Fibrosis in Apparently Uninvolved Areas in Patients with Acute Pancreatitis

Necrotizing pancreatitis is often accompanied by interstitial pancreatitis some distance from the areas of necrosis (fig. 3). Several authors have noted that acute pancreatitis may cause fibrosis [3, 4]. However, interlobular fibrosis is a characteristic finding in chronic pancreatitis [5], and it is unclear whether the fibrosis in apparently uninvolved areas occurs before or after acute pancreatitis.

Our previous study revealed apparently uninvolved areas that were distant from frank parenchymal necrosis in all patients with acute pancreatitis; these areas are frequently accompanied by interlobular fibrosis [6]. The appearance and increase in interlobular fibrosis also correlates with the duration of disease, as shown in table 2, and as follows: (1) no fibrosis with illness of less than 5 days' duration (fig. 4); (2) linear fibrosis with positive immunoreactivity against anti-collagen type III between 8 days and a month (fig. 5), and (3) broad fibrosis with positive immunoreactivity against both types I and III anti-collagen with illness of 2 months or longer (fig. 6). The interlobular fibrosis is often accompanied by hemosiderin deposition, which is assumed to be due to previous inflammation with hemorrhage. Hence, fibrosis in apparently univolved areas appears to develop in relation to acute pancreatitis. This finding is supported by the interlobular distribution of hemorrhage in two patients without

Table 2. Fibrosis in apparently uninvolved areas and fat necrosis in cases of acute pancreatitis fö

Table 2. Fibrosis in apparently uninvolved areas and fat necrosis in cases of acute pancreatitis

Case

Age/ Sex

Duration of illness, days

Cause

Interlobular spaces

Fat necrosis

Fibrosis*

Hemosiderin

Types I/III collagen

Fibrin thrombi

Hemorrhage/ hemosiderin

Reparative change

Venous thrombus

1

57/F

4

gallstones

(inflammation with hemorrhage)

+

+/ +

-

+

2

47 /M

5

alcohol

(inflammation with hemorrhage)

+

+/ +

-

3

51 /F

8

unknown

linear

+

-/+

+

+/ +

+/-

4

72 /M

28

gallstones,

linear

+

-/+

+

+/ +

G

+

after ERCP

and EST

5

36 /M

30

alcohol

linear

-

-/+

+

-/+

G

6

50 /M

34

alcohol

linear and broad

+

+/ +

+

-/+

G

+

7

37/M

70

alcohol

broad

+

+/ +

+

+/ +

G

8

70 /M

91

alcohol

broad

+

+/ +

+

+/ +

G

+

9

69 /M

95

alcohol,

linear and broad

+

+/ +

+

+/ +

G

after ERCP

interlobular fibrosis, except for the thin connective tissue septa. ERCP = Endoscopic retrograde choledochopancreatography; EST = endoscopic sphincterotomy; G = granulation tissue.

Fig. 4. Interlobular distribution of hemorrhage in a patient with an illness of 4 days. HE. X100. From [6] with permission.

fibrosis. It is also known that pancreatic lobules appear to be more resistant to the digestive process than the interlobular spaces.

As 6 of the 9 patients had been heavy drinkers, one may consider such interlobular fibrosis as a finding in chronic pancreatitis due to chronic alcohol abuse [7]. However, one patient (case 2) with an illness of 5 days showed no interlobular fibrosis. Moreover, our previous study [5] showed no chronic pancreatitis/fibrosis in 33 of 53 cases of chronic alcoholism and in 13 of 46 cases of alcohol-dependence syndrome. Therefore, we consider such interlobular fibrosis to occur after acute pancreatitis.

Fibrosis in pancreatic tissue is one of the most characteristic findings in chronic pancreatitis [8]. Sarles et al. report chronic and acute pancreatitis to be different disease entities [9]. However, other authors [3, 4] have noted that acute pancreatitis may cause fibrosis, as mentioned above.

Immunoreactivity against anti-collagen types I and III was positive in 4 patients with an illness of 34 days to two months or longer, whereas anti-collagen type I was negative in the other 3 patients with an illness of 8 days to a month. More type III than type I collagen is present in newly formed connective tissue. So although fibrosis after acute pancreatitis may contain reversible type III collagen as in that of WBN/Kob rats [10], we emphasize that fibrosis is ultimately followed by irreversible type I collagen, corresponding to the duration of disease.

Fig. 5. Interlobular fibrosis in a patient with an illness of 28 days. a The fibrosis shows a linear type. HE. X100. b The fibrosis was accompanied by hemosiderin deposition. Berlin's blue. X100. c The fibrosis stained positively for anti-collagen type III. Immunostaining for anti-collagen type III. X100. d The fibrosis stained negatively for anti-collagen type I. Immunostaining for anti-collagen type I. X100. From [6] with permission.

Fig. 5. Interlobular fibrosis in a patient with an illness of 28 days. a The fibrosis shows a linear type. HE. X100. b The fibrosis was accompanied by hemosiderin deposition. Berlin's blue. X100. c The fibrosis stained positively for anti-collagen type III. Immunostaining for anti-collagen type III. X100. d The fibrosis stained negatively for anti-collagen type I. Immunostaining for anti-collagen type I. X100. From [6] with permission.

Fig. 6. Interlobular fibrosis in a patient with an illness of 2 months and 10 days. a The fibrosis shows a broad type. HE. X50. b The fibrosis was accompanied by hemosiderin deposition. Berlin's blue. X50. c The fibrosis stained positively for anti-collagen type I (arrows). Immunostaining for anti-collagen type I. X50. From [6] with permission.

Fig. 6. Interlobular fibrosis in a patient with an illness of 2 months and 10 days. a The fibrosis shows a broad type. HE. X50. b The fibrosis was accompanied by hemosiderin deposition. Berlin's blue. X50. c The fibrosis stained positively for anti-collagen type I (arrows). Immunostaining for anti-collagen type I. X50. From [6] with permission.

We therefore consider that fibrosis in apparently uninvolved areas develops in relation to acute pancreatitis, and it may consist of type I collagen in patients surviving longer.

Was this article helpful?

0 0

Post a comment