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1.
Am J Surg Pathol ; 6(2): 109-17, 1982 Mar.
Article in English | MEDLINE | ID: mdl-7102891

ABSTRACT

Omenta removed either at surgery or autopsy were examined for benign glandular inclusions. Multiple random sections failed to reveal these inclusions in any of the 37 male or 27 female autopsy specimens. None of the 22 male surgical specimens contained benign cysts, whereas these inclusions were found in 19 of 128 (14.8%) of the female surgical specimens. One female patient had endometriotic cysts, two had mesothelial cysts, and 13 had inclusions histologically similar to oviduct epithelium (endosalpingiosis). Another female had both endometriotic cysts and endosalpingiosis, whereas two had both mesothelial cysts and endosalpingiosis. All 16 patients with endosalpingiosis had inflammatory tubal disease (e.g., chronic salpingitis, hydrosalpinx, tubal pregnancy). Four of these 16 females also had an ovarian tumor. These ovarian tumors included one serous cystadenoma, two serous cystadenomas of borderline malignancy, and one serous cystadenocarcinoma. We conclude that the endosalpingiotic inclusions are benign and occur exclusively in females. Since they are found in association with ovarian tumors, it is important to exclude well-differentiated metastases. Our findings support a close relationship between inflammatory tubal disease and endosalpingiosis.


Subject(s)
Endometriosis/pathology , Omentum , Peritoneal Neoplasms/pathology , Adolescent , Adult , Aged , Child , Child, Preschool , Endometriosis/complications , Endometriosis/diagnosis , Fallopian Tube Diseases/complications , Female , Humans , Infant , Male , Middle Aged , Omentum/pathology , Peritoneal Diseases/diagnosis , Peritoneal Neoplasms/complications
2.
Hum Pathol ; 17(6): 600-3, 1986 Jun.
Article in English | MEDLINE | ID: mdl-3710472

ABSTRACT

Enteritis cystica profunda (ECP), an uncommon condition, is characterized by nonneoplastic cystic spaces within the wall of the small bowel. The cases of two patients who had ECP in association with Crohn's disease are reported, and the role of mucosal damage in the pathogenesis of ECP is discussed. Pathologists must recognize this entity and distinguish it from adenocarcinoma, which may arise with increased frequency in the small bowel in patients with Crohn's disease.


Subject(s)
Crohn Disease/complications , Cysts/complications , Enteritis/complications , Intestinal Diseases/complications , Adult , Crohn Disease/pathology , Cysts/diagnosis , Cysts/pathology , Diagnosis, Differential , Enteritis/diagnosis , Enteritis/pathology , Female , Humans , Intestinal Diseases/diagnosis , Intestinal Diseases/pathology , Male
3.
Hum Pathol ; 14(1): 42-61, 1983 Jan.
Article in English | MEDLINE | ID: mdl-6832749

ABSTRACT

Most previous studies of Barrett's metaplasia have used biopsy material to document cell, gland, and architectural types, leading to inaccurate or incomplete conclusions. The present study presents data from eight esophagogastrectomy specimens of Barrett's metaplasia with associated neoplasia, which were evaluated topologically by use of dissecting microscopy, specimen radiography, scanning electron microscopy, and routine histologic examination. Barrett's metaplasia was found to be mosaic of cell, gland, and architectural types, showing variable degrees of atrophy and maturation toward intestinal and gastric epithelium. Zonation was not found. Surface mucous, goblet, absorptive, mucous neck, mucous gland, and neuroendocrine cells were found in all cases; Paneth, chief, and parietal cells were found in approximately half. The presence of villar architecture with lining goblet and absorptive cells is unique and can be used to make a biopsy diagnosis. In one case, only a minute residual focus of Barrett's metaplasia was found, suggesting that the pathogenesis of some cases of adenocarcinoma of the lower esophagus and gastric cardia unassociated with Barrett's metaplasia may be the same. Nine cases of adenocarcinoma of the gastroesophageal junction unassociated with Barrett's metaplasia, studied during the same time period, had similar epidemiologic characteristics including mean age, age range, and sex distribution. Multifocal dysplasia and carcinoma in situ were found in all but one case. In two of eight cases adenomatous change was present; one of these resembled a villous adenoma of the colon with malignant degeneration. Barrett's metaplasia thus appears to be important as a precursor of adenocarcinoma in the region of the lower esophagus and gastroesophageal junction. The significance of these findings in relation to previous reports is discussed.


Subject(s)
Adenocarcinoma/etiology , Barrett Esophagus/complications , Esophageal Diseases/complications , Esophageal Neoplasms/etiology , Esophagogastric Junction/pathology , Adenocarcinoma/pathology , Adenocarcinoma/ultrastructure , Aged , Barrett Esophagus/pathology , Esophageal Neoplasms/pathology , Esophageal Neoplasms/ultrastructure , Female , Humans , Male , Microscopy, Electron, Scanning , Middle Aged
4.
JPEN J Parenter Enteral Nutr ; 7(4): 337-45, 1983.
Article in English | MEDLINE | ID: mdl-6413709

ABSTRACT

Forced feeding has been shown to effectively stimulate tumor metabolism in numerous animal models. Significant acceleration of tumor growth by exogenous nutrient administration is generally considered to be detrimental to the host. The present study was performed to determine if substrate-induced alterations in tumor metabolism could be exploited to enhance tumor response to cycle-specific chemotherapy. Following subcutaneous mammary tumor implantation (AC-33) and protein depletion, 39 female Lewis/Wistar rats were randomly assigned to one of four nutritional regimens for 48 hr: (1) protein-depleted food (0.03% protein) ad libitum po, (2) parenteral carbohydrate (18.6% dextrose), (3) parenteral amino acids (2.8% amino acids), or (4) total parenteral nutrition (18.6% dextrose/2.8% amino acids). Methotrexate (5 mg/kg im) was administered to all animals 2 hr after initiating these nutritional regimens. Tumor volume and host toxicity were monitored throughout the study. At sacrifice, significant reduction in tumor volume was observed in animals receiving parenteral amino acids (0.37 +/- 0.24 cm3) and total parenteral nutrition (0.25 +/- 0.18 cm3) compared to the group receiving protein-depleted food po (0.70 +/- 0.22 cm3) (p less than 0.01). In this animal model, the parenteral administration of amino acids with or without the addition of hypertonic dextrose was found to effectively potentiate tumor response to methotrexate without increasing host toxicity.


Subject(s)
Adenocarcinoma/therapy , Amino Acids/administration & dosage , Mammary Neoplasms, Experimental/therapy , Methotrexate/therapeutic use , Parenteral Nutrition , Adenocarcinoma/pathology , Animals , Dietary Proteins/administration & dosage , Disease Models, Animal , Female , Glucose/administration & dosage , Mammary Neoplasms, Experimental/pathology , Methotrexate/toxicity , Nitrogen/metabolism , Parenteral Nutrition, Total , Rats
5.
J Surg Res ; 39(2): 103-13, 1985 Aug.
Article in English | MEDLINE | ID: mdl-3927061

ABSTRACT

Exogenous nutrient administration has been shown to significantly stimulate tumor growth in numerous animal models. The present study was performed to determine if substrate-induced alterations in tumor metabolism could be exploited to potentiate tumor response to cycle-specific chemotherapy. Following subcutaneous mammary tumor (AC-33) implantation, 55 female Lewis/Wistar rats were randomly assigned to one of three nutritional regimens for 48 hr: (1) protein-depleted chow (0.03% protein) ad lib per os, (2) standard rat chow (22.0% protein) ad lib per os, or (3) total parenteral nutrition (TPN; 18.6% dextrose/2.8% amino acids). One-half of the animals in each group received a single dose of methotrexate (5 mg/kg im) while the remaining animals received placebo (saline) injections. At sacrifice, methotrexate-treated animals receiving TPN demonstrated a significantly smaller tumor volume (0.47 +/- 0.44 cm3) compared to animals given either protein depleted chow (1.30 +/- 0.76 cm3) or standard rat chow (1.34 +/- 0.83 cm3) (P less than 0.01). In this animal model, adjuvant TPN was found to significantly potentiate tumor response to cycle-specific chemotherapy with no detectable exacerbation of host toxicity.


Subject(s)
Mammary Neoplasms, Experimental/drug therapy , Methotrexate/therapeutic use , Parenteral Nutrition, Total , Parenteral Nutrition , Adenocarcinoma/drug therapy , Adenocarcinoma/metabolism , Animals , Body Composition , Body Weight , Energy Intake , Female , Leukocyte Count , Mammary Neoplasms, Experimental/metabolism , Methotrexate/adverse effects , Nitrogen/metabolism , Random Allocation , Rats , Rats, Inbred Strains
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