on clinical, biochemical and histopathological findings.


METHODS
We studied 81 patients with hepatic iron overload not explained by known genetic and acquired causes. The metabolic syndrome (MS) was defined according to ATPIII criteria. Iron overload was assessed by liver biopsy. Liver histology was evaluated by Ishak's score and iron accumulation by Deugnier's score; steatosis was diagnosed when present in >or=5% of hepatocytes.


RESULTS
According to transferrin saturation levels, we observed significant differences in the amount of hepatic iron overload and iron distribution, as well as the number of metabolic abnormalities. Using Receiving Operating Curve analysis, we found that the presence of two components of the MS differentiated two groups with a statistically significant different hepatic iron overload (P<0.0001). Patients with >or=2 metabolic alterations and steatosis had lower amount of hepatic iron, lower transferrin saturation and higher sinusoidal iron than patients with <2 MS components and absence of steatosis.


CONCLUSIONS
In our patients, the presence of >or2 alterations of the MS and hepatic steatosis was associated with a moderate form of iron overload with a prevalent sinusoidal distribution and a normal transferrin saturation, suggesting the existence of a peculiar pathogenetic mechanism of iron accumulation. These patients may have the typical dysmetabolic iron overload syndrome. By contrast, patients with transferrin saturation>or=60% had more severe iron overload, few or no metabolic abnormalities and a hemochromatosis-like pattern of iron overload.
Riva
Alessia
A
Department of Clinical Medicine, University of Milano-Bicocca, San Gerardo Hospital, Via Pergolesi 33, Monza 20052, Italy.
Trombini
Paola
P
Mariani
Raffaella
R
Salvioni
Alessandra
A
Coletti
Sabina
S
Bonfadini
Silvia
S
Paolini
Valentina
V
Pozzi
Matteo
M
Facchetti
Rita
R
Bovo
Giorgio
G
Piperno
Alberto
A
D000328:Adult; D000368:Aged; D005234:Fatty Liver / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006432:Hemochromatosis / Q000235:genetics / Q000378:metabolism; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I / Q000235:genetics; D006801:Humans; D007333:Insulin Resistance; D007501:Iron / Q000378:metabolism*; D019190:Iron Overload / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D024821:Metabolic Syndrome / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008875:Middle Aged; D011237:Predictive Value of Tests; D012372:ROC Curve; D012307:Risk Factors; D012720:Severity of Illness Index; D014168:Transferrin / Q000378:metabolism
C103673:HFE protein, human; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I; D008565:Membrane Proteins; D014168:Transferrin; D007501:Iron