Histologic and clinical outcome after laparoscopic Nissen fundoplication for gastroesophageal reflux disease and Barrett's esophagus.

BACKGROUND: The effectiveness of laparoscopic Nissen fundoplication for the regression of Barrett's esophagus in gastroesophageal reflux disease remains controversial. The aim of this study, therefore, was to review endoscopic findings and clinical changes after laparoscopic Nissen fundoplication for gastroesophageal reflux disease, particularly for patients with Barrett's esophagus. METHODS: From September 1995 through June 2004, 127 patients with gastroesophageal reflux disease underwent laparoscopic Nissen fundoplication. All the patients had clinical and endoscopic follow-up evaluation. We further analyzed the course of 37 consecutive patients with Barrett's esophagus (29% of all laparoscopic fundoplications performed in our institution) using endoscopic surveillance with appropriate biopsies and histologic evaluation. The median follow-up period for all the patients after fundoplication was 34 months (range, 3-108 months). The median follow-up period for the patients with Barrett's esophagus was 19 months (range, 3-76 months). RESULTS: During the 9-year period, 70 women (55 %) and 57 (45%) men were treated with laparoscopic Nissen fundoplication. The median age of these patients was 42 years (range, 7-81 years). The clinical results were considered excellent for 67 patients (53%), good for 51 patients (40%), fair for 7 patients (6%), and poor for 2 patients (1%). Endoscopic surveillance showed regression of the macroscopic columnar segment in 23 patients with Barrett's esophagus (62%). Regression at a histopathologic level occurred for 15 patients (40%). The histopathology remained unchanged for 14 patients with Barrett's esophagus (38%). CONCLUSION: Laparoscopic Nissen fundoplication effectively controls intestinal metaplasia and clinical symptoms in the majority of patients with Barrett's esophagus.

The effect of epithelial and myoepithelial differentiations on survival in a parotid gland undifferentiated carcinoma: case report and review of the literature.

Undifferentiated carcinoma of the parotid gland is a rare tumor, with an incidence of 5-10% among all parotid tumors. Salivary gland tumors frequently present myoepithelial cell differentiation. Recognition of myoepithelial cell differentiation is not easily apparent on routinely stained sections and it often requires immunohistochemical or ultrastructural studies. The relationship between these differentiations and survival is still not clear. We report on a 71-year-old male with left parotid undifferentiated small cell carcinoma with epithelial and myoepithelial differentiation that relapsed at the parotid region and neck nodes 4 years after he had undergone superficial parotidectomy. The relapsing disease was treated with total parotidectomy and radical left neck dissection. Also, postoperative radiotherapy was given to the left parotid region and the neck. In total, he is alive 8.5 years from the beginning of the disease, and 54 months after the second surgery and radiotherapy. No disease recurrence has occurred ever since. Undifferentiated carcinomas with epithelial and myoepithelial differentiation are rarely seen and differential diagnosis should be made with salivary gland myoepitheliomas and epithelial-myoepithelial carcinomas. Better understanding of the impact of these differentiations on survival will come with the evaluation of more cases of this unusual malignancy.

Immunohistochemical detection of E-cadherin, alpha- and beta-catenins in papillary thyroid carcinoma.

E-cadherin and catenins play a major role in neoplastic cell behavior as a suppressor of invasion and/or metastasis. The aim of this study was to determine E-cadherin, alpha-catenin and beta-catenin expressions in papillary thyroid carcinoma (PTC) and to correlate the results of expression to initial clinicopathological parameters and clinical outcome. Forty-one cases (mean age 37.3 +/- 11.2 yr) with PTC were studied. Patients were followed-up with a mean period of 47.6 +/- 27.0 months. A retrospective immunohistochemical analysis of E-cadherin, alpha-catenin and beta-catenin was performed on paraffin-embedded tissue sections. Tissues from ten patients with benign goiter were used as controls. E-cadherin, alpha- and beta-catenin immunoreactivities were found in 80% (33/41), 76% (31/41) and 97% (40/41) of patients respectively. No correlation was found between E-cadherin, alpha- and beta-catenin immunoreactivities and sex, local invasion or lymphatic spread at the time of initial examination. Distant metastases and/or local recurrences developed in 6 patients during follow-up. Recurrences/metastases developed both E-cadherin, alpha- and beta-catenin positive and negative primary tumors. Disease-free survival curves according to Kaplan-Meier analysis and log-rank test did not show any significant differences between E-cadherin, alpha- and beta-catenin positive and negative patients. According to our findings, E-cadherin, alpha- and beta-catenin expressions may not add any valuable information to the follow-up in a subgroup of PTC patients with a relatively benign course.

Cushing's syndrome caused by ectopic corticotropin secretion by multiple peripheral pulmonary carcinoids and tumorlets of carcinoid type.

Multiple peripheral pulmonary carcinoid tumors or their smaller counterparts (tumorlets of carcinoid type) are the most unusual form of carcinoids as a cause of ectopic corticotropin syndrome. Only three case reports were found in the literature. We describe a 35 year-old female patient with ectopic corticotropin secretion due to multiple peripheral pulmonary carcinoid tumors and tumorlets. A high-dose dexamethasone suppression test result led to the diagnosis of Cushing's disease in our case. But no tumor was identified on sella imaging and bilateral inferior petrosal sinus sampling was non-diagnostic. Computed tomography of the lungs revealed multiple acinar-nodular parenchymal infiltrations confined to the left lung. Corticotropin-dependent hypercortisolism persisted after bilateral adrenalectomy. A second operation was necessary to remove the hyperplastic adrenal remnants. Meanwhile, computed tomography findings of the thorax were unchanged. We decided to explore these nodules by open lung biopsy. During the procedure multiple nodules ranging 12 to 3 mm in diameter scattered throughout the left lung were observed and left pneumonectomy was performed. Histopathological diagnosis was multiple peripheral carcinoid tumors and tumorlets of carcinoid type showing positive immunostaining with corticotropin. This observation emphasizes a rare form of carcinoids as a cause of ectopic corticotropin secretion and its unusual response to high dose dexamethasone suppression test.

Pancreatobiliary adenosquamous carcinoma (report of two cases).

Adenosquamous carcinomas are rare malignant tumors of the pancreas and periampullary region. We present two cases of pancreatic and periampullary adenosquamous carcinoma with clinicopathologic, histo- and immunohistochemical findings. A 51-year-old and a 48-year-old man presented with right upper quadrant pain of three months duration and jaundice for two weeks. Both cases had an elevation of liver enzymes and CA 19-9. In the first case, computerized tomography showed a 3 cm-mass at the pancreatic head. In the second one, endoscopic retrograde choledocopancreatography (ERCP) revealed a mass at the ampulla Vateri localization. A pancreatoduodenectomy was performed for both cases. Gross pathologic examination displayed a solid, gray-white colored 4 cm-tumor at the pancreatic head and a solid, pink-white colored, 2 cm-tumor at the periampullary region bulging into the duodenal lumen. Microscopically, both tumors were composed of solid nests of squamous cells with pearl formation and mucin-containing glandular cells and diagnoses were adenosquamous carcinoma. Furthermore, histo- and immunohistochemical findings were consistent with microscopic diagnoses.

Anaplastic thyroid cancer with transient thyrotoxicosis: case report and literature review.

A 55-year-old woman with anaplastic thyroid carcinoma presented with hyperthyroidism and neck swelling, hoarseness, and cervical lymphadenopathy. On physical examination, she was found to be clinically hyperthyroid with an enlarged, nontender multinodular goitre. Her serum thyroid hormone levels confirmed hyperthyroidism and technetium-99m pertechnetate scan failed to visualize the thyroid gland. Open biopsy showed an invasion of the thyroid gland by anaplastic thyroid carcinoma. The thyrotoxic phase lasted 60 days with predominantly increased thyroxine level and triiodothyronine/thyroxine (T3/T4) ratio decreased below 15. The thyrotoxic period was followed by subclinical hyperthyroidism and hypothyroidism which continued until she died of lung metastasis.

Bombesin ameliorates colonic damage in experimental colitis.

In the present study we investigated the possible therapeutic effects of bombesin on an experimentally induced colitis model in rats. Inflammation of the colon was induced by a single intracolonic administration of 30 mg of 2,4,6-trinitrobenzene sulfonic acid (TNBS) at 8 cm from the anus. Immediately after the induction of colitis, some rats were given bombesin (10 microg/kg; subcutaneously) three times a day for 14 days, while another group received vehicle treatment. On day 14, the rats were decapitated and plasma carbonyl content and tissue myeloperoxidase level, as an index of granulocyte infiltration into intestinal tissue, were determined in order to obtain an objective evaluation of colonic injury. In the colitis group, increased macroscopic damage score, elevated MPO level and high plasma carbonyl content, together with the microscopic appearance revealed severe inflammatory changes resembling IBD. Bombesin treatment attenuated the TNBS-induced colonic damage and stimulated histopathologically apparent mucosal proliferation, suggesting that bombesin may play a role in protecting gut integrity.

Role of endothelins in trinitrobenzene sulfonic acid-induced colitis in rats.

To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4+/-0.4), acute (4.8+/-0.6) and chronic (3.8+/-0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3+/- 0.5) and chronic (2.3+/-0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1+/-44.9 and 431.8+/-54.6 U/g wet weight) as compared with the control group (73.6+/-11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1+/-63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3+/-23.1, 490+/-52.2 and 422.2+/-50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5+/-46.9 nmol/ml) and MPO activity (167.5+/-35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.

Steroid cell tumor of the ovary as a rare cause of virilization.

BACKGROUND: Virilization is associated with either ovarian causes, including polycystic ovary syndrome, hyperthecosis, and ovarian tumor, or with adrenal causes, including tumors and congenital adrenal hyperplasia. In establishing the diagnosis, levels of dehydroepiandresterone sulfate, testosterone, and 17 alpha-hydroxyprogesterone (17-OHP), with their response to dexamethasone treatment, should be assessed; and, where indicated, computerized tomography, ultrasound, and selective venous catheterization should be undertaken. CASE REPORT AND RESULTS: A 21-year-old woman presented with a 17-year history of early accelerated linear growth and virilization. During this time, a putative diagnosis of nonclassic congenital adrenal hyperplasia had been made, and she had been treated with glucocorticoids, with no regression in virilization, for 8 years. On presentation to our group, the failure of low- and high-dose dexamethasone suppression tests to decrease blood levels of testosterone and 17-OHP, combined with a relatively low blood level of corticotropin, led us to investigate an androgen-secreting tumor of ovarian origin. When ultrasonography and computerized tomography of the ovaries and adrenal glands displayed no abnormality, selective venous catheterization was performed, revealing an abnormal ovarian-peripheral gradient for testosterone, 17-OHP, estradiol, and androstenedione in the right ovarian vein. On exploratory laparotomy, a neoplasm adjacent to the right ovary was resected and was found to be a steroid cell tumor of the ovary not otherwise specified, one of the rarest tumors causing virilization in children. Symptomatic resolution followed tumor removal. CONCLUSION: Selective ovarian and adrenal venous catheterization for hormone assays is an efficient method of identification and localization of an androgen source in virilizing syndromes when noninvasive methods fail.