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At least 1,477 records · Page 82Linked to original sources
PubMed2001

High grade prostatic intraepithelial neoplasia is a disease.

High grade prostatic intraepithelial neoplasia (PIN) is now widely accepted as the main premalignant lesion that has the potential to progress to prostate adenocarcinoma. High grade PIN is a standard diagnosis that must be included as part of the reported pathologic evaluation of prostate biopsies. Premalignant lesions that affect other organs have been identified and are treated when diagnosed such that the premalignant lesions itself are a disease (eg, carcinoma in situ of the bladder, colon polyps, and cervical dysplasia). Urologists should recognize that high grade PIN is a dangerous lesion and that it should be aggressively managed either by saturation biopsies of the prostate following the diagnosis of high grade PIN, or the more common recommendation--repeated prostate biopsies every 3 to 6 months for 2 years, then annually. Treatment of these precancerous lesions would appear to be of clinical benefit notwithstanding the potential for cancer prevention. These clinical benefits would reduce morbidity, enhance the quality of life, delay surgery or radiation, and increase the interval for surveillance requiring invasive procedures.

Adenocarcinoma↗
PubMed1990

Immunochemical detection of human blood in feces.

We have developed a new immunochemical test for fecal occult blood utilizing enzyme-linked immunosorbent assay (ELISA) of human hemoglobin (HbAo) and transferrin (Tf) simultaneously. The ELISA had a sensitivity of about 15 ng/ml Hb, and the measurable range was 1.5-750 micrograms Hb per g feces. The stability of Tf in feces was greater than that of Hb. In 17 out of 18 patients with colon cancer, 8 out of 15 patients with colon polyps, and 11 out of 20 patients with upper-gastrointestinal disorders. The Hb and Tf values were more than 10 micrograms/g feces, in terms of Hb concentration. The ELISA for human fecal HbAo and Tf might be useful for the diagnosis of gastrointestinal disorders.

Animals↗
PubMed1990

Na+-dependent bile acid transport in the ileum: the balance between diarrhea and constipation.

Ileal Na+-dependent bile acid transport was quantified in vitro as the uptake of 3H-taurocholate into brush-border membrane vesicles. Vesicles were prepared from ileal biopsies of 158 patients placed in 10 diagnostic categories. Active bile acid transport (expressed as picomoles taurocholate uptake per milligram brush-border membrane protein per 15 s, median and interquartile ranges indicated) did not differ significantly in 6 categories: irritable bowel syndrome (71, 35-97; n = 21), colon polyps (42, 30-89; n = 29), colitis (62, 33-91; n = 31), postvagotomy or postcholecystectomy (69, 37-97; n = 11), diarrhea without increased bile acid loss (58, 48-85; n = 12), and lack of gastrointestinal pathology (74, 45-103; n = 22). A decreased active bile acid transport was found in 3 categories: ileal disease (4, 1-36; n = 11), partial ileal resection (5, 1-35; n = 5), and constipation (41, 22-50; n = 8). Bile acid transport was increased in patients with bile acid-losing diarrhea with endoscopically and histologically normal ilea (111, 94-135; n = 8). These findings indicate that a low fecal bile acid loss, presumed to be present in constipated patients, is associated with a low Na+-dependent ileal bile acid transport and a high bile acid loss is associated with a high active bile acid transport. Ileal bile acid transport might be regulated by the availability of bile acids to the ileal enterocytes.

Bile Acids and Salts↗
PubMed1987

Trisomy 14 in refractory anemia with excess of blasts in transformation.

Trisomy 14 was demonstrated on four occasions over a 2-year period in the bone marrow cells of a 63-year-old patient with refractory anemia with excess of blasts in transformation (RAEB-t). Trisomy 14 as the sole karyotype abnormality has been documented in only six malignancies, namely, in two cases of acute leukemias, one Philadelphia-negative chronic myeloid leukemia, one pancytopenia, and in two colonic polyps. In hematologic neoplasms, this rare primary change preferentially occurs in elderly adults and seems exclusively associated with the myeloid cell lineage.

Anemia, Refractory, with Excess of Blasts↗
PubMed1995

The Muir-Torre syndrome: a 25-year retrospect.

The Torre or Muir-Torre syndrome consists of certain types of sebaceous neoplasms of the skin, with or without keratoacanthomas, and one or more low-grade visceral malignancies in the absence of other predisposing factors. The sebaceous tumors are relatively uncommon or rare: sebaceous adenoma, sebaceous epithelioma, basal cell epithelioma with sebaceous differentiation, and sebaceous carcinoma. Sebaceous hyperplasia and hamartomas such as nevus sebaceus of Jadassohn, with or without a sebaceous epithelioma within it, are not a defining part of this syndrome. Sebaceous hyperplasia is common in elderly light-complexioned people with or without this syndrome. Nevus sebaceus of Jadassohn is not rare and is predisposed to the development of other neoplasms within it, including occasionally a sebaceous epithelioma. Colonic polyps are frequently present. Muir-Torre syndrome requires recognition because affected patients are at risk of multiple primary malignancies. The skin lesions may be the first sign of this syndrome, although more often its cutaneous signs follow the diagnosis of at least the first visceral malignancy. The Muir-Torre syndrome portends the greater possibility of a favorable prognosis than might be anticipated otherwise because the visceral cancers are usually low-grade malignancies. However, they are often multiple, so identifying such patients will affect their management in a few ways. Because these indolent visceral malignancies tend to permit prolonged survival, even metastatic disease may respond well to aggressive surgical treatment. The sebaceous cancers in this syndrome, like the visceral malignancies, are less aggressive than their counterparts unassociated with this syndrome. Because this syndrome is inherited in an autosomal dominant manner, identifying one patient means delineating an entire family, which should be investigated. This syndrome may be caused by a defective mismatch DNA repair gene.

Diagnosis, Differential↗
PubMed2006

The colorectal malignant polyp: scoping a dilemma.

Colorectal adenomas containing invasive carcinoma represent the majority of early colorectal cancers. The malignant polyp carries a significant risk of lympho-haematic metastasis and mortality due to the penetration of cancerous cells into the submucosal layer. The therapeutic dilemma is whether to perform endoscopic or surgical resection. A thorough assessment of the endoscopic, histological and clinical variables is needed to unravel the best treatment for each patient. In particular, a unique staging of such lesions, based on certain histopathological features, has been deeply implicated in the therapeutic choice. Aim of this article is to review the main endoscopic, histological and clinical features of the malignant polyp in order to propose a systematic management of this lesion.

Adenomatous Polyps↗
PubMed2004

A 55-year-old man with hypogammaglobulinemia, lymphopenia, and unrelenting cutaneous warts.

A 55-year-old white man with a history of hypertension, fibromyalgia, and colonic polyps presented with unrelenting plantar warts on his hands and feet for the past 4 years. He was otherwise healthy and without a history of recurrent infections. Physical examination was unremarkable except for extensive warts on his hands and feet. Pertinent laboratory findings included hypoalbuminemia, hypogammaglobulinemia, and lymphopenia most severely affecting CD4(+) T cells. Testing for HIV infection was negative. This clinical and laboratory presentation suggested a combined humoral and cellular immunodeficiency syndrome that could be best explained by loss of lymphocytes, immunoglobulins, and other serum proteins. Additional immunologic testing revealed a marked reduction in peripheral blood naive (CD4(+)CD45RA(+)) T cells. A 24-hour stool collection showed a markedly elevated alpha(1)-antitrypsin level. These findings were most consistent with the diagnosis of intestinal lymphangiectasia, a type of protein-losing enteropathy associated with hypoalbuminemia, hypogammaglobulinemia, and lymphopenia, characterized by a preferential loss of naive CD4(+) T cells into the gastrointestinal tract. This case illustrates the importance of considering intestinal loss of immunoglobulins and lymphocytes in the differential diagnosis of the adult patient who presents with laboratory evidence of a combined humoral and cellular immunodeficiency. It also underscores the diagnostic utility of the clinical immunology laboratory and how flow cytometry, in particular, can contribute to an understanding of pathogenic mechanisms.

Agammaglobulinemia↗
PubMed2005

Ocular manifestations of familial adenomatous polyposis (Gardner syndrome).

Familial adenomatous polyposis (FAP) is a colon cancer predisposition syndrome in which hundreds to thousands of precancerous colonic polyp become evident at a mean age of 16 years (range, 7-36 years). By age 35 years, 95% of patients have polyps. Gardner syndrome is the eponym given to a subgroup of FAP with extracolonic manifestations, such as pigmented ocular fundus lesions that resemble congenital hypertrophy of the retinal pigment epithelium, among others.

Fluorescein Angiography↗
PubMed2001

Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms.

BACKGROUND: The standard evaluation of a patient with iron deficiency anemia includes a complete evaluation of the gastrointestinal tract to identify a source of bleeding. However, even after a careful examination, many patients remain without a diagnosis. Because iron deficiency anemia results from iron loss or defective absorption, we sought to determine the prevalence of potential gastrointestinal sources for iron deficiency anemia in patients without gastrointestinal symptoms. METHODS: Over a 10-month period, 668 outpatients were referred to the University Hematology Department with iron deficiency anemia, defined by a hemoglobin concentration less than 14 g/dL (less than 12 g/dL in women), mean corpuscular volume less than 80 fL, and ferritin level less than 30 microg/L. After excluding patients with obvious causes of blood loss, inadequate diet, chronic diseases, or malignancies, there were 81 eligible patients, 10 of whom refused investigation. The remaining 71 patients (51 women, median age 59 years) underwent colonoscopy, as well as gastroscopy with gastric (antrum and body) and duodenal biopsies. RESULTS: A likely cause of iron deficiency anemia was detected in 60 patients (85%). Diseases associated with bleeding were found in 26 patients (37%), including colon cancer (10 patients), gastric cancer (2), peptic ulcer (7), hiatal hernia with linear erosions (5), colonic vascular ectasia (3), colonic polyps (2), and Crohn's disease (1). Causes not associated with bleeding were found in 36 patients (51%), including 19 with atrophic gastritis, 4 with celiac disease, and 13 with Helicobacter pylori gastritis. Six (8%) patients had coincident gastrointestinal findings, and 11 (15%) had no cause identified. Patients with an identified nonbleeding-associated cause were younger than those with a bleeding-associated cause (median, 56 vs 70 years; P = 0.001) and included 59% of women (n = 30) versus 30% of men (n = 6) (P = 0.04). Hemoglobin level was not related to the site and severity of disease. CONCLUSION: Gastrointestinal diseases that do not usually cause bleeding are frequently associated with iron deficiency anemia in patients without gastrointestinal symptom or other potential causes of gastrointestinal bleeding.

Adult↗
PubMed1988

Peutz-Jeghers syndrome: a clinicopathologic survey of the "Harrisburg family" with a 49-year follow-up.

Of the original Peutz-Jeghers families reported by Jeghers, the "Harrisburg Family" has now been followed for 49 yr. Their 12 affected family members comprise the largest Peutz-Jeghers kindred reported. The course of this family illustrates that Peutz-Jeghers syndrome is not a benign disease. One family member developed a duodenal carcinoma in a hamartoma with adenomatous changes; this progression in the duodenum has not previously been reported. Ten patients underwent 75 polypectomies. One patient developed short bowel syndrome. Three patients died in young adulthood. The development of gastrointestinal malignancy in 2 of 12 affected patients suggests that Peutz-Jeghers syndrome may be a premalignant condition. Consequently, even asymptomatic gastric, duodenal, and colonic polyps should be removed endoscopically. If surgical intervention is necessary, intraoperative endoscopy with polypectomy may prevent the development of a short bowel syndrome. Colonoscopic screening of patients and their family members may be beneficial and surveillance for extraintestinal malignancy appears to be warranted.

Adolescent↗
PubMed1995

A prospective controlled evaluation of endoscopic detection of angiodysplasia and its association with aortic valve disease.

BACKGROUND: In view of controversy about the association of aortic stenosis and angiodysplasia of the gut, we performed a prospective, controlled study to evaluate the relationship between aortic valve disease and gastrointestinal angiodysplasia. METHODS: Forty patients who had endoscopy for clinical indications such as gastrointestinal bleeding, anemia, polyps, colon cancer, and dyspepsia, and who were found to have angiodysplasia of the gastrointestinal tract, underwent two-dimensional and Doppler echocardiography. Thirty-seven controls matched for age, sex, indication, and nature of endoscopic examination, but without angiodysplasia, underwent similar echocardiographic examination. RESULTS: None of the patients in either group had aortic stenosis. The prevalence of aortic sclerosis, aortic insufficiency, and low left ventricular ejection fraction was similar in patients with and without angiodysplasia. CONCLUSIONS: This study does not support the role of aortic valve disease as the cause of angiodysplasia of the gastrointestinal tract. A subgroup of patients with angiodysplasia with aortic sclerosis, with or without other valvular disease (but none with aortic stenosis), had increased prevalence of gastrointestinal bleeding when compared with controls. When aortic valve disease or decreased left ventricular ejection fraction were analyzed as independent predictors, none of them in and of itself appeared to be a factor in bleeding from these gastrointestinal lesions.

Aged↗
PubMed1997

The pathologic measurement of polyp size is preferable to the endoscopic estimate.

BACKGROUND: There is no standardized technique to measure polyp size. Estimation of polyp size at endoscopy is difficult. Polyp size measurement by pathologists would seem to be an accurate alternative, but tissue fixation may alter polyp size. To evaluate methods of determining polyp size, we compared endoscopists' estimates and pathologists' measurements with measurements made by an independent examiner. METHODS: Polyps were measured by an independent investigator before and after formalin fixation. The investigator's measurement before fixation (the "gold standard") was compared with the endoscopists' estimates and the pathologists' measurements. RESULTS: Ten endoscopists removed 61 polyps with a snare in 33 patients: 82% were adenomatous and 72% were pedunculated. Mean size was 0.85 +/- 0.6 cm (SD) (range: 0.3 to 3.6 cm, 26% > or = 1 cm). Polyps remained in formalin for a mean of 239 minutes (46 to 1164 minutes). Polyps neither consistently shrank nor enlarged in formalin (maximum change +/- 0.2 cm, r = 0.99 [p < 0.001]). Interobserver agreement between pathologists' and the investigator's post-formalin measurements showed that 55 of 57 polyps (97%) were within +/- 0.3 cm. Endoscopists inaccurately estimated 11 of 56 polyps (20%) (> 0.3 cm difference from the independent examiner). Polyp size was underestimated in three instances (range 0.5 to 0.9 cm) and overestimated in eight (range 0.4 to 0.8 cm). In 5 of 11 instances (46%), this inaccuracy altered polyp size classification across the 1 cm threshold. Results were not dependent on endoscopist, histology, or polyp location. CONCLUSIONS: (1) Polyp size is not significantly affected by formalin fixation; 2) Endoscopists' estimates of polyp size are often unreliable; and, when possible, (3) Pathologists' measurements of polyp size should be used in clinical trials and in clinical practice.

Adenomatous Polyps↗
PubMed2002

The role of sigmoidoscopy and colonoscopy in the diagnosis and management of lower gastrointestinal disorders: endoscopic findings, therapy, and complications.

Flexible sigmoidoscopy and colonoscopy have revolutionized the clinical management of colonic diseases. Colonoscopy is a highly sensitive and specific test. Colonic diseases often produce characteristic colonoscopic findings, as well as characteristic histologic findings, as identified in colonoscopic biopsy or polypectomy specimens. Colonoscopy is relatively safe, with a low incidence of serious complications, such as colonic perforation, hemorrhage, cardiopulmonary arrest, or sepsis. Colonoscopy is becoming more important clinically because of more widespread use of screening colonoscopy for colon cancer, application of therapeutic colonoscopy, and exciting new technical improvements.

Angiodysplasia↗
PubMed2000

Colorectal cancer update. Prevention, screening, treatment, and surveillance for high-risk groups.

Great advances have been made in understanding the cause and molecular genesis of colorectal cancer. The disease can be prevented by a healthful diet and lifestyle or by resecting the precursor of most of these cancers, the advanced adenomatous polyp. Screening the average-risk population plus special surveillance for high-risk groups now is recommended by evidence-based guidelines. Surgery is highly curative for patients without distant metastases, and adjuvant therapy improves survival in selected patients with advanced cancers.

Adenomatous Polyps↗