Massive ovarian edema associated with ovarian serous cystadenoma: a case report and review of the literature.

Massive ovarian edema is a rare entity that can be confused with an ovarian neoplasm. A few ovarian lesions have been reported that are associated with massive ovarian edema. This article describes the first case of an ovarian serous cystadenoma associated with a massive ovarian edema. The patient was a 17-year-old female who was referred to the emergency room because of lower abdominal pain. Subsequent ultrasound and computed tomography scanning studies revealed an abdominopelvic cystic mass suggestive of an ovarian neoplasm. She underwent an exploratory laparoscopy, and a left salpingo-oophorectomy was performed. The specimen weighed 1610 g and consisted of a cystic mass measuring 17 x 15 x 8 cm attached to a solid mass measuring 13 x 11 x 4 cm. Microscopy revealed a cystic and a solid lesion. The cystic structure was composed of a flat or cuboidal single-layer lining showing ciliated epithelium and focal areas of papillary structures compatible with a diagnosis of ovarian serous cystadenoma. The solid mass had an intact capsule and diffuse interstitial edema, preserving the overall structure of the ovary and sparing the outer cortex. These findings are compatible with the diagnosis of ovarian massive edema. This report of an association of serous cystadenoma with massive ovarian edema broadens the histologic spectrum in which a massive ovarian edema may be encountered.

Small-cell tumors of the liver: a cytological study of 91 cases and a review of the literature.

This study was designed to consider the cytomorphological spectrum, differential diagnosis, and the role of ancillary studies in small-cell tumors of the liver. Three independent pathologists reviewed cytological slides from 91 cases of small-cell tumors of the liver. The results were compared with the findings of three recently published studies (Cytopathology 11 (2000) 262-267; Diagn Cytopathol 19 (1998) 29-32; and Acta Cytol 40 (1996) 937-947). The role of immunohistochemistry in reaching timely and specific diagnoses was also examined. The diagnostic categories included 44 cases of metastatic small-cell undifferentiated carcinoma, 15 cases of metastatic neuroendocrine carcinoma, 10 cases of metastatic adenocarcinoma, 7 cases of malignant lymphoma, 4 cases of hepatocellular carcinoma with small-cell features, 2 cases of cholangiocarcinoma, 1 case of poorly differentiated carcinoma, and 8 cases of rare tumors including granulosa cell tumor (2 cases), sarcoma (4 cases), malignant melanoma with small-cell features (1 case), and meningioma with small-cell features (1 case). Metastatic granulosa cell-tumor, metastatic melanoma, and metastatic meningioma should be included in the differential diagnoses of small-cell malignancies found in the liver.

Primary malignant melanoma of the urinary bladder diagnosed by urine cytology: a case report.

BACKGROUND: Primary melanoma of the urinary bladder is a rare neoplasm, and there have been no prior reports in which the initial diagnosis was made by urinary cytology. CASE: An 82-year-old woman presented with vaginal spotting, gross hematuria and dysuria. Voided urine cytology revealed malignant cells, several of which exhibited cytoplasmic melanin pigment and were accompanied by many macrophages also containing melanin. Cystoscopy revealed a darkly pigmented, polypoid mass at the bladder neck. Biopsy confirmed the diagnosis. CONCLUSION: Primary melanoma of the urinary bladder is rare. The diagnosis can be made on cytologic examination of voided urine if careful study of exfoliated malignant cells reveals cytoplasmic melanin pigment. Macrophages may also harbor melanin pigment, and their presence should alert the cytopathologist to search carefully for pigmented malignant cells. Clinical and radiologic studies are essential to rule out melanoma metastatic to the bladder.

SpinThin, a simple, inexpensive technique for preparation of thin-layer cervical cytology from liquid-based specimens: data on 791 cases.

BACKGROUND: Acceptance of liquid-based fixatives for cervical cytology has been limited by the more complex slide-preparation procedures, increased cost, and reports that increased sensitivity has been based largely on comparison with conventional cytology without histologic correlation. Here the authors describe and evaluate a technically simple and relatively inexpensive method (which they call SpinThin) for preparing Cytospin (Shandon Inc., Pittsburgh, PA) cervical cytology slides from samples in liquid fixative using a modified electric toothbrush holder to put the cells in suspension. Results are compared with conventional cytology and histologic biopsy. METHODS: A total of 791 cervical cytology specimens from 2 patient groups at high risk of uterine cervical neoplasia were entered into this study, and a spatula and cytobrush (174 specimens) or cytobroom (617 specimens) were used to collect conventional smears. The collection device with remaining cellular sample was placed in an alcohol-based fixative solution; the cells were put into suspension by a brief burst of vibration using a modified electric toothbrush holder, then cytocentrifuged on a slide and stained with the Papanicolaou technique. RESULTS: Specimen adequacy in SpinThin slides was better than that of conventional cytology smears. However, the prevalence of dysplasia, including atypical squamous cells of undetermined significance (ASCUS-D), in conventional smears and SpinThin slides was the same--27% and 25%, respectively--and excluding ASCUS-D, it was 20% in both. The prevalence of neoplasia (low or high grade squamous intraepithelial lesion, or carcinoma) histologically was 31% in the 647 cases biopsied, and agreement with histology was similar for SpinThin and conventional smears. CONCLUSIONS: Using a simple and relatively inexpensive new technique (Spin-Thin), slides prepared from fluid-based cervical cytology specimens obtained with the cytobrush or cytobroom correlated very well with the corresponding conventional smears within major diagnostic categories, and both correlated well with histology.

Pancreatic metastasis of cardiac rhabdomyosarcoma diagnosed by fine needle aspiration. A case report.

BACKGROUND: Fine needle aspiration (FNA) is a valuable technique in the diagnosis of soft tissue tumors or their metastases. CASE REPORT: A rhabdomyosarcoma of the left atrium with metastasis to the pancreas was diagnosed by FNA in a 74-year-old female. The patient presented with dyspnea, weight loss and generalized weakness and was found to have a cardiac arrhythmia. Magnetic resonance imaging showed a 9-cm mass in the left atrium and anterior mediastinum. Computed tomography (CT) of the abdomen revealed a 2.8-cm nodule within the head of the pancreas. The patient underwent CT-guided percutaneous aspiration biopsy of the pancreatic mass on the first hospital day and, on the second day, transvenous FNA biopsy of the intracardiac mass. The cytologic morphology and immunocytochemistry of the aspirated material from both sites established a diagnosis of cardiac rhabdomysarcoma with metastasis to the pancreas. CONCLUSION: This is the fifth reported case of rhabdomysarcoma metastatic to the pancreas and the first in which the diagnosis was made by FNA, thereby eliminating the need for open biopsy.

Effect of HCl on transmembrane potentials and intracellular pH in rabbit esophageal epithelium.

BACKGROUND/AIMS: Acidification of the basolateral membrane by adding HCl to the serosal solution of esophageal epithelium leads to more necrosis than acidification of the apical membrane by adding HCl to the luminal solution. The aim of this study was to examine the mechanism for this difference. METHODS: The effect of low extracellular pH (pHo) (HCl) on intracellular pH (pHi) and transmembrane potentials was examined in rabbit esophageal cells by impalement with intracellular microelectrodes. RESULTS: Lowering luminal pH to 3.0 had no effect on membrane voltage and/or pHi in either luminally or serosally impaled cells, although a decline in both parameters occurred at pH 1.5 in luminally impaled cells. In contrast, lowering serosal pH from 7.4 to 3.0 progressively reduced membrane voltage and/or pHi. Membrane depolarization at low pHo was inhibited by a high-potassium solution or barium and mimicked by lowering pHi (gassing with CO2) at neutral pHo. CONCLUSIONS: Basolateral, but not apical, membranes of esophageal epithelial cells are highly permeable to H+, accounting for the greater susceptibility to damage from exposure to serosal than luminal acid. Membrane depolarization at low pHo is mediated by low pHi through inhibition of basolateral membrane K+ conductance.

Potassium conductance in rabbit esophageal epithelium.

K+ conductance in apical and basolateral cell membranes of rabbit esophageal epithelial cells was investigated within intact epithelium by impalement with conventional microelectrodes from luminal or serosal sides. Under steady-state conditions, K+ conductance was demonstrated in basolateral, but not apical, membranes by showing 1) membrane depolarization upon exposure to either solutions high in K+ (20-65 mM) or containing Ba2+, tetraethylammonium, or quinine, and 2) a resistance ratio that increased on exposure to high K+ solution and decreased on exposure to Ba2+, quinine, and tetraethylammonium. From exposures to high K+, the apparent K+ transference number and electromotive force generated at the basolateral membrane were calculated and found to be 0.42 +/- 0.01 and -83 +/- 3 mV, respectively. Furthermore, basolateral K+ conductance was shown to be important for maintaining resting net transepithelial Na+ absorption in that high K+ or barium inhibited the transepithelial potential difference and short-circuit current of Ussing-chambered epithelia. We conclude that under steady-state conditions the basolateral, but not apical, membranes of esophageal epithelial cells contain a K(+)-conductive pathway and that this pathway is important for active sodium absorption.

Na(+)-dependent and -independent Cl-/HCO3- exchangers in cultured rabbit esophageal epithelial cells.

BACKGROUND: The mechanisms by which esophageal epithelial cells regulate intracellular pH (pHi) in a physiological solution are unknown. METHODS: Basal-type esophageal cells growing in primary culture were loaded with the fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) to study pHi by microfluorimetry. RESULTS: The pHi in HEPES buffer was 7.7 +/- 0.03, a value higher than that in CO2/HCO3- buffer, 7.2 +/- 0.1. Cells in HEPES switched to CO2/HCO3- buffer rapidly acidified to pHi of 7, then alkalinized to a new steady-state pHi. The mechanisms for alkalinization in CO2/HCO3- were dependent on two exchangers, one amiloride-sensitive and the other 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)-sensitive, the latter dependent on Nao and Cli, and so indicative of an Na(+)-dependent Cl-/HCO3- exchanger. Cells in a CO2/HCO3- buffer rapidly alkalinized to pH 8.2 when switched to HEPES, then acidified to a new steady-state pHi. Acidification in HEPES was largely caused by a DIDS-sensitive, Clo-dependent, non-Nao-requiring mechanism, indicative of a cell-acidifying Na-independent Cl-/HCO3- exchanger. CONCLUSIONS: In a physiological buffer, esophageal cells have at least three exchangers for regulation of pHi.

Involvement of cell calcium and transmembrane potential in control of hepatocyte volume.

This study examined the role of hepatocyte calcium and cytoskeleton in activation of hyposmotic stress-induced increases in hepatocyte transmembrane potential and control of cell volume. Hepatocyte transmembrane potential was measured by glass microelectrodes in mouse liver slices before and after exposure to hyposmotic medium. Hepatocytes were loaded with tetramethylammonium by briefly exposing liver slices to nystatin, a cation poreforming antibiotic. Changes in hepatocyte steady-state water volume were determined by changes in intracellular tetramethylammonium activity measured with tetramethylammonium-sensitive, double-barrel micro-electrodes 4 min after exposure to hyposmotic medium. Hyposmotic stress of 74% of the control osmolality (approximately 280 mOsm) hyperpolarized hepatocyte transmembrane potential by 1.83 times the control hepatocyte transmembrane potential, and cell water volume increased by a factor of 1.19. The Ca2+ channel blocker verapamil (100 mumol/L) completely inhibited hyposmotic stress-induced hyperpolarization of hepatocyte transmembrane potential. This inhibitory effect diminished at doses of 37.5 or 50 mumol/L, but even these hyperpolarizations were decreased significantly compared with control. Hyposmotic stress during added verapamil dosage (50 mumol/L) also resulted in 23% greater cell swelling compared with control. Ca(2+)-free medium plus ethylene glycol-bis (beta-aminoethylether)-N,N'-tetraacetic acid (5 mmol/L) inhibited hyposmotic stress-induced increases in hepatocyte transmembrane potential and resulted in 16% greater cell swelling compared with control. Calmodulin inhibitors trifluoperazine (100 mumol/L) and promethazine (100 mumol/L) inhibited the hyperpolarization of hepatocyte transmembrane potential caused by hyposmolality, as did 3,4,5-trimethoxybenzoate 8-(N,N-diethylamino)octyl ester) (50 mumol/L), which inhibits mobilization of Ca2+ from intracellular stores. Cytochalasin B (50 mumol/L), which disrupts microfilaments, also inhibited hyperpolarization of hepatocyte transmembrane potential with osmotic stress.(ABSTRACT TRUNCATED AT 250 WORDS)

An electrophysiological technique to measure change in hepatocyte water volume.

We have applied an electrophysiologic technique (Reuss, L. (1985) Proc. Natl. Acad. Sci. USA 82, 6014) to measure changes in steady-state hepatocyte volume during osmotic stress. Hepatocytes in mouse liver slices were loaded with tetramethylammonium ion (TMA+) during transient exposure of cells to nystatin. Intracellular TMA+ activity (alpha 1TMA) was measured with TMA(+)-sensitive, double-barrelled microelectrodes. Loading hepatocytes with TMA+ did not change their membrane potential (Vm), and under steady-state conditions alpha iTMA remained constant over 4 min in a single impalement. Hyperosmotic solutions (50, 100 and 150 mM sucrose added to media) and hyposmotic solutions (sucrose in media reduced by 50 and 100 mM) increased and decreased alpha iTMA, respectively, which demonstrated transmembrane water movements. The slope of the plot of change in steady-state cell water volume, [(alpha iTMA)0/(alpha iTMA)4min] -1, on the relative osmolality of media, (experimental mosmol/control mosmol) -1, was less predicted for a perfect osmometer. Corresponding measurements of Vm showed that its magnitude increased with hyposmolality and decreased with hyperosmolality. When Ba2+ (2 mM) was present during hyposmotic stress of 0.66 X 286 mosmol (control), cell water volume increased by a factor of 1.44 +/- 0.02 compared with that of hyposmotic stress alone, which increased cell water volume by a factor of only 1.12 +/- 0.02, P less than 0.001. Ba2+ also decreased the hyperpolarization of hyposmotic stress from a factor of 1.62 +/- 0.04 to 1.24 +/- 0.09, P less than 0.01. We conclude that hepatocytes partially regulate their steady-state volume during hypo- and hyperosmotic stress. However, volume regulation during hyposmotic stress diminished along with hyperpolarization of Vm in the presence of K(+)-channel blocker, Ba2+. This shows that variation in Vm during osmotic stress provides an intercurrent, electromotive force for hepatocyte volume regulation.