Disclosure of potential conflicts of interest is found at the end of this article.

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Previous studies of umbilical vein varix diagnosed prenatally have been small, and the results have been contradictory. We wanted to determine whether prenatally diagnosed umbilical vein varix is associated with an increased risk of fetal anomalies or poor perinatal outcomes. We identified all cases of fetal intra-abdominal umbilical vein varix diagnosed on the basis of prenatal ultrasonography at Brigham and Women's Hospital between 1988 and 1998. Cases were reviewed to determine the presence of other sonographic findings as well as pregnancy and neonatal outcomes. We identified 25 cases and included those 23 for which follow-up was available. In 11 cases (48%), pregnancies and neonatal outcomes were normal, with full-term delivery, appropriate birth weight, and no evidence of anomalies. Three cases (13%) had preterm deliveries, and 1 had Kell isoimmunization requiring postnatal transfusion. In the remaining 8 cases (35%), structural anomalies were present. One fetus had a chromosomal abnormality (69,XXX). Prenatal diagnosis of fetal umbilical vein varix appears to be associated with a high rate of fetal anomalies. Detection of an umbilical vein varix should prompt a thorough examination of the fetus, including a fetal survey and echocardiogram. Isoimmunization should be ruled out, and consideration of karyotyping should be discussed if other anomalies are present.

BACKGROUND Adenosquamous carcinoma (ASCa) is a rare subtype of ductal adenocarcinoma of the pancreas with what to the authors' knowledge are limited cytologic descriptions. In the current study, the authors describe their experience with the fine‐aspiration biopsy (FNAB) diagnosis of ASCa and characterize cytologic features in 14 cases. METHODS Fourteen cases of ASCa were identified from pathology case files. Cytologic material was examined for cellularity, grade, tumor cell necrosis, and specific features of glandular and squamous differentiation. RESULTS The 10 females and 4 males had an average age of 70 years. Nine patients (64%) were reported to have Stage IV disease at the time of presentation. All tumors were high grade, with moderate to high cellularity. Tumor cell necrosis was noted in 12. Nine of the 14 cases (64%) demonstrated predominantly squamous differentiation with keratinization. Seven of these nine contained at least focal intracellular mucin or honeycombed glandular sheets. Two of the nine had rare cytoplasmic vacuoles as the only evidence of glandular differentiation. Five cases (36%) were predominantly glandular. All but one of these five cases contained atypical to malignant keratinized cells. One of the five cases lacked keratinization but had tumor cells with dense cytoplasm; the diagnosis of ASCa was confirmed on histology. In 13 patients for whom followup was known, 12 had died of disease (mean, 5.6 months) and 1 was alive at 13 months of follow‐up. CONCLUSIONS A specific diagnosis of ASCa is possible when aspirates show evidence of both squamous and glandular differentiation, although one component often predominates and features of dual differentiation may be focal. A purely squamous tumor should raise the suspicion of a metastasis, but also may represent undersampling of an ASCa. Cancer (Cancer Cytopathol) 2003;99:372–8. © 2003 American Cancer Society.

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Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is a distinct subtype of Hodgkin lymphoma in which T-cell subsets have not been studied specifically. We reviewed 24 cases of NLPHL and compared flow cytometric results with those of 13 progressively transformed germinal centers (PTGC) cases, 78 nonspecific reactive hyperplasia (RH) cases, and 31 classical Hodgkin lymphoma (CHL) cases. A double-positive (CD4+CD8+) T-cell population was present in 58% of NLPHL cases, constituting 10% to 38% of T cells. The cells were CD3+, CD5+, CD2+, CD7+, CD1a- and terminal deoxynucleotidyl transferase-. Similar CD4+CD8+ T cells were identified in 38% of PTGC cases (P = .31), 4% of RH specimens (P < .00001), and 6% of CHL specimens (P < .0001). The presence of a CD4+CD8+ T-cell population in NLPHL may reflect an activated or reactive T-cell subset and should not lead to a misdiagnosis of T-cell lymphoma. This population may be a clue to the diagnosis of NLPHL, particularly in cases with limited tissue.

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Rare cases of CD20+ T-cell lymphoma (TCL) have been reported, but the clinicopathologic spectrum of this disorder is not known. We identified 9 cases of CD20+ TCL diagnosed at our institution and 26 additional cases through a search of the English language literature. Among current cases, there were 7 men (ages 71 to 81, median 75 y) and 2 women (ages 36 and 37 y). Five patients presented with predominantly nodal disease (localized in 3 and widespread in 2 cases) and 4 patients presented with purely extranodal disease involving the parotid glands, skin, or small intestine. CD20 was uniformly and strongly expressed in 5 cases and dimly expressed or present on a subset of neoplastic cells in 4 cases. The proportion of CD20+ T cells changed over time in 3 cases. Three cases fulfilled diagnostic criteria for clinicopathologically defined subtypes of TCL (2 mycosis fungoides; 1 enteropathy-type TCL), whereas 6 were peripheral TCL unspecified with variable cytomorphology, T-cell immunophenotype, and sites of involvement. In 8 of 9 cases, a clonal T-cell population was identified by molecular genetic analysis. Among 8 cases with clinical follow-up, 5 behaved aggressively with death from disease within 3 years of diagnosis in 4 cases (median survival: 11 mo, range: 1 to 35 mo), and recurrent disease at 10 months in 1 case; 1 patient died of an EBV+ B-cell lymphoma (BCL) 66 months after the original diagnosis; in the remaining 2 cases, patients were alive and undergoing treatment (follow-up: 4 and 18 mo). Historical cases showed similar clinicopathologic variability. CD20+ TCL is rare, and clinically and pathologically heterogeneous. When CD20 expression is present in TCL, it may be dimmer than that of normal B cells, suggesting neoplastic transformation of a normal CD20dim+ T-cell subset. Cases of CD20+ TCL in which the proportion of CD20+ cells changes over time may reflect aberrant expression of CD20, possibly as an activation marker, by neoplastic T cells. CD20+ TCL may cause diagnostic difficulty, particularly in cases that clinically and pathologically mimic BCL. Knowledge of the unusual phenomenon of CD20 expression in TCL, in conjunction with careful morphologic analysis, the use of a panel of antibodies, and molecular genetic studies, is important in avoiding a misdiagnosis of BCL.