Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases.

A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.

Pancreatitis associated with alcoholic liver disease. A review of 1022 autopsy cases.

The prevalence with which alcoholic pancreatitis is associated with alcoholic liver disease is unclear. To investigate this association further, we have reviewed the autopsy findings of 1022 patients who died from alcoholic liver disease and compared these findings with those from 352 patients who died from cardiac or pulmonary disease. All patients who died from liver disease had a history of chronic alcoholism with clinical and biochemical evidence of severe liver damage. Death resulted from hepatic coma, gastrointestinal bleeding, or infection. Liver disease patients were classified into two groups: (1) those with cirrhosis (77%) and (2) those without cirrhosis but with acute and/or chronic sclerosing hyaline necrosis (23%). Anatomic and histopathologic changes characteristic of chronic pancreatitis were found in 203 patients in approximately the same frequency (20% and 18%, respectively) in both groups. Acute pancreatitis without chronic lesions was observed in 8% and 10% of both groups, respectively. In the control group of 352 autopsies (122 cardiac and 230 pulmonary patients), the overall prevalence of pancreatitis, at 2.6%, was significantly (P less than 0.001) lower than that observed in the alcoholic liver disease groups. A total of 22 cases (50%) dying from acute or chronic sclerosing hyaline necrosis had severe chronic calcifying pancreatitis compared to 29 patients (18%) (P less than 0.001) dying from cirrhosis. By contrast, dense fibrosis was significantly (P less than 0.001) more commonly observed in patients with cirrhosis. We conclude that pancreatitis occurs frequently in patients dying from alcoholic liver disease but is an uncommon finding in patients dying from other causes.(ABSTRACT TRUNCATED AT 250 WORDS)

Idiopathic retroperitoneal fibrosis producing common bile duct and pancreatic duct obstruction.

Idiopathic retroperitoneal fibrosis is a rare finding usually confined to the retroperitoneal space. Symptoms caused by this fibrotic process are usually secondary to compression and constriction of local anatomic structures. The ureters are the most common site of involvement, although the biliary tree, duodenum, and vasculature may also be affected. This case report describes a patient with retroperitoneal fibrosis involving the pancreas and common bile duct, and whose clinical course and investigative results stimulated cancer of the pancreas.

Mutations preventing transpositions of yeast mating type alleles.

Homothallic strains of Saccharomyces cerevisiae can switch from one mating type to the other as often as every cell division. The conversion of mating type alleles (from MATa to MATalpha or vice versa) depends on other, unexpressed copies of a or alpha information that can be transposed to MAT. Previously, "inconvertible" mutations within MATalpha and MATa have been described that block the excision of the MAT allele. In this paper we describe two cis-acting mutations that also impair mating type switching and lie very near, but outside, the MAT locus. Both "stuck" mutations, stk1 and stk2, diminish the efficiency of converting MATa to MATalpha to less than 10% of normal. The stk1 mutation also slightly reduces conversion of MATalpha to MATa, whereas stk2 has no discernible effect. Unlike the inconvertible MATalpha-inc and MATa-inc mutations within MAT, the stk mutations are not replaced by wild-type sequences after the "stuck" cells occasionally switch to the opposite mating type. Because these mutations are not "healed" by mating type conversions, they must lie in sequences outside of the transposable mating type information. These results indicate that the efficient replacement of MAT alleles depends on sequences both within and adjacent to the MAT locus. Among subclones of homothallic stk MATa strains, approximately 2% show "illegal" transpositions of mating type genes. In these colonies the silent copy of alpha information at the HMLalpha locus has been converted to a, without any change of MATa or the silent a copy at HMRa. Such conversions of the unexpressed library genes are not found in wild-type homothallic strains that can switch mating type efficiently, but they are found in MATa-inc and MATalpha-inc strains. It appears that all of the cis-acting mutations within or adjacent to mating type result in these unusual switches of mating type information at HML and HMR.