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In Herpes simplex virus pancreatitis the primary and also the most pronounced lesion is intense necrosis of acinar cells due to a direct cytopathic effect of Herpes simplex virus and although severe hemorrhage is seen, fat necrosis remains minimal. In addition, the alterations of the nuclei of acinar cells are easily observed and help greatly in the pathologic diagnosis.

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The gross and histopathologic changes seen in HSV pancreatitis are fairly characteristic and clearly distinguishable from those of the usual acute hemorrhagic pancreatitis (or acute pancreatic necrosis).

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Acute hemorrhagic pancreatitis :  Severe edema and acute inflammatory cell infiltration in the interlobular stroma (interstitial pancreatitis) ; the released pancreatic enzymes induce severe vascular injury resulting in prominent hemorrhage and also extensive fat necrosis with saponification.  Although injury of acinar cells occurs as the initial event in the disease process, necrosis of acinar cells is usually not a prominent feature, especially in its mild form .

HSV pancreatitis : Most pronounced lesion is intense necrosis of acinar cells due to a direct cytopathic effect of HSV, and although severe hemorrhage is seen, fat necrosis remains minimal.

Gross examination of the pancreas show scattered, small, and discrete foci of fresh hemorrhagic necrosis, each measuring a few millimeters in diameter.

Histopathologically, multiple foci of necrosis of the parenchyma accompanied by intense hemorrhage are scattered throughout the pancreas. These are present in the peripheral areas of each lobule.

Fat necrosis with saponification is minimal.

Acinar cells surrounding the necrotic foci show atrophy and necrobiotic changes, and numerous eosinophilic intranuclear inclusions with clear halos (Cowdry type A) are noted.

Many multinucleated giant cells with hyperchromatic irregular nuclei and eosinophilic cytoplasm are noted around these necrotic foci.

                       

Herpes simplex pancreatitis.Arch Pathol Lab Med. 2003 Feb;127(2):231-4.

Lesions of the pancreas induced by viral infection have drawn relatively little attention because of their low incidence, and the histopathologic features of viral pancreatitis have not been fully elucidated. We report the autopsy findings of 2 patients, a 59-year-old woman with allergic granulomatous angiitis and a 73-year-old man with invasive pulmonary aspergillosis who had a disseminated visceral herpes simplex virus (HSV) infection. In both cases, the liver was the organ most severely affected by the viral infection. The pancreas showed multiple small foci of hemorrhagic necrosis, which were not accompanied by fat necrosis of the surrounding adipose tissue. Histopathologically, Cowdry type A intranuclear inclusions and a ground-glass appearance of the nuclei were found in many degenerated acinar cells around the necrotic foci. The gross appearance and histopathologic features of HSV pancreatitis were characteristic and, in particular, distinct from those of the more common acute hemorrhagic pancreatitis. Immunohistochemistry using an anti-HSV antibody revealed immunoreactivity in the intranuclear inclusions and ground-glass nuclei, and polymerase chain reaction analysis disclosed that the causative virus in these 2 cases was HSV-1. Herpes simplex virus pancreatitis constitutes a rare, but distinct pathologic entity among a group of acute pancreatitis diseases with diverse etiopathogenesis.

 

August 2007

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