Hemangiomas constitute a heterogeneous group of benign vascular proliferations of skin and mucous membranes and very rarely known to develop in the brain or spinal cord. We report here a case of multiple intracranial capillary hemangiomas presenting with transient neurological deficit. The patient underwent stealth MRI brain utilizing 15 ml of Magnevist for stereotactic localization and biopsy was done to establish the diagnosis. It is pivotal to differentiate benign hemangiomas from primary cerebral vascular tumors including hemangioblastoma, hemangioendothelioma and hemangiopericytoma, as later are known for more aggressive biologic behavior.

No abstract

There has been little study of how pleural fluids are interpreted in actual practice, including the use of immunocytochemistry and nondefinitive diagnoses. Pleural fluid reports (n = 1,330) from 1991–1997 and the University of Iowa cancer database were retrospectively reviewed to determine the cytologic diagnosis, requisition form history, patient survival, and use of immunocytochemistry. Nondefinitive diagnoses were made in 11.3% of cases. Immunocytochemistry was used in 2.6% of cases and aided in making a definitive diagnosis in 71.9% of cases. For patients with a clinical suspicion of malignancy, the percentages of patients who had a nondefinitive, benign, and malignant diagnosis and died of disease were 81.6%, 94.0%, and 90.6%, respectively. In conclusion, if patients had a history of malignancy and a clinical suspicion of recurrence, patient survival was dismal, regardless of the cytologic diagnosis. Immunocytochemistry was used sparsely but often aided in making a definitive diagnosis. Diagn. Cytopathol. 2000;22:281–285. © 2000 Wiley‐Liss, Inc.

Parachordomas are rare cutaneous tumors that show virtually identical histologic findings to chordomas. Therefore, the major differential diagnosis in a case of parchordoma is metastatic chordoma. Parachordomas are benign neoplasms and most often develop on the extremities adjacent to tendons, synovium or osseous structures, as opposed to chordomas, which are malignant tumors located along the craniospinal axis. While recurrences may occur in cases of parachordoma, metastases have not been reported. In this report, two cases of parachordomas are reported and the literature reviewed. By light microscopy, parachordomas show eosinophilic bands of fibrous tissue separating lobules of cells with variably vacuolated cytoplasm (physaliphorous cells) admixed with more epithelioid cells in a myxoid stroma. Parachordomas and chordomas share immunohistochemical and ultrastructural features. Both stain with S-100 protein and vimentin, and ultrastructurally both demonstrate cytoplasmic vacuoles, intermediate filaments, pinocytotic vesicles, celljunctions, and cytoplasmic membranes with microvillous processes. Chordomas more frequently express cytokeratin (98% vs. 66% in parachordomas) and epithelial membrane antigen (90% vs. 20% in parachordomas) and chordomas have a larger number of rough endoplasmic reticulum-mitochondrial complexes. Thus, positive staining with epithelial membrane antigen and the identification of a large number of rough endoplasmic reticulum-mitochondrial complexes are suggestive of metastatic chordoma. However, the definitive distinction remains a clinical one after appropriate radiologic studies of the skull and spinal chord.

Antibodies to antigens in the Kell blood group system are usually immunoglobulin G, and, notoriously, anti-K, anti-k, and anti-Kp a can cause severe hemolytic transfusion reactions, as well as severe hemolytic disease of the fetus and newborn (HDFN). It has been shown that the titer of anti-K does not correlate with the severity of HDFN because, in addition to immune destruction of red blood cells (RBCs), anti-K causes suppression of erythropoiesis in the fetus, which can result in severe anemia. We report a case involving anti-Kp a in which one twin was anemic and the other was not. Standard hemagglutination and polymerase chain reaction (PCR)-based tests were used. At delivery, anti-Kp a was identified in serum from the mother and twin A, and in the eluate prepared from the baby's RBCs. PCR-based assays showed twin A (boy) was KEL*841T/C (KEL*03/KEL*04), which is predicted to encode Kp(a+b+). Twin B (girl) was KEL*841C/C (KEL*04/ KEL*04), which is predicted to encode Kp(a-b+). We describe the first reported case of probable suppression of erythropoiesis attributable to anti-Kp a . One twin born to a woman whose serum contained anti-Kp a experienced HDFN while the other did not. Based on DNA analysis, the predicted blood type of the affected twin was Kp(a+b+) and that of the unaffected twin was Kp(a-b+). The laboratory findings and clinical course of the affected twin were consistent with suppression of erythropoiesis in addition to immune RBC destruction.