Sinusoidal caliber in alcoholic and nonalcoholic liver disease: Diagnostic and pathogenic implications

Abstract

Portal hypertension in alcoholic liver disease has been attributed to an increased resistance to blood flow either of sinusoidal or of postsinusoidal origin. The former should be accompanied by sinusoidal compression while the latter is expected to result in an increased or a normal sinusoidal diameter. Patients with alcoholic liver disease showed a marked reduction (p less than 0.001) in relative sinusoidal area (995 +/- 135 micron 2; n = 19) when compared to nonalcoholic patients with normal liver histology (5,100 +/- 389 micron 2; n = 6), or to patients with nonalcoholic liver disease (6,242 +/- 467 micron 2; n = 19). Hepatocyte surface area was significantly increased in patients with alcoholic liver disease when compared to hepatocytes from normal biopsies (563 +/- 32 micron 2 vs. 301 +/- 26 micron 2; p less than 0.001). Patients with nonalcoholic liver disease had hepatocyte surface areas within the normal range (327 +/- 14 micron 2). There was a significant inverse correlation between hepatocyte size and sinusoidal area (r = -0.63; p less than 10(-6); n = 44), indicating that larger hepatocytes were associated with sinusoidal compression. In the alcoholic patients, portal pressure correlated inversely (r = -0.77; p less than 0.01) with sinusoidal area only after the sinusoidal area was markedly reduced to areas below 20% of normal. Such a threshold was not reached in patients with nonalcoholic liver disease, in whom no correlation between sinusoidal area and portal pressure was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Identification of Factors Contributing to Hepatomegaly in Severely Burned Children

“…Intracellular volume increases can also result in an increase in intrahepatic pressure (13). Studies have shown that an increase in hepatocyte surface area is associated with a reduction in the relative liver sinusoidal area and an increase in portal pressure (14). It has also been demonstrated that hepatocyte size correlates well with hepatic wedge pressures and intrahepatic pressures, which are independent of fatty liver or cirrhosis (13).…”

Development of risky varices in alcoholic cirrhosis with a well-maintained nutritional status

“…The present study showed that alcoholic compensated cirrhotic patients can develop severe portal hypertension even with a relatively well-maintained liver pressure and portal hypertension depending on several conditions which vary from hepatitis virus-related CLDs, such as compression of the hepatic sinusoid by enlarged hepatocytes in the form of ballooning [6][7][8] . In addition, perivenular fibrosis, one of histological characteristics of ALD, is also suggested to contribute to the development of portal hypertension [15][16][17] .…”

“…For instance, the enlargement of hepatocytes with ballooning was reported to mechanically compress the sinusoid and contribute to increased pressure of the portal vein [6][7][8] . Therefore, the severity of portal hypertension in alcoholic liver cirrhosis tends to be more remarkable than that in hepatitis virus-related cirrhosis, and patients with alcoholic liver cirrhosis are suggested to develop large varices even with a relatively well-maintained liver function and general clinical conditions [9][10][11] .…”

Pathophysiology of portal hypertension

“…More significant however, are the variable factors which modulate the intrahepatic vascular resistance 10 . Portal flow may be obstructed by compression of simusoids by swollen hepatocytes in alcoholics—even before frank cirrhosis appears 11 …”