Fibrosis periportal

E. histolytica invades mucosal cells of colonic epithelium, producing the classic flask-shaped ulcer in the submucosa. The trophozoite toxin has a cytocidal effect on cells. If the trophozoite gets into the portal circulation, it will be carried to the liver, where it produces abscess and periportal fibrosis. Liver abscesses are more common in men than women and are rarely seen in children. Amebic ulcerations can affect the perineum and genitalia, and abscesses may occur in the lung and brain. 

Findings from studies of schistosomiasis-induced liver fibrosis, as well as other models of pulmonary, kidney, and liver fibrosis, strongly support the role of CD4+ Th2 cells in the progression of fibrosis (4). In this regard, analyses of gene and protein expression after stimulation by Thl (vs. Th2) cytokines indicates that IL-4 is found at increased concentrations in the bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis, as well as in the peripheral blood mononuclear cells of those afflicted with periportal fibrosis (10,53-56). 

Booth M, Mwatha JK, Joseph S, et al. Periportal fibrosis in human Schistosoma mansoni infection is associated with low IL-10, low IFN-gamma, high TNF-alpha, or low RANTES, depending on age and gender. J Immunol 2004 172(2) 1295-1303. 

Alves Oliveira LF, Moreno EC, Gazzinelli G, et al. Cytokine production associated with periportal fibrosis during chronic schistosomiasis mansoni in humans. Infect Immun 2006 74(2) 1215-1221. 

Hepatic Fibrosis/Cirrhosis Fibrosis usually results from chronic inflammation which can be the result of continuous exposure to a variety of hepatotoxic chemicals such as organic arscnicals, vinyl chloride, or high doses of vitamin A (Zimmerman, 1999), chronic ethanol ingestion and nonalcoholic fatty liver disease. Fibrosis usually occurs around the portal area, in the space of Disse, and around the central veins. This results in loss of liver architecture and function. The hepatocytes are replaced with fibrous material and thus there is hepatocyte loss. Periportal fibrosis may lead to portal hypertension. 

Toxically induced hepatoportal sclerosis/periportal fibrosis... 

Various infectious, toxic or immunological lesions lead to a presinusoidal block in adults. From a primary endothelial lesion, endophlebitis ensues. Rich in fibres and deficient in cells, it is ultimately responsible for the obliteration and even disappearance of the portal branches. Obliterative portal venopathy (N.C. Nayak et al., 1969) with portal and periportal fibrosis and subsequent perisinusoidal sclerosis is referred to as hepatoportal sclerosis (W P. Mikkelsen et al., 1965). This is a complex disorder involving splenomegaly, hypersplenism and portal hypertension, which has also been described as non-cirrhotic portal fibrosis (XL. Boyer et al., 1967) or idiopathic portal hypertension (K. Okuda et al., 1982). (I2l, 127) Band s syndrome (7) probably fell into this group ... 

Fig. 14.2 Slight lobular inflammation. Periportal/perisinusoidal delicate fibrosis as a result of chronic vitamin A intoxication (same patient as in fig. 14.3) (Ladewig)...

Shlbayama, Y., Nakata, K. The relation of periportal fibrosis to portal hypertension. J. Hepatol. 1990 11 313-317... 

Standstill It can be assumed that fibrogenesis will initially come to a standstill upon cessation of the causative factors or stimulating signals. When the extracellular matrix is only moderately increased, the lobular structure, the vascular supply and the bile flow from the periportal fields are undisturbed. A balance between the stimulation and inhibition of fibrogenesis can develop, stopping liver fibrosis at the point which has been reached. 

Fibrosis is usually the consequence or concomitant symptom of a chronic hepatobiliary disease, the course of which can itself in turn be unfavourably influenced by the fibrosis. The matrix substances, which are being produced in greater quantities, are increasingly deposited in Disse s space in the portal field and periportal area as well as around the terminal liver vein. 

A fibrotic widening of the portal fields (with differing intensity and often variable regional distribution) is a frequent finding in chronic hepatitis, and it plays an important role in staging, (s. p. 694) However, it may also be a remnant of previous hepatitis. In many cases, strands of connective tissue extend into the periportal parenchyma. Mostly, there is portal/periportal fibrosis with an irregular star-shaped pattern, (s. fig. 21.14)... 

Fig. 21.14 Periportal and septal fibrosis following severe acute viral hepatitis B liver architecture clearly disrupted older collapse fields with condensed reticular fibres (Gomori s reticulin stain)...

A case report of blastomycosis of the hepatobiliary i yi -tem describes the following conditions (39) development of chronic cholangitis in the area of the left hepatic duct with encroachment of the mycotic inflammation to the left lobe of liver in cases of predisposing and/or preexisting choledocholithiasis histological evidence of liver granulomas and periportal fibrosis marked increase in alkaline phosphatase and y-GT. (40)... 

Fig. 28.6 Alcohol-induced periportal and centrilobular fibrosis, partially spider leg-like (Sirius red) (s. fig. 21.14)...

Fig. 28.11 Chronic moderate periportal and portal inflammatory reaction with septal fibrosis and centrilobular steatosis in chronic alcoholic liver damage (DD mild chronic viral hepatitis C ) (van Gieson)...

Fig. 30.3 Thorotrast liver deposits of thorotrast in portal and perisinusoidal macrophages periportal fibrosis and inflammation...

The development of FNH due to thoratrast was reported for the first time in 1998. (6) In the liver, thorotrast is initially stored in the Kupffer cells after their destruction, it is deposited in the periportal areas. From here, periportal and periacinar fibrosis as well as Glisson s capsule fibrosis develop, (s. figs. 30.2, 30.3)... 

Fig. 32.4 Chronic cholangitis. Periportal fibrosis dark red/brown-ish discolouration of the hver with greenish patches finely nodular surface (= scattered light reflection)...

Fig. 32.11 Primary sclerosing cholangitis following cholecystectomy (due to involvement of the gall bladder) distinct periportal fibrosis with initial surface roughness...

Stage II The periportal stage presents an encroachment of the inflammatory changes on the parenchyma with piecemeal necrosis connective tissue proliferations also break into the lobule (so-called periportal hepatitis + fibrosis). Liver cell necroses are also found sporadically, whereby CD4 cells, CD56-NK cells and lymphocytes are markedly increased. In places, reduction in and fibrosis of bile ducts are already in evidence, (s. fig. 32.13) (335, 349, 384)... 

Fig. 32.13 PSC marked concentric fibrosis around a septal bile duct as well as slight periportal inflammation (HE)...

Stage ni The septal stage displays periportal and bridging necrosis as well as an increasing loss of bile ducts with a simultaneous decline in portal inflammatory infiltrations. Dense concentric fibrosis develops around... 

---