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Forty-two patients each with a colorectal polyp have been treated in our hospital over the past 10 years. In twenty-two cases the polyps were noted in the rectum, nine in the sigmoid colon, seven in the descending colon and four in the transverse colon. Each patient had only one polyp. Hematochezia was the main symptom in 29 patients, prolapse of the polyp from the anus in 10, abdominal pain due to intussusception in two and no symptoms were observed in one. Auto-amputation of the polyp was considered to have occurred in five patients. Twelve rectal polyps were resected from a transanal operation, and another 25 polyps were removed endoscopically with electric cautery. We have had no experience of endoscopic complications such as bleeding or perforation. A histological examination revealed an adenoma in one patient. Other polyps were non-neoplastic and were classified as juvenile, inflammatory and hyperplastic in 30, two and four patients, respectively. There have been no recurrences of polyps to date.
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PMID:Management of colorectal polyps in children. 846 May 42

Ileostomy polyps are uncommon and poorly described. The aim of this study was to undertake a retrospective clinicopathological review of ileostomy polyps. Seven patients with 60 polyps arising on ileostomies performed for ulcerative colitis were studied. The histopathological evaluation of archival ileostomy biopsy specimens, polypectomy or excision specimens, and clinical review of patient records was undertaken. Fifty of 60 polyps were inflammatory cap polyps and six further polyps were composed of granulation tissue only. They occurred anywhere on the stoma at any time after ileostomy construction and were strongly associated with overt stomal prolapse. Four neoplastic polyps were identified in two patients 27-36 years after ileostomy construction; all occurred at the mucocutaneous junction. One patient presented with a 2 cm polypoid invasive adenocarcinoma while in the second a 1.7 cm polypoid mucinous adenocarcinoma and a 0.7 cm ileal tubular adenoma with high grade dysplasia occurred at the site of excision of a cap polyp showing focal low grade adenomatous dysplasia six years previously. Neoplastic and non-neoplastic polyps could not be differentiated clinically. It was found that most ileostomy polyps are inflammatory cap polyps associated with stomal prolapse. Less common are polypoid adenomas or adenocarcinomas arising at the mucocutaneous anastomosis > 20 years after ileostomy construction. To prevent ileostomy carcinoma it is recommended that a biopsy of all polyps at the mucocutaneous anastomosis and of any non-prolapse associated polyps elsewhere on the stoma occurring > 15 years after ileostomy construction is done.
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PMID:Ileostomy polyps, adenomas, and adenocarcinomas. 853 59

Coumarin is the basic structure of numerous naturally occurring compounds with important and diverse physiological activities. More than a thousand coumarin derivatives have been described, varying from simple coumarins containing alkyl and hydroxyl side chains to complex coumarins with benzoyl, furanoyl, pyranoyl, or alkylphosphorothionyl substituents. Coumarin and 3,4-dihydrocoumarin were nominated by the Food and Drug Administration and the National Cancer Institute for study because of the widespread use of coumarin in perfumes, cosmetics, and other products as a fragrance, continued interest in coumarin compounds as flavor-enhancing agents for foods, and the interest in structure-activity relationships of this important group of compounds. Coumarin is believed to be metabolized to a 3,4-epoxide intermediate, which may be responsible for its toxic effects, while 3,4-dihydrocoumarin, which lacks the 3,4-double bond, is not considered likely to form an epoxide intermediate. Toxicity and carcinogenicity studies were conducted by administering coumarin (97% pure) in corn oil by gavage to groups of male and female F344/N rats and B6C3F1 mice for 16 days, 13 weeks, and 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, Drosophila melanogaster, and B6C3F1 mice. 16-DAY STUDY IN RATS: Groups of five male and five female rats received coumarin in corn oil by gavage at doses of 0, 25, 50, 100, 200, or 400 mg per kg body weight, 5 days a week for a total of 12 doses in a 16-day period. All female rats and four male rats receiving 400 mg/kg died. The mean body weight gains and final mean body weights of surviving dosed male and female rats were similar to those of the controls. There were no clinical signs of organ-specific toxicity, and there was no evidence of impaired blood coagulation from measurements of capillary clotting time or prothrombin and activated partial thromboplastin time. 16-DAY STUDY IN MICE: Groups of five male and five female mice received coumarin in corn oil by gavage at doses of 0, 40, 75, 150, 300, or 600 mg per kg body weight, 5 days a week for a total of 12 doses in a 16-day period. All mice receiving 600 mg/kg, two male mice receiving 300 mg/kg, and one male mouse receiving 75 mg/kg died. The mean body weight gains and final mean body weights of surviving dosed male and female mice were similar to those of the controls. Clinical findings of inactivity, excessive lacrimation, piloerection, bradypnea, ptosis, or ataxia were observed in some mice from the 300 and 600 mg/kg groups within the first several hours after dosing. Capillary clotting time and platelet counts of dosed mice were similar to those of controls. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats received coumarin in corn oil by gavage at doses of 0,19, 38, 75,150, or 300 mg per kg body weight. Three male and three female rats receiving 300 mg/kg died. The mean body weight gains and final mean body weights of male rats that received 150 and 300 mg/kg were significantly lower than those of the controls. There were no clinical signs related to specific organ toxicity. Male and female rats receiving coumarin exhibited dose-related decreases in mean erythrocyte volume and mean erythrocyte hemoglobin, and dose-related increases in erythrocyte counts. Serum levels of total bilirubin and one or more cytoplasmic enzymes including alanine aminotransferase, aspartate aminotransferase, ornithine carbamoyltransferase, and/or sorbitol dehydrogenase in males and females receiving 300 mg/kg were higher than those of controls. The absolute and relative liver weights of male and female rats that received 150 and 300 mg/kg were significantly greater than those of the controls. Centrilobular hepatocellular degeneration and necrosis, chronic active inflammation, and bile duct hyperplasia were observed in the liver of rats receiving 150 or 300 mg/kg. The high dose selected for the 2-year study was 100 mg/kg, which was just below the level at which mortality, lower final mean body weiody weights, and treatment-related liver lesions were observed in the 13-week study. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female mice received coumarin in corn oil by gavage at doses of 0, 19, 38, 75, 150, or 300 mg per kg body weight. Two male mice receiving 300 mg/kg died. The mean body weight gain and final mean body weight of surviving male mice that received 300 mg/kg were significantly lower than those of the controls. No clinical signs of toxicity were observed. Male and female mice receiving coumarin exhibited dose-related decreases in mean erythrocyte volume and mean erythrocyte hemoglobin. The absolute and relative liver weights of males and females that received 150 and 300 mg/kg were significantly greater than those of the controls. Centrilobular hepatocellular hypertrophy was observed in male and female mice receiving 300 mg/kg. The high dose selected for the 2-year study was 200 mg/kg, which was just below the level at which mortality and liver lesions were observed in the 13-week study. 2-YEAR STUDY IN RATS: Groups of 60 male and 60 female rats were administered coumarin in corn oil by gavage at doses of 0, 25, 50, or 100 mg per kg body weight. After 15 months, 10 animals from each group were evaluated. Survival, Body Weights, and Clinical Findings: None of the male rats receiving 100 mg/kg and only two males receiving 50 mg/kg survived until the end of the study (vehicle control, 28/50; 25 mg/kg, 9/50; 50 mg/kg, 2/51; 100 mg/kg, 0/50). Survival of dosed female rats was similar to that of the controls (29/50, 38/50, 36/50, 30/50). The reduced survival in dosed male rats was primarily attributed to chemical-related exacerbation of spontaneously occurring renal disease. Final mean body weights of female rats that received 100 mg/kg and all dosed groups of male rats were lower than those of the controls. There were no clinical signs of toxicity in rats, other than nonspecific signs relating to debilitation as a result of renal or other spontaneous disease. Hematology and Clinical Chemistry: At the 15-month interim evaluation, the values for one or more hematologic parameters including mean erythrocyte volume, mean erythrocyte hemoglobin in 50 and 100 mg/kg rats, and hematocrit or hemoglobin in 100 mg/kg rats were significantly lower than those of controls. Activated partial thromboplastin times were also significantly lower in 50 and 100 mg/kg males, while platelet counts were significantly higher. Activities of alanine aminotransferase, sorbitol dehydrogenase, or g-glutamyltransferase in 50 and 100 mg/kg male and 100 mg/kg female rats were significantly higher than those of the controls at the 15-month interim evaluation. Pathology Findings: The principal lesions associated with the administration of coumarin to rats for up to 2 years occurred in the liver, kidney, and forestomach. While the hepatic lesions were seen in all groups of males, they occurred only in the 50 and 100 mg/kg females. The lesions consisted of a spectrum of changes including hepatocellular necrosis, fibrosis, cytologic alteration, and increased severity of bile duct hyperplasia. The incidences of hepatocellular neoplasms were not increased in dosed rats. There was a chemical-related increase in the average severity of nephropathy in all groups of dosed male and female rats. There were corresponding increased incidences of parathyroid gland hyperplasia in all groups of dosed males, probably as a result of compromised renal function. In the standard evaluation of single kidney sections, a low incidence of renal adenomas was seen in all groups of males and in 100 mg/kg females (males: vehicle control, 1/49; 25 mg/kg, 2/50; 50 mg/kg, 2/51; 100 mg/kg, 1/50; females: 0/49, 0/50, 0/50, 2/49). An evaluation of step sections identified additional individuals with renal tubule focal hyperplasia (males: 2/49, 12/50, 10/51, 6/50; females: 1/49, 0/50, 4/50, 2/49) and adenoma (males: 0/49, 4/50, 5/51, 4/50; females: 0/49, 0/50, 1/50,1/49) in the dosed groups. The incidences of forestomach ulcers in all groups of dosed male rats and in 100 mg/kg female rats were significantly greater than those of the controls (males: 7/48, 24/50, 35/51, 34/50; females: 1/48, 1/49, 6/50, 9/48). STOP-EXPOSURE EVALUATION: A group of 40 male rats received 100 mg/kg coumarin in corn oil by gavage for 9 months, when 20 of the animals were necropsied and evaluated. The remainder of the male rats received only the corn oil vehicle during the 15-month recovery period. Similarly, a group of 30 male rats received 100 mg/kg coumarin in corn oil by gavage for 15 months, when 10 of the rats were necropsied and evaluated. The remaining 20 rats received only corn oil during the 9-month recovery period. A group of 20 vehicle control male rats were necropsied at 9 months, and another 10 vehicle control male rats were necropsied at 15 months. While chemical-related hepatic lesions were seen at both the 9- and 15-month interim evaluations, the incidences and severities of these lesions following the recovery period were generally similar to controls. Thus, the hepatic lesions produced by 9 or 15 months of exposure were reversible. In contrast to the liver lesions, the severity of nephropathy in male rats following the recovery period was significantly greater than that of males examined at the 9- and 15-month interim evaluations. This is not unexpected, since nephropathy is a progressive degenerative disease that naturally increases in severity with age. The incidence of renal tubule hyperplasia in the 15-month stop-exposure group (dosed for 15 months followed by the recovery period) and the incidence of renal tubule adenoma in the 9-month stop-exposure group were significantly greater than those of the control group. 2-YEAR STUDY IN MICE: Groups of 70 male and 70 female mice were administered coumarin in corn oil by gavage at doses of 0, 50, 100, or 200 mg per kg body weight for up to 2 years. After 15 months, 19 or 20 mice from each group were evaluated. Survival, Body Weights, and Clinical Findings: Survival of dosed male and female mice was similar to that of the controls (males: vehicle control, 43/50; 50 mg/kg, 47/50; 100 mg/kg, 42/50; 200 mg/kg, 37/51; females: 33/50, 40/50, 42/51, 28/51). The mean body weights of 200 mg/kg male and female mice were lower than those of controls throughout much of the study. There were no clinical findings related to chemical administration. Hematology and Clinical Chemistry: Mean erythrocyte volume, mean erythrocyte hemoglobin, and hematocrit of 200 mg/kg males and mean erythrocyte volume of 200 mg/kg females were significantly lower than those of the controls. Blood platelet counts of 200 mg/kg males and females were significantly higher than those of controls. There were no biologically significant differences in enzyme activities between dosed and control mice. Pathology Findings: The principal toxic lesions associated with the administration of coumarin to mice occurred in the liver. The incidences of centrilobular hypertrophy in 100 and 200 mg/kg males and 200 mg/kg females were significantly greater than those of controls. The incidences of syncytial alteration in all male dose groups and in 200 mg/kg females were also significantly greater than controls. The incidences of eosinophilic foci, a putative preneoplastic lesion, and of hepatocellular adenoma were significantly greater in the 50 and 100 mg/kg females. Hepatocellular carcinomas occurred with low incidences in the dosed females, but none occurred in the controls. The overall incidence of hepatocellular neoplasms (benign and malignant combined) in the 50 and 100 mg/kg females (control, 8/50; 50 mg/kg, 27/49; 100 mg/kg, 31/51; 200 mg/kg, 13/50) exceeds the range in historical controls (range 2%-34%; 129/898, 14.4%) from recent NTP studies. The reason for a lack of liver response in 200 mg/kg female mice is not known, but may be due in part to the decrease in body weight. While the incidences of eosinophilic foci were marginally greater in dosed male mice, the incidences of hepatocellular neoplasms were similar among the dosed and control groups. The incidences of alveolar/bronchiolar adenomas were significantly greater in 200 mg/kg male and female mice than in the controls. Further, the incidence of alveolar/bronchiolar carcinoma in 200 mg/kg females was also significantly greater than in controls. The overall incidence of pulmonary neoplasms (benign and malignant combined) in the 200 mg/kg groups (males: 14/50, 9/50,15/50, 25/51; females: 2/51, 5/49, 7/49, 27/51) exceeds the range in historical controls (males: range 6%-28%; 166/900, 18.4%; females: range 0%-14%; 58/899, 6.5%) from recent NTP studies. The incidence of squamous cell papilloma of the forestomach in 50 mg/kg males was greater than that of the controls (2/50, 8/50, 2/50, 0/51) and also exceeds the range of this neoplasm in control male mice from recent NTP studies (range 0%-14%; 27/902, 3.0%). The incidence of squamous cell papilloma of the forestomach in 50 mg/kg female mice was also slightly increased (1/52, 5/50, 2/51, 2/51); however, the incidence did not exceed the NTP historical range (27/901, 3%; range, 0%-10%). GENETIC TOXICOLOGY: Coumarin induced gene mutations in Salmonella typhimurium strain TA100 in the presence, but not in the absence, of exogenous metabolic activation (S9); no mutations were induced in strains TA98, TA1535, or TA1537, with or without S9. In Chinese hamster ovary cells, coumarin induced sister chromatid exchanges in the absence of S9, and chromosomal aberrations in the presence of S9. Coumarin did not induce sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster treated either as adults by feeding or injection, or as larvae by feeding. No increase in the frequency of micronucleated erythrocytes was observed in peripheral blood of male and female B6C3F1 mice administered coumarin by gavage for 13 weeks. CONCLUSIONS: Under the conditions of these 2-year gavage studies there was some evidence of carcinogenic activity of coumarin in male F344/N rats based on increased incidences of renal tubule adenomas. There was equivocal evidence of carcinogenic activity of coumarin in female F344/N rats based on a marginally increased incidence of renal tubule adenomas. There was some evidence of carcinogenic activity of coumarin in male B6C3F1 mice based on the increased incidence of alveolar/bronchiolar adenomas. There was clear evidence of carcinogenic activity of coumarin in female B6C3F1 mice based on increased incidences of alveolar/bronchiolar adenomas, alveolar/bronchiolar carcinomas, and hepatocellular adenomas. The marginally increased incidences of squamous cell papillomas of the forestomach in male and female mice receiving 50 mg/kg may have been related to coumarin administration. The administration of coumarin to rats was also associated with an increased severity of nephropathy in the kidney and of bile duct hyperplasia in the liver, increased incidences of ulcers of the forestomach, and necrosis, fibrosis, and cytologic alteration of the liver. Administration of coumarin to mice was also associated with centrilobular hypertrophy, syncytial alteration, and eosinophilic focus in the liver. Synonyms: 5,6-benzo-alpha-pyrone, 2H-1-benzopyran-2-one, 2H-benzolblpyran-2-one, 1,2-oxo-1,2-benzopyran, 1,2-benzopyrone, cis-o-coumarinic acid lactone, coumarinic anhydride, cumarin, o-hydroxycinnamic acid lactone, kumarin, [2-propenoic acid, 3-(-2-hydroxyphenyl)-delta-lactone], Rattex, tonka bean camphor
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PMID:NTP Toxicology and Carcinogenesis Studies of Coumarin (CAS No. 91-64-5) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1261 89

A 63-year-old woman with diplopia and bilateral ptosis underwent brain MRI that showed a pituitary mass with signal characteristics suggestive of adenoma. Within one week she had developed nearly complete bilateral ophthalmoplegia. A repeat MRI showed extension of the mass into both cavernous sinuses. Hypophysectomy disclosed an amelanotic melanoma. Extensive search for a primary source was unsuccessful. Despite local radiation treatment, the tumor continued to grow and the patient became blind and died within several months of diagnosis. There are seven reported cases of melanoma arising primarily in the sella turcica. Two cases of metastatic melanoma to the cavernous sinuses have been reported. Amelanotic melanoma has not been reported as a cause of cavernous sinus syndrome.
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PMID:Rapidly progressive bilateral ophthalmoplegia and enlarging sellar mass caused by amelanotic melanoma. 1651 68

Pituitary abscess secondary to an adenoma is rare. To date, only 19 cases have been reported. This is the first report of a patient who presented with bilateral total ophthalmoplegia. A 59-year-old male patient presented with headache, nausea, vomiting, decreasing visual acuity, diplopia and bilateral ophthalmoplegia with ptosis. Magnetic resonance imaging was suggestive of a pituitary abscess with adenoma. Transphenoidal surgery was performed and, during debulking of the tumour, the abscess was seen and excised. After the operation, the patient received antibiotic therapy and his neurological condition improved. Pituitary abscess with adenoma is a serious condition that has a high mortality rate. Therefore, early diagnosis and surgical intervention with antibiotic therapy are necessary.
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PMID:Abscess formation within invasive pituitary adenoma. 1693 Oct 19

Pituitary apoplexy (PA), which is one of the most serious life-threatening complications of pituitary adenoma, is characterized by abrupt onset of headache, nausea, vomiting, visual disturbances and oculomotor paresis. Combination of oculomotor cranial nerve paralysis with normal visual fields is very rare in PA. We report a 60-year-old acromegalic man presented with panhypopituitarism and bilateral total opthalmoplegia without a visual field defect. At initial evaluation his clinical findings were compatible with adrenal crisis and eye examination revealed total opthalmoplegia, bilateral ptosis and normal vision. MRI showed a large heterogeneous mass in the pituitary fossa. Although clinical findings due to adrenal crisis improved after glucocorticoid therapy there was no improvement in opthalmoplegia and ptosis. The patient underwent transsphenoidal excision of the pituitary mass. Histological examination revealed an adenoma with large areas of hemorrhagic infarction and most of the cells were positive for GH in immunohistochemical analysis. Although opthalmoplegia was severe at presentation, total recovery was achieved 3 months after transsphenoidal surgery. Therefore the presented case clearly demonstrates that opthalmoplegia without a visual field defect due to PA has a good prognosis and early diagnosis and treatment including surgical decompression are crucially important.
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PMID:Complete surgical resolution of bilateral total opthalmoplegia without visual field defect in an acromegalic patient presented with pituitary apoplexy. 1778 21

We removed 12 intraorbital tumors (5 schwannomas, 3 meningiomas, 2 cavernomas, 1 pleomorphic adenoma, and 1 neuroblastoma) using the frontozygomatic approach. No patients died. Postoperatively, 1 patient developed transient ptosis, and 3 patients had mild enophthalmos. Two patients with a meningioma developed transient worsening of their visual acuity and visual field. The frontozygomatic approach for surgical treatment of intraorbital tumors provides a wide visual field exposing the entire optic nerve. This approach is indicated for large intraorbital tumors, tumors affecting the optic nerve or orbital apex, intraorbital tumors that have extended into the intracranial cavity, and intracranial tumors that have extended into the orbit. The operative procedure for intraorbital tumor is determined by the location of the lesion and by the direction of its growth. The procedure is applicable to all intraorbital tumors. It reduces discomfort for surgeons while providing a relatively wide surgical field.
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PMID:Frontozygomatic approach to intraorbital tumors. 1833 Apr 28

Pituitary apoplexy after coronary bypass operations is a rare complication with very serious neurologic consequences. Anisocory, unilateral ptosis, and third cranial nerve palsy after coronary bypass surgery developed in a patient. The diagnosis was assured by computerized tomographic scan showing pituitary macro adenoma.
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PMID:Pituitary apoplexy after cardiac surgery. 2273 16

Pseudoinvasion or pseudocarcinomatous invasion in an adenomatous polyp of the colon can be unfamiliar to an endoscopist. Pseudoinvasion in an adenomatous polyp represents prolapse of the adenomatous epithelium into its stalk. In most cases its morphology does not differ from of general adenomatous polyps, but in some cases it can morphologically mimic a malignant polyp with submucosal invasion due to mass-like lesioning of its stalk. This makes it difficult for endoscopists to differentiate pseudoinvasion in an adenoma from an invasive carcinoma by conventional endoscopy; instead, endoscopic ultrasonography can provide useful information for differentiating these conditions. We report on an 82-year-old man who presented with a large pedunculated polyp with a thick stalk in the sigmoid colon, which mimicked a submucosal invasive carcinoma. The patient was diagnosed with pseudoinvasion in an adenomatous polyp after segmental resection of the sigmoid colon.
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PMID:Pseudoinvasion in an adenomatous polyp of the colon mimicking invasive colon cancer. 2043 36

The author investigated histopathology of 1,438 consecutive rectal specimens in the last 10 years of our pathology laboratory in Japan. A computer review of pathologic reports was done. Observations of pathologic slides were performed, when appropriate. The rectal specimens were composed of 1,022 benign lesions and 416 malignant lesions. The 1,022 benign lesions were composed non-specific proctitis (n=460, 45%), adenoma (n=248, 24%), ulcerative colitis (n=98, 10%), hyperplastic polyp (n=54, 5%), carcinoma in adenoma (n=40, 4%), rectal ulcer (n=37, 4%), serrated adenoma (n=24, 2%), hyperplastic nodule (n=21, 2%), Crohn's disease (n=9, 1%), ischemic proctitis (n=8, 0.8%), mucosal prolapse syndrome (n=7, 0.6%), juvenile polyp (n=6, 0.6%), lymphoid hyperplasia (n=5, 0.5%), lipoma (n=4, 0.4%) and amebic dysentery (n=2, 0.2%), and mature cystic teratoma (n=1, 0.1%). In this article, histopathological features of these benign lesions were described in details. In particular, adenomas were classified into adenomas with mild, moderate, and severe atypia, serrated adenoma, and carcinoma in adenoma. The later are mainly seen in large adenoma with severe atypia. Ulcerative colitis was characterized by continuous lesion, crypt abscess, abnormal branching, and deletion of goblet cells. Crohn's disease was characterized by transmural inflammation and epithelioid granulomas. Ischemic colitis was characterized by ischemic necrotic changes and pseudomembrane formation. Mucosal prolapse syndrome was characterized by abnormal muscle in the mucosa (fibromuscular obliterance). Juvenile polyp was characterized by abnormal dilations of the crypts. Lymphoid hyperplasia must be differentiated from MALT lymphoma. Lipoma was ordinary lipoma without lipoblasts. Amebic dysentery was characterized by ulcer and presence of histiocyte-like entamoeba histolitica. Mature cystic teratoma was characterized by hairs and other elements of skin and mesodermal and endodermal components.
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PMID:Histopathologic study of the rectum in 1,438 consecutive rectal specimens in a single Japanese hospital: I. benign lesions. 2341 70


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