Pancreatic Pathology Online: Chronic Pancreatitis

Histopathology Image of Chronic Pancreatitis:

Visit: Pancreatic Pathology Online ; Exocrine Pancreatic Tumours.

Chronic pancreatitis is thought to result from recurrent bouts of acute pancreatitis, which lead to a progressive destruction of acinar cells, followed by healing and fibrosis.Pancreatitis ; Autoimmune Pancreatitis

As a result, exocrine and endocrine functions are lost.

Like acute pancreatitis, chronic pancreatitis is associated with alcoholism and, less commonly, with biliary tract disease, hypercalcemia, or hyperlipidemia.

About one half of cases are seen in patients without any of these risk factors.

In the acute phase, focal pancreatic necrosis is accompanied by a polymorphonuclear infiltrate, which is replaced by lymphocytes and plasma cells.

Healing is characterized by the removal of necrotic tissue by macrophages, a proliferation of capillaries and fibroblasts, and finally the collagen.

In advanced cases, large areas of the pancreas are replaced by fibrosis, and the exocrine and endocrine tissues become atrophic.

The most common type of chronic pancreatitis is chronic calcifying pancreatitis, a disorder most frequently associated with alcoholism.

Intraductal protein plugs eventually calcify and lead to the formation of stones in the ducts.

In chronic pancreatitis following sustained alcohol abuse, ductules and ducts are so often filled with thick proteinaceous secretion that some have concluded that such secretions may be an important mechanism of obstruction.

Image Link1 ; Image Link2 ; Image Link3 ; Image Link4

Since alcohol is potent secretagogue for the exocrine glands, one can visualize a situation of secretion against obstruction.

In another form of this disease, chronic obstructive pancreatitis, stenosis of the sphincter of Oddi is associated with gallbladder stones.

Although in this condition the pancreatic ducts are filled with thick proteinaceous secretions, they are rarely the focus of calcification or stone formation.

Chronic pancreatitis is more common in men, and in about 10% of cases it is associated with the pancreas divisum (incomplete fusion of the ventral and dorsal pancreatic anlage).

Diabetes mellitus, pancreatic insufficiency with its attendant steatorrhea and malabsorption, and pancreatic pseudocyst are frequent complications in the late stages of chronic pancreatitis.

A rare variant of chronic pancreatitis, familial hereditary pancreatitis, requires special mention.

It occurs with increased frequency in certain families, predominantly in girls, and become apparent in early childhood.

Its pattern of inheritance is autosomal dominant, and in some instances the disease is associated with an aminoaciduria, in which the pattern of excretion resembles that of the recessive form of cystinuria.

A second biochemical abnormality in some cases is hypercalcemia, secondary to hyperplasia or adenomas of the parathyroid glands.

Hereditary pancreatitis is not associated with alcohol abuse or chronic biliary disease.

It is noteworthy that about 20% of such patients have subsequently developed ductal adenocarcinoma of the pancreas.

In view of the rarity of this disease, these data must be interpreted with caution.

Except for the features noted previously, hereditary pancreatitis is indistinguishable from chronic relapsing pancreatitis, including its associated late complications.

Duct-narrowing chronic pancreatitis without immunoserologic abnormality: comparison with duct-narrowing chronic pancreatitis with positive serological evidence and its clinical management.Dig Dis Sci. 2005 Aug;50(8):1414-21

Histopathologic correlates of noncalcific chronic pancreatitis by EUS: a prospective tissue characterization study.Gastrointest Endosc. 2007 Jul 17;

BACKGROUND: Studies that correlated EUS features of chronic pancreatitis (CP) with histopathology are retrospective and only include patients with severe disease or calcific pancreatitis. Controversies regarding the significance of EUS features of noncalcific CP (NCCP) remain unresolved. OBJECTIVE: To correlate EUS criteria for NCCP with histology from surgical specimens. DESIGN: Prospective study. SETTING: Tertiary referral center. PATIENTS: All patients who underwent EUS for pancreaticobiliary indications and subsequent pancreatic surgery. Patients with calcific pancreatitis were excluded. METHODS: Individual CP features on EUS were carefully documented with relation to different parts of the pancreas. Standard EUS criteria for CP were adopted. All patients underwent surgery within 2 months of EUS. A single pathologist blinded to EUS findings reviewed the specimens and graded fibrosis (total score, 12; >/=6 = unequivocal CP). A quantitative receiver operating characteristic (ROC) curve analysis was performed, and Spearman rank correlation coefficients were calculated. MAIN OUTCOME MEASUREMENTS: Correlate EUS criteria for NCCP, with histology from surgical specimens. RESULTS: Of the 42 patients evaluated, NCCP was diagnosed histologically in 21 patients (50%). None of the patients had CP diagnosis by CT. ROC curve analysis revealed that 4 or more EUS criteria provided the best sensitivity (90.5%), specificity (85.7%), and accuracy (88.1%) for diagnosing NCCP. Parenchymal EUS features that were significantly associated with histopathologic NCCP were foci (P < .0001), stranding (P < .001), and lobulations (P = .04); ductal features that were significantly associated with histopathologic NCCP were dilated (P < .0001) or irregular main pancreatic duct (P < .0001), side branches (P < .001), and hyperechoic duct margins (P = .03). There was a significant correlation between the number of EUS criteria and severity of NCCP on histology (r = 0.85; P < .0001). LIMITATIONS: Small number of patients. CONCLUSIONS: An excellent correlation exists between EUS and histologic findings of NCCP.

Chronic pancreatitis in primary hyperparathyroidism: Comparison with alcoholic and idiopathic chronic pancreatitis.J Gastroenterol Hepatol. 2007 Aug 6;

Background: Primary hyperparathyroidism is a rare cause of chronic pancreatitis and there is a paucity of data on this interesting association. There is also no data comparing the clinical profile of chronic pancreatitis secondary to primary hyperparathyroidism with that of alcohol related and idiopathic chronic pancreatitis. Methods: The clinical and biochemical spectrum of chronic pancreatitis secondary to primary hyperparathyroidism was evaluated retrospectively and compared with nine age-matched patients with alcohol related and idiopathic chronic pancreatitis. Results: Renal colic, nephrolithiasis, nephrocalcinosis, bone disease, palpable neck nodule, and psychiatric abnormality were significantly more common in chronic pancreatitis due to hyperparathyroidism in comparison to alcoholic and idiopathic groups. The corrected calcium (10.8 +/- 0.9 vs 9.3 +/- 0.6 vs 9.2 +/- 0.8 mg/dL; P = 0.001) and intact parathormone (425 +/- 130 [SE]vs 22.2 +/- 14.3 [SE]vs 30 +/- 27.3 [SE] pg/mL; P = 0.009) levels were significantly elevated, while levels of serum phosphate were significantly less (3.1 +/- 0.4 vs 3.9 +/- 0.5 vs 3.4 +/- 0.7 mg/dL, respectively; P = 0.04) in chronic pancreatitis due to hyperparathyroidism in comparison to the alcoholic and idiopathic groups. No significant difference was observed in the frequency of steatorrea, diabetes mellitus, pancreatic calcification, and pseudocyst between the three groups. Six out of nine patients underwent parathyroidectomy and none had recurrence of pancreatic pain over 14.3 +/- 13.8 months. Conclusions: Chronic pancreatitis due to hyperparathyroidism has important characteristics in its biochemical and clinical manifestations. Parathyroidectomy relieves pancreatic pain in majority of patients.

The natural course of chronic pancreatitis--pain, exocrine and endocrine pancreatic insufficiency and prognosis of the disease.Zentralbl Chir. 1995;120(4):278-86.

The natural course of the classical symptoms of chronic pancreatitis, i.e. pain, exocrine and endocrine pancreatic insufficiency, was followed up in 335 patients over a median of 9.8 years (mean 11.3 +/- 8.3 years). Pain relief was not obtained in the majority of patients, even after a longterm observation of > 10 years, and severe exocrine and/or endocrine insufficiency, severe duct abnormalities and pancreatic calcifications developed. Alcohol abstinence failed to have a significant beneficial effect on pain. Pancreatic surgery led to pain relief immediately after operation, but later on the pain course between operated and nonoperated patients was not significantly different. Repeated exocrine pancreatic function tests in 143 patients showed that functional exocrine impairment came to a standstill (46%), or improved (11%). At the end of the observation, 22% of 335 patients still had normal endocrine function and only 40% required insulin treatment. Alcohol abstinence had a significant beneficial effect on endocrine, but not on exocrine pancreatic insufficiency. Chronic pancreatitis led to a sharp increase in unemployment and retirement. Pancreatic carcinoma occurred in 3% and extrapancreatic carcinoma in 4%. The mortality rate within the observation period was 22%, pancreatitis-induced complications accounted for 13% of these deaths.

Natural course in chronic pancreatitis. Pain, exocrine and endocrine pancreatic insufficiency and prognosis of the disease. Digestion. 1993;54(3):148-55.

The natural course of the classical symptoms of chronic pancreatitis, i.e. pain, exocrine and endocrine pancreatic insufficiency, was followed up in 335 patients over a median of 9.8 years (mean 11.3 +/- 8.3 years). Pain relief was not obtained in the majority of patients, even after a long-term observation of > 10 years, and severe exocrine/endocrine insufficiency, severe duct abnormalities and pancreatic calcifications developed. Alcohol abstinence failed to have a significant beneficial effect on pain. Pancreatic surgery led to pain relief immediately after operation, but later on the pain course between operated and nonoperated patients was not significantly different. Repeated exocrine pancreatic function tests in 143 patients showed that functional exocrine impairment came to a standstill (46%), or improved (11%). At the end of observation, 22% of 335 patients still had normal endocrine function and only 40% required insulin treatment. Alcohol abstinence had a significant beneficial effect on endocrine, but not on exocrine pancreatic insufficiency. Chronic pancreatitis led to a sharp increase in unemployment and retirement. Pancreatic carcinoma occurred in 3% and extrapancreatic carcinoma in 4%. The mortality rate within the observation period was 22%, pancreatitis-induced complications accounted for 13% of these deaths.

Chronic alcoholism and evolution of pain and prognosis in chronic pancreatitis. Dig Dis Sci. 1989 Jan;34(1):33-8.

To evaluate the influence of chronic alcoholism on clinical features of chronic pancreatitis in Japan, pain evolution, pancreatic insufficiency, and long-term prognosis were studied by comparing chronic alcoholic pancreatitis (N = 88) with idiopathic pancreatitis (N = 67). The 155 patients with known course of the disease over three years were followed-up further for five more years, and pain evolution was evaluated once at the start and once at the end of the follow-up period. At the time of diagnosis, severe pain (59 vs 33%, P less than 0.001), pancreatic calcification (63 vs 31%, P less than 0.001), advanced exocrine pancreatic insufficiency (72 vs 60%, NS), and overt diabetes (48 vs 17%, P less than 0.001) were more common in alcoholic than in idiopathic pancreatitis, respectively. Pain evolution was similar in both pancreatitis, and the pain decreased with time. The rate of abstinence was higher in groups with pain relief than without in alcoholic pancreatitis. Cumulative mortality rate during the five years was higher in alcoholic than idiopathic pancreatitis (26 vs 10%, P less than 0.01). These results suggest more favorable evolution of the disease can be expected by abstinence from alcohol.

Your Ad Here