Newsgroup: it.salute
Titolo: Steatosi epatica

Ad un'ecografia dell'addome mi e' stata dignostica una steatosi epatica.
Dato che sono gravemento obeso (121 Kg - 1.70 di altezza), vorrei sapere
se e' quasi fisiologico che abbia il fegato grasso, oppure se e' un
disturbo serio per il quale dovrei prendere provvedimenti.
L'epatosteatosi puo' evolvere in cirrosi?
Grazie a chi mi vorra' rispondere.
Un cordiale saluto a tutti.
Antonio

 L'epatosteatosi puo' evolvere in cirrosi?
si'.


 si'.
Uhu? Uhmmm...sicuro sicuro sicuro? :-)
Saluti
Lella

In 9fhcsp$3vc77$
7...@ID-55447.news.dfncis.de
, Lella, 
lella...@vene.dave.it
,


la concezione tradizionale della steatosi e' che si tratta di una patologia
benigna e reversibile; tuttavia sta crescendo la consapevolezza della
correalazione tra steatosi e cirrosi. La domanda era "Puo' evolvere". Allo
stato la risposta e' si', anche se questo non significa che "Deve evolvere".
BTW chi ha postato la domanda non ha escluso la correlazione con l'alcool o
con l'epatite C che farebbe crescere notevolmente la possibilita' di
un'evoluzione in tal senso.
cosi' il Merck:
Potentially reversible, macrovesicular fatty liver usually is not in itself
harmful. It is reversible even in potentially fatal instances (eg, in fatty
liver of pregnancy, early delivery may be lifesaving). Alcoholic fatty liver
may be accompanied by inflammation and necrosis (alcoholic hepatitis) and
permanent damage in the form of cirrhosis. Microvesicular fatty liver
presents acutely but is reversible if the patient survives.
No specific therapy is available except to eliminate the cause or treat the
underlying disorder. Even obesity and diabetes mellitus with fatty liver are
thought not to progress to cirrhosis. Although hepatotoxins such as alcohol
and carbon tetrachloride (which also produce necrosis) can eventually result
in cirrhosis, there is no evidence that a fatty liver per se leads to
cirrhosis. Some other event must occur.
Nonalcoholic fatty liver disease generally has a good prognosis, without
histologic or clinical progression. Some livers may show increased fibrosis
and progression to cirrhosis. Management includes weight loss for obese
patients, although this is of unproven benefit. Anecdotal reports indicate a
benefit from ursodeoxycholic acid therapy.
che riporta in sostanza la posizione piu' consolidata. Ma gli articoli piu'
recenti implicano costantemente questa possibilita' (questi abstracts non
sono scelti ma presi a caso tra molti altri dalla ricerca "nash+cirrhosis"):
Semin Liver Dis 2001;21(1):3-16    Related Articles, Books
Nonalcoholic steatohepatitis: definition and pathology.
Brunt EM.
Department of Pathology, 4th Floor, Saint Louis University Hospital, 3635
Vista Ave., St. Louis, MO 63110, USA. 
bru...@slu.edu
Nonalcoholic steatohepatitis (NASH) is a significant form of chronic liver
disease in adults and children. The natural history of NASH ranges from
indolent to end-stage liver disease. Current studies are focusing on
identification of histologic and/or clinical markers of progression. NASH
may be an underlying cause of cryptogenic cirrhosis, and the lesions of NASH
may recur in allograft livers. An expanding array of clinical conditions and
pathogenetic mechanisms have been identified, but many cases remain
"idiopathic"; lack of significant alcohol use is, by definition, common to
all cases. Neither clinical evaluation nor laboratory values can ensure
either the diagnosis or the exclusion of NASH, and liver biopsy
interpretation continues to be considered the "gold standard" for diagnosis.
The lesions in NASH are similar but not identical to those of alcoholic
steatohepatitis; exact, specific histologic criteria for the diagnosis are
currently under discussion. The lesions most commonly accepted for NASH
include steatosis, hepatocyte ballooning degeneration, mild diffuse lobular
mixed acute and chronic inflammation, and perivenular, perisinusoidal
collagen deposition. Zone 3 accentuation may be detected. Mallory's hyaline,
vacuolated nuclei in periportal hepatocytes, lobular lipogranulomas, and
PAS-diastase-resistant Kupffer cells are common. In biopsy specimens from
children, portal inflammation may be more prominent than in adults.
Progression of fibrosis may result in bridging septa and cirrhosis. The
lesions of steatohepatitis may be noted concurrently with other forms of
chronic liver disease. A histological "grading and staging" system has been
developed to reflect the unique features of steatohepatitis, gradations of
severity and fibrosis, and to promote uniform reporting of the
histopathology.
PMID: 11296695 [PubMed - in process]
J Assoc Physicians India 2000 Mar;48(3):311-3    Related Articles, Books
Nonalcoholic steatohepatitis: clinicopathological profile.
Amarapurkar DN, Amarapurkar AD.
Bombay Hospital and Medical Research Centre.
AIMS: To evaluate clinicopathological spectrum of nonalcoholic
steatohepatitis (NASH) METHODOLOGY: Total 210 patients with chronic liver
disease were evaluated. Detailed history has taken with clinical
examination, laboratory investigations, radiological findings and liver
biopsy whenever possible. RESULTS: From 210 patients of chronic liver
disease, 13 (6.19%) were diagnosed to have NASH (M:F = 9:4, age range 37-72
years, mean age 55.4 +/- 9 years). Of 13 patients, four were referred for
asymptomatic enzyme elevation, nine had right hypochondriac pain. Risk
factors were diabetes in four cases, obesity four, steroid treatment two and
hyperlipidemia in three cases. Laboratory investigations showed abnormal
liver enzymes in all the cases. Ultrasonography and CT scan was helpful in
predicting fatty liver. Liver biopsy showed steatosis with inflammation in
all, fibrosis in two and cirrhosis in one patient. CONCLUSION: NASH is an
important form of chronic liver disease, and is characterised by
hepatomegaly, elevated liver enzymes. It is essential to diagnose this
condition due to its progression to liver fibrosis and cirrhosis in some
patients.
PMID: 11229116 [PubMed - indexed for MEDLINE]
 Mayo Clin Proc 2000 Jul;75(7):733-9    Related Articles, Books, LinkOut
Nonalcoholic steatohepatitis.
Kumar KS, Malet PF.
Division of Digestive and Liver Diseases, University of Texas Southwestern
Medical Center at Dallas 75390-9151, USA.
Nonalcoholic steatohepatitis (NASH) is a liver disease that, until recently,
has been underrecognized as a common cause of elevated liver enzymes. This
distinct clinical entity is characterized by liver biopsy findings similar
to those seen in alcoholic hepatitis but in the absence of alcohol
consumption sufficient to cause such changes. Patients with NASH are often
middle-aged and obese, with coexisting diabetes or hyperlipidemia, but NASH
also occurs in younger lean, otherwise healthy individuals and even in
children. Although NASH is generally a benign disorder, it may be
progressive, leading to cirrhosis and complications of portal hypertension.
Liver biopsy remains the gold standard for diagnosis. Therapy for NASH
remains poorly defined, although weight reduction and ursodeoxycholic acid
may have a beneficial effect.
PMID: 10907390 [PubMed - indexed for MEDLINE]
Can J Gastroenterol 2000 Apr;14(4):321-6    Related Articles, Books, LinkOut
Nonalcoholic steatohepatitis: an evolving diagnosis.
Neuschwander-Tetri BA.
Saint Louis University, MO 63110, USA. 
tet...@slu.edu
Nonalcoholic steatohepatitis (NASH) is a histological diagnosis applied to a
constellation of liver biopsy findings that develop in the absence of
alcohol abuse. Steatosis, a mixed cellular inflammatory infiltrate across
the lobule, evidence of hepatocyte injury and fibrosis are the findings that
can be seen. This entity is often identified during evaluation of elevated
aminotransferases after exclusion of viral, metabolic and other causes of
liver disease. Obesity is a major risk factor for NASH. The role of diabetes
is less certain, although evidence is accumulating that hyperinsulinism may
play an important pathophysiological role. Patients sometimes suffer from
right upper quadrant abdominal pain and fatigue; examination may reveal
centripetal obesity and hepatomegaly. Although patients are often discovered
because of persistent aminotransferase elevations, these enzymes can be
normal in NASH. When they are elevated, the alanine aminotransferase level
is typically significantly greater than the aspartate aminotransferase
level. This can be particularly helpful for excluding occult alcohol abuse.
Imaging studies identify hepatic steatosis when the amount of fat in the
liver is significant; however, imaging does not distinguish benign steatosis
from NASH. Ultimately a liver biopsy is needed to diagnose NASH. The biopsy
may be useful for establishing prognosis based on the presence or absence of
fibrosis and for excluding other unexpected causes of liver enzyme
elevations. Weight loss is the mainstay of treatment for obese patients.
About 15% to 40% of NASH patients develop fibrosis; how many of these cases
progress to cirrhosis is unknown, but about 1% of liver transplants are
performed with a pretransplant diagnosis of NASH.
PMID: 10799085 [PubMed - indexed for MEDLINE]
quindi sicuro sicuro sicuro no, ma certo il rischio di avere una cirrosi e'
sigificativamnte piu' elevato nei cfr. di chi non ha steatosi. Questo
dovrebbe incoraggiare la persona a prendere dei provvedimenti in primo luogo
dietetici.
saluti,
Marko

 PAS-diastase-resistant Kupffer cells are common.
Allora...la steatosi (quello di cui si stava parlando) è solo *una*
componente della NASH, giusto? Ovvero, se manca il danno,
l'infiammazione, la fibrosi, stiamo parlando di un'altra cosa! :-)
IMHO, la steatosi non evolve in cirrosi, certo che se i fattori che
hanno portato alla steatosi perdurano o peggiorano, portando ad un danno
epatico etc etc...bhè...
Mi spiego meglio. Se il pz, una volta informato sul problema, interrompe
i fattori di rischio, tutto torna nella norma. La steatosi regredisce.
La fibrosi rimane, ma magari non crea altri danni. La cirrosi rimane ed
evolve, anche se in maniera più lenta. Ecco, intendevo questo! :-)))
Saluti
Lella ed i puntini sulle I