Fifty-eight immature ovarian teratomas were studied. Neoplasms with other germ cell elements (endodermal sinus tumor, choriocarcinoma, and dysgerminoma) were excluded so that the clinical and pathologic features of "pure" immature teratomas could be defined and correlated with the prognosis. T h e primary tumors and their metastatic growths were graded from 0 to 3. Forty were stage I; nine, stage 11; and nine, stage 111. The size and stage of teratomas were related to survival, but it was the grade of the primary tumor that best determined the likelihood of extraovarian spread, and it was the grade of the metastases that related best to the subsequent course. Actuarial survival was 63% at 5 years and also at 10 years. Regardless of the grade of the primary tumor, only one of six with grade 0 metastases progressed, and that neoplasm may not have been adequately sampled. Two of five neoplasms having grade 1 metastases did not progress, and two of six patients with grade 2 metastatic growths were living after relatively long intervals. All seven patients with grade 3 metastases died with tumor, none surviving more than 2.1 years. Survival of patients with grade 1, 2, and 3 neoplasms was 81, 60, and 30%, respectively.T h e importance of adequate sampling of primary tumor and metastases for estimating prognosis and determining therapy is stressed.

Purpose To assess p53 gene expression in pterygia with and without recurrence. The pathogenesis of pterygium has not yet been determined. The most widely recognized etiologic factor is ultraviolet radiation, which leads to degeneration of the conjunctiva. However, pterygium was recently found to have several tumor-like characteristics. The p53 gene is a common marker for neoplasia, and is known to control cell cycle, cell differentiation and apoptosis. In this study we examined the expression of the p53 gene in primary pterygia with and without recurrence, searching for the pathogenesis of this very common lesion and for a prognostic factor for recurrence. Methods Immunohistochemical staining using a monoclonal antibody to human p53 (DO-7) was performed on 13 consecutive patients with primary pterygia, four pterygia without recurrence and nine pterygia which recurred during a 12-month follow-up. As a control we used two specimens of normal conjunctiva. Results Seven of the 13 pterygia specimens (54%) were positive for abnormal p53 expression. There was no difference between the groups with and without recurrence. Two out of four pterygia (50%) without recurrence and five out of nine (55.5%) pterygia with recurrence were positive. No pathological staining was observed in the control specimens. Conclusions In this study, abnormal p53 expression was found in pterygial epithelium, suggesting that pterygium could be a result of uncontrolled cell proliferation, and not as a degenerative lesion. There seems to be no connection between abnormal p53 expression and recurrence.

Fifty-eight immature ovarian teratomas were studied. Neoplams with other germ cell elements (endodermal sinus tumor, choriocarcinoma, and dysgerminoma) were excluded so that the clinical and pathologic features of "pure" immature teratomas could be defined and correlated with the prognosis. The primary tumors and their metastatic growths were graded from 0 to 3. Forty were stage I; nine, stage II; and nine, stage III. The size and stage of teratomas were related to survival, but it was the grade of the primary tumor that best determined the likelihood of extraovarian spread, and it was the grade of the metastases that related best to the subsequent course. Actuarial survival was 63% at 5 years and also at 10 years. Regardless of the grade of the primary tumor, only one of six with grade 0 metastases progressed, and that neoplasms may not have been adequately sampled. Two of five neoplasms having grade 1 metastases did not progress, and two of six patients with grade 2 metastatic growths were living after relatively long intervals. All seven patients with grade 3 metastases died with tumor, none surviving more than 2.1 years. Survival of patients with grade 1, 2, and 3 neoplasms was 81, 60, and 30% respectively. The importance of adequate sampling of primary tumor and metastases for estimating prognosis and determining therapy is stressed.

The objective of this study was to test the hypothesis that excessive severity of ischaemic heart disease in diabetics is due, in part, to capillary inadequacy. Sections from autopsied hearts of diabetic patients with and without myocardial infarction as well as from those of patients with infarcts and no diabetes were used for morphometric studies of intramural microvessels in areas without infarction. Normoglycaemic patients with normal hearts were also examined. Two to five transverse sections from each of 44 hearts (stained with methenamine silver) were examined for capillary numerical density, capillary to myofibre ratios, and myofibre diameters. Averages for each case and totals for each group were calculated and compared. Normoglycaemic patients with infarcts had increased morphometric values. Diabetics with infarcts had significantly lower capillary densities than the other groups. In conclusion, it is suggested that in diabetes there is an inadequate ischaemia-induced, reactive angiogenesis. This may contribute towards increased myocardial vulnerability in further ischaemic injury and perhaps to diabetic cardiomyopathy.

We report two sibs who were the products of a consanguineous mating, and who had an extensive form of aplasia cutis congenita (ACC). In one of them the generalized skin disorder was manifested by slipping off of the epidermis and mucous membranes with the slightest trauma. This sib also had pyloric atresia and other congenital malformations. Two hypotheses are presented to explain the discordance between the siblings for the abnormalities other than the ACC. One hypothesis assumes varying degrees of severity of the same autosomal recessive disease. The second suggests linkage between the gene for ACC and the gene for an epidermolysis bullosa (EB)-like disorder and pyloric atresia. a recombination event involving the EB-pyloric atresia gene in one carrier parent would then lead to an offspring with only ACC. Prenatal diagnosis is suggested by monitoring alpha-fetoprotein levels in aminotic fluid.

Murine typhus is a febrile systemic illness, presenting with headache and undulating fever. Neurological involvement is considered a rare complication. During 1994 and 1995, 34 patients admitted to our hospital were diagnosed as having murine typhus. Five of these patients presented with a syndrome of subacute "aseptic" meningitis or meningoencephalitis. Three had bilateral papilloedema and 2 had focal neurological signs. None had a rash or other systemic findings suggestive of rickettsial disease. The diagnosis was based on serum and cerebrospinal fluid serology and on prompt response to doxycycline therapy. These cases suggest that neurological involvement in murine typhus is more common than previously suspected and that murine typhus should be included in the differential diagnosis of subacute meningitis in endemic areas.

The clinicopathological aspects of 15 patients with necrotizing soft-tissue infections in the head and neck are reviewed. Our relatively large series suggests that the disease occurs more frequently than described in the literature. Histological studies showed that tissue superficial and deep to the fascia is frequently involved with the infectious inflammatory process, even in early stages of the disease. These pathologic changes were also found in healthy-appearing tissues at the periphery of the lesions. The early recognition of the disease and the prompt and aggressive surgical and medical therapeutic approach have resulted in far lower mortality rates (7%) than those reported in the literature. Frozen-section examination contributed to the maximal eradication of the pathologic process. This successful outcome was achieved in spite of the adverse associated clinical conditions, such as old age, debilitating disease, or complications, observed in half of the patients.

Occurrence of sporadic colorectal neoplastic lesion in patients with diffuse hyperplastic gastric polyposis and hypergastrinaemia may represent a new syndrome. Gastrin is not secreted by the gastric polyps or colonic carcinomas and may be related to gastric mucosal changes and H. pylori colonization. In patients with hyperplastic gastric polyposis and hypergastrinaemia, colorectal neoplasms should be ruled out.