High F-18 FDG uptake in a low-grade supratentorial ganglioma: a positron emission tomography case report.

PURPOSE: Positron emission tomography (PET) with fluorine-18 fluorodeoxyglucose (F-18 FDG) is used for the noninvasive monitoring and grading of primary brain tumors. Here the FDG uptake is positively correlated with the malignant extent of the lesion and thereby negatively correlated with patient survival. Little is known about the FDG PET features of primary brain tumors in children, such as mixed neuronal-glial tumors. METHODS: The authors describe a 13-year-old boy who had partial complex seizures since early childhood caused by a brain tumor in the left temporal lobe. RESULTS: Magnetic resonance and computed tomographic examinations yielded uncharacteristic results: mixed density, marked calcifications, little contrast enhancement, a nearly absent mass effect, and no edema. The FDG PET scan revealed a large hypermetabolic tumor, with a tumor: contralateral gray matter FDG uptake ratio of 1.45. In contrast to this intense hypermetabolism, the pathologic analysis after gross total resection revealed a low-grade ganglioglioma (WHO grade 1), which is usually associated with an excellent prognosis. CONCLUSIONS: Mixed neuronal-glial tumors such as gangliogliomas must be considered in making differential diagnoses by judging hypermetabolic FDG PET scans in young patients with brain tumors in the presence of uncharacteristic imaging features.

Postmenopausal hyperandrogenism of ovarian origin. A clinicopathologic study of four cases.

Postmenopausal hyperandrogenism with overt clinical effects is rare and often related to ovarian stromal disorders. We present a clinicopathologic study of 4 cases. The patients (age range 41-75 years; mean 62 years) had evidence of hirsutism or frank virilization. Their serum testosterone was elevated with or without increases in their serum androstenedione and DHEA levels. There were two right-ovarian hilus cell tumors, one associated with left-ovarian stromal hyperplasia and the other with bilateral hyperthecosis and nodular hilus cell hyperplasia. The other tumor was a small corticomedullary stromal luteoma with bilateral hyperthecosis and nodular hilus cell hyperplasia. The fourth patient had bilateral hilus cell hyperplasia with mild cortical-stromal hyperplasia. All these patients had rapid normalization of androgen levels after surgery without recurrence after a 2- to 10-year follow-up.

Different genes code for alkaline phosphatases from human fetal and adult intestine.

Alkaline phosphatases from human adult intestine and fetal intestine (meconium) were purified and compared. Electrophoresis in SDS showed one band of protein in the former. There were three bands of protein in the latter, all with essentially the same peptide map. Thus, two of the bands probably arose by proteolysis of the third, which was largest (Mr 73000). In gradient gels of polyacrylamide the alkaline phosphatase from fetal intestine showed only one band of protein coincident with the band of activity (Mr 151000). Radiolabeled mapping showed that the tryptic peptides of the alkaline phosphatase from fetal intestine were distinctly different from those of adult intestine and human liver, and placenta, indicating a gene distinct from the three that code for the enzyme in liver/kidney/bone, placenta, and adult intestine.

Isoenzymes of alkaline phosphatase in infantile hypophosphatasia.

Infantile hypophosphatasia is a rare inborn error of metabolism in which the expression of the liver/kidney/bone locus of the alkaline phosphatase gene is defective. Analysis of tissues from a suspected case of hypophosphatasia for alkaline phosphatase activity demonstrated very low levels of activity in liver, kidney, and rib as compared to tissues from a case of osteogenesis imperfecta or normal adult tissues. Intestinal and placental tissues demonstrated significant levels of activity. Gene-specific amino acid inhibitors and isoelectric focusing demonstrated that the activity which was present in the liver, kidney, and rib tissues from the case of hypophosphatasia was of the intestinal type and not the normal liver/kidney/bone form of the enzyme.