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A 21-year-old female underwent a hysterectomy with the finding of an endometrial stromal sarcoma (7-9 mitoses/10 HPF) confined to the uterus. However, within 30 months of hysterectomy, metastases occurred in the spinal cord, femur and lungs. Treatment consisted of surgery and irradiation for the spinal cord metastases and ten courses of combination chemotherapy, Adriamycin, vincristine, cyclophosphamide (6 courses) and megestrol acetate (continuous since course 7). This therapy resulted in a complete clinical remission which has been maintained for eight months since completion of chemotherapy. It is suggested that this regimen be employed in patients with this rare and lethal tumor.

Amylase assays measure total activity without differentiating the relative contributions of pancreatic- and salivary-type amylase isozymes. Since polyacrylamide electrophoresis allows identification of salivary-and pancreatic-type isoxymes and their respective variants, serum and urine specimens from patients with the clinical diagnoses of mumps (4), pancreatitis (16), or undiagnosed hyperamylasemias (5) were compared with specimens from control subjects. Patients with mumps had elevations of salivary-type isozymes, while those with pancreatitis had elevations of pancreatic-type isozymes. Elevation of salivary-type isozymes was identified in the five patients who had undiagnosed hyperamylasemias; among these, the isozymes of two originated in neoplastic ovarian tissue and those of three, probably in the salivary glands. Amylase isozyme differentiation cannot unamibiguously identify the tissue source of hyperamylasemia. However, in patients whose hyperamylasemia is of unknown etiology or who respond atypically to therapy, amylase electrophoresis provides identification of the elevated isozyme type, thus providing the basis for the rational selection of further diagnostic procedures.

Although thyroid medications are commonly prescribed, there are only nine case reports describing the consequences of acute excessive ingestion of thyroid hormones. Two additional cases are presented and the prior nine cases are reviewed. The potential for toxicity is discussed in relationship to the cellular mechanisms of action of thyroid hormones. Although the potential for toxicity is low, the following therapy is recommended to decrease further the toxic potential: (1) lavage and activated charcoal to decrease absorption, (2) cholestyramine to decrease enterohepatic circulation (3) prednisone and/or propylthiouracil to decrease conversion of thyroxine to triiodothyronine, and (4) propranolol to block metabolic effects. If symptoms of toxicity develop, then attempts to remove thyroid hormones should be undertaken using exchange transfusion.

Patients with hypertension and altered neurologic status represent difficult diagnostic problems. If these patients are presumed to have hypertensive encephalopathy, specific diagnostic procedures and therapy may be delayed. Our case report and discussion emphasize the difficulty of differentiating hypertensive encephalopathy from other conditions and illustrate hypertensive encephalopathy should not be a primary diagnosis, but only a diagnosis of exclusion.

A 54-year-old man developed mild renal insufficiency after treatment with gentamicin and cephalothin. He then received tetracycline for eight days, 500 mg orally four times daily, for a total dose of 15 gm. Twelve days after discontinuation of the drug, a severe but reversible aplastic anemia developed. We propose that bone-marrow-toxic concentrations of tetracycline resulted from the preexisting renal insufficiency. Because of the temporal relationship between tetracycline administration and aplastic anemia, and the lack of any other explanation, we conclude that this case illustrates a rare but potentially fatal complication of this drug.

In the chicken population at large, three electrophoretically distinct pancreatic alpha-amylase isozymes were discovered. The isozymes were designated Pa 1, Pa 2, and Pa 3. The local population of chickens, however, possessed only isozymes Pa 2 and Pa 3 present as three phenotypes: Amy-2 B, consisting of isozyme Pa2; Amy2 BC, consisting of isozymes Pa 2 plus Pa 3; and Amy2 C, consisting of isozyme Pa 3. Pancreatic biopsy permitted the establishment of a breeding flock with defined amylase phenotypes. Matings of this flock established that amylases are inherited as codominant alleles at a single genetic locus. Further, there was no evidence of ontogenetic modification of the amylase isozymes. It was observed that amylase isozymes Pa 2 and Pa 3 each generated a family of at least three faster-migrating amylolytic proteins. These post-translationally modified amylases were designated Pa Xa, Pa Xb, and Pa Xc, where X represents the number of the progenitor amylase. Structural analyses of purified amylases demonstrated that all amylase isozymes are nonglycosidated, monomeric molecules of molecular weight 55,000. In addition, the data are consistent with the hypothesis that the faster-migrating amylases are produced by deamidation of asparagine and/or glutamine residues.

The origins and clinical significance of hyperamylasemia during diabetic ketoacidosis are unclear. We have therefore correlated important clinical and laboratory indices of diabetic ketoacidosis with sequential determinations of serum and urine amylase concentrations, amylase/creatinine clearance ratios, and specific amylase isozyme types. Hyperamylasemia occurred in 79% of our patients with diabetic ketoacidosis, often after admission to the hospital. Among these patients, 48% had pancreatic-type, 36% salivary-type, and 16% mixed-type (pancreatic and salivary) hyperamylasemia. There were no correlations between the presence, degree, or isozyme type of hyperamylasemia and most laboratory or clinical characteristics, including gastrointestinal symptoms. Patients with pancreatic-type hyperamylasemia tended to have higher amylase/creatinine clearance ratios, but it was not possible to unequivocably diagnose acute pancreatitis during diabetic ketoacidosis with current routine clinical or laboratory procedures.

A patient with an amylase-producing serous cystadenocarcinoma of the ovary had elevated serum and urine amylase levels and high levels of amylase in pleural and ascitic fluids. Serum and urine amylase levels reflected both surgical removal of tumor mass and response to chemotherapy. Tumor homogenates had pronounced amylase activity. Salivary type amylase isozyme patterns were found in electrophoresis of samples from all sources. Ascites tumor cells were successfully cultured and salivary type amylase was found in the culture media throughout 5 passages. The tumor was classified by light microscopy as poorly differentiated serous cystadenocarcinoma. Ultrastructural studies on the tumor were consistent with that diagnosis. Amylase was detected in the cells of the tumor examined by the immunoperoxidase technique.