Early gastric cancer in a fundic diverticulum.
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Biomedical subjects
Publications and source records attributed to C Lindström.
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BACKGROUND: Beta-microseminoprotein is a 94-kDa protein present on most mucosal surfaces in the body. It is produced in mucin cells but is also found in a particular type of cells (E-cells) in the gastric antral mucosa. Most of these cells also contain gastrin. In atrophic corpus gastritis the gastrin-producing cells become hyperplastic, and the patients have hypergastrinemia. We wanted to ascertain whether there is a similar effect on the E-cells and on the concentration of beta-microseminoprotein in serum. METHODS: Antral biopsy specimens from 10 patients with atrophic corpus gastritis and 10 controls were stained immunohistochemically for beta-microseminoprotein and gastrin. beta-Microseminoprotein and gastrin were measured by radioimmunoassay in serum from 15 women with atrophic corpus gastritis and 31 healthy female blood donors. RESULTS: There was a 3.5-fold increase of the number of E-cells (which also were hypertrophic) and a 2.1 times higher serum concentration of beta-microseminoprotein in the patients with atrophic corpus gastritis than in the control subjects. Gastrin was seen in 28% of the E-cells in patients with atrophic corpus gastritis, compared with 87% in normal antral mucosa. There was no correlation between the serum concentrations of beta-microseminoprotein and gastrin. CONCLUSIONS: In atrophic corpus gastritis antrum E-cells undergo hyperplasia and hypertrophy, and the proportion of E-cells containing gastrin decreases. Increased amounts of beta-microseminoprotein are secreted to the blood but uncorrelated with gastrin.
A study was conducted to determine the time dependency of myocardial perfusion improvement after coronary artery bypass graft (CABG) surgery. Seventeen 3-vessel diseased patients (16 male, 1 female) scheduled for CABG surgery from a cardiac surgical and intensive-care unit were examined. Ten of the 17 patients returned for examination after 1 year. A titrated adenosine infusion was used to expose reversible ischemia. Tc99m-sestamibi was injected at rest and at maximum adenosine infusion rate, and isotope distribution was determined using ectomographic myocardial scintigraphy. Visually scored percent isotope uptake defect size and percent uptake reduction were assessed. It was found that resting isotope uptake defects were unchanged 1 h after surgery, increased in severity after 1 week, and after 1 year were 24% less than the preoperative scores (p < 0.01) and 55% less than after 1 week (p < 0.001). It was found that adenosine infusion induced a 57% increase in average defect score preoperatively (p < 0.001) but no increase postoperatively. No differences were seen between regions supplied by arterial or venous grafts. Isotope uptake defects increased between 1 h and 1 week after CABG surgery, and after 1 year the scores were less than those recorded preoperatively and after 1 week. Adenosine-induced reversible isotope uptake changes seen preoperatively were eliminated postoperatively in all vessel regions.
UNLABELLED: This study compared myocardial perfusion scintigraphy performed with ectomography to corresponding SPECT studies. METHODS: In a comparative study between SPECT and ectomography, 19 patients with suspected coronary artery disease were imaged under similar conditions. A two-day protocol using 99mTc-sestamibi was followed. In SPECT, 32 projection images were acquired by rotating the gamma camera detector through 180 degrees, from 45 degrees left posterior oblique to 45 degrees right anterior oblique. Short-axis view sections and polar tomograms were reconstructed. In ectomography, a 30 degrees slant-hole collimator was rotated through 360 degrees in front of a stationary detector to obtain 64 projection images with different projection directions. The gamma camera was orientated perpendicular to the long axis of the left ventricle; the orientation was determined from the SPECT examination. Short-axis section images through the projected conical volume were reconstructed using a two-dimensional filtered back projection technique. In a blind test, the relative diagnostic value and image quality of the two methods were evaluated by three independent observers assessing short-axis view sections and polar tomograms. An objective evaluation based on relative values in the polar tomograms was also performed. The interpretations were evaluated with analysis of variance. RESULTS: After injection during exercise, there was no significant difference between SPECT and ectomography. After injection at rest, visualization of the left ventricle was superior (p < 0.05) and influence of external activity was less (p < 0.005) in ectomography. The activity level within a perfusion defect was significantly lower (p < 0.05) and its extension significantly larger (p < 0.05) in ectomography than in SPECT. There was no difference between the diagnosis based on SPECT or ectomography. CONCLUSION: In myocardial perfusion imaging with 99mTc-sestamibi, ectomography provides information similar to that obtained with SPECT and can, therefore, be used clinically for evaluation of myocardial perfusion when the gamma camera is postitioned perpendicular to the long axis of the left ventricle.
Secretory leukocyte protease inhibitor (SLPI) is the dominant protease inhibitor in the mucus secretions of the repiratory and genital tracts, and local production seems likely, as immunoreactive SLPI has been found in the corresponding mucosa. To our knowledge, SLPI has not been previously demonstrated in intestinal epithelia or secretions. In an earlier study, however, we found surprisingly high levels of SLPI in peritonitis exudate from patients with gastrointestinal perforations. This study extends these observations by demonstrating the presence of immunoreactive SLPI in intestinal mucosa. In the small intestine, SLPI was present in Paneth cells and in scattered mucosa cells of goblet-type. In normal mucosa of the large bowel, SLPI was also found in scattered cells of goblet-type in the epithelium. In addition, immunoreactive SLPI was frequently found in colonic adenomas. The findings in this study raise several interesting questions on the possible role of SLPI in the gut epithelial defense against inflammatory assaults.
PURPOSE: Changes in morbidity pattern of ulcerative colitis have created a need to update understanding of the course of the disease. METHOD: A follow-up study was done of relapse rates and progression of inflammation in 571 non-selected patients with ulcerative and indeterminate colitis. RESULTS: Relapse rate ten years after diagnosis was 70 percent in definite ulcerative colitis, 22 percent in probable ulcerative colitis, and 77 percent in indeterminate colitis. During the study period, there was no change in the relapse rate. In relapsing proctitis, 52 percent developed more extensive inflammation. Fifty-four percent of patients with only one attack of colitis had persistent signs of inflammatory bowel disease. CONCLUSIONS: Shift in morbidity pattern to a greater proportion of patients with proctitis at diagnosis and a shorter time from onset of symptoms to diagnosis had no influence on the relapse rate. Indeterminate colitis has a worse prognosis than definite ulcerative colitis. Considering the documented efficacy of sulfasalazine, the high relapse rate calls for studies of the effectiveness of such treatment in everyday practice.
OBJECTIVE: To assess the need for operative treatment for ulcerative colitis and indeterminate colitis. DESIGN: Retrospective study. SETTING: University Hospital, Sweden. SUBJECT: All patients diagnosed from 1958 to 1982, in Malmö, Sweden-ulcerative colitis (n = 471) and indeterminate colitis (n = 100). MAIN OUTCOME MEASURES: Incidence of colectomy. RESULTS: The mean follow-up was 15 years. The incidence of colectomy was 7.51, 1.90 and 36.13/1000 person years for definite ulcerative colitis, probable ulcerative colitis and indeterminate colitis, respectively. The incidence of colectomy in patients with definite ulcerative colitis in the present study was low compared with other studies. In contrast to other reports, men had a threefold risk while extent of inflammation did not influence the incidence. Patients with indeterminate colitis were a high risk group with a high incidence of colectomy. The high incidence among patients with indeterminate colitis compared with that in patients with definite ulcerative colitis was also seen in subgroups such as patients with total colitis at diagnosis, in patients in remission after the first attack, and in patients with a severe attack. CONCLUSION: As patients with indeterminate colitis seem to be at increased risk of colectomy it could be important to distinguish them from those with ulcerative colitis. Today, however, it is not possible to identify all patients with indeterminate colitis early in the course of the disease.
Cancer morbidity and all cause mortality were studied prospectively in all patients with definite and probable ulcerative colitis and indeterminate colitis diagnosed from 1958 to 1982, in the city of Malmö, Sweden. The follow-up to Jan. 1, 1990 was complete for all but ten patients. Nine of the 471 patients with ulcerative colitis and three of the 100 patients with indeterminate colitis developed colo-rectal cancer. The incidence of colorectal cancer in ulcerative colitis was 1.4 per 1000 person-years. The observed number of cases was 2.1 times higher than expected; (95% C.I. 1.0-4.1), based on the age- and sex-specific cancer incidence in the city during the study period. Indeterminate colitis was associated with a higher colorectal cancer risk than ulcerative colitis; 2.4 per 1000 person-years; (SMR 8.6, 95% C.I. 1.8-25.1). Both conditions were associated with a slight increased mortality rate, for ulcerative colitis 12.6 per 1000 person-years; (SMR 1.3, 95% C.I. 1.0-1.5), and for indeterminate colitis 11.7 per 1000 person-years; (SMR 2.7, 95% C.I. 1.6-4.4). Complications of colitis were the main cause of death in both groups. The cancer risk was related to extent of disease, duration of disease and female gender. Ten out of the 12 cases with cancer had or developed total colitis. However, only seven of the 134 cases with total ulcerative colitis and two of 87 cases with total indeterminate colitis developed cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
Brunner's glands (duodenal glands) in humans are located mainly in the two proximal thirds of the duodenum. They are known to produce and secrete mucin. In recent years, human Brunner's glands have also been shown to express immunoreactivity toward epidermal growth factor-urogastrone (EGF-uro) and lysozyme. These proteins are considered to have a protective function within the gastrointestinal canal. Human pancreatic secretory trypsin inhibitor (PSTI) was recently identified in Brunner's glands. This present study was done by an immunohistochemical method, using monospecific polyclonal antibodies against human PSTI and human lysozyme, respectively. McManus/Alcian blue mucin staining was used to clarify the distribution of mucin. We found immunoreactive PSTI (irPSTI) in seven out of ten specimens. Lysozyme and mucin were present in all ten. While virtually all cells were stained for lysozyme and mucin, irPSTI was restricted to separate lobules and to cells in the ducts.
BACKGROUND: This study was designed to assess time trends in the incidence of ulcerative colitis and indeterminate colitis in an urban population. METHODS: Medical records of in- and out-patients with inflammatory bowel disease were reviewed by a panel to establish the diagnosis. All histopathologic specimens and almost all radiographs were re-examined. RESULTS: During the time period 1958 to 1982 there were 354 new cases of definite ulcerative colitis, 117 of probable ulcerative colitis, and 100 of indeterminate colitis. This corresponds to an average annual incidence per 100,000 of 5.5, 1.8, and 1.6, respectively. The incidence was higher in men than in women. Peak incidence was between 20 and 29 years, but indeterminate colitis was most common in 10- to 19-year-old males. The incidence was stable from 1958 to 1972 but then increased in almost all age groups in both sexes. The increase in annual incidence of definite ulcerative colitis from 4.2 to 9.4/10(5) corresponds to an average annual increase of about 5% (p < 0.001). The increase in the incidence of definite ulcerative colitis was due to an increased proportion of patients with proctitis. CONCLUSIONS: This study has shown an increased incidence of ulcerative colitis and indeterminate colitis, and we have found no reason to believe that this is a spurious finding.
Reactions from the rectal mucosa often give rise to troublesome side-effects during and after radiotherapy in the pelvic region. Local vasoconstriction in the rectal mucosa will cause an ischemia which will decrease the sensitivity of the mucosal cells to radiation and thereby these side-effects can be reduced. Triglycyl-lysine-vasopressin applied rectally in 1% Blanose solution gave in the present study significant radioprotection of the rectal mucosa in the doses of 0.8, 1.6, and 3.2 mg. These doses are, however, very high. Triglycyl-lysine-vasopressin in 1.2% Natrosol solution in a dose of 128 micrograms did not show any certain protective effects. However lysine-vasopressin in 1.2% Natrosol solution in a dose of 16 micrograms gave significant radioprotection of the rectal mucosa. This dose level has in a previous study not given any significant effects on the systemic circulation. Lysine-vasopressin in Natrosol solution seems to be a suitable combination for further studies.
OBJECTIVE: To compare digital examination, endoluminal ultrasound (ELU), and plain magnetic resonance imaging (MRI), with histopathological findings in the preoperative staging of rectal cancer. DESIGN: A prospective comparative study. SETTING: University hospital, Sweden. SUBJECTS: 35 patients with rectal cancer who presented during the period February 1987 to February 1991. RESULTS: The digital examination of 19 patients could be assessed and was correct in 13 (68%). ELU was done in 34 patients; the accuracy was 88%. Extension of tumour was overestimated in two and underestimated in two. MRI was done for 35 patients with an accuracy of 66%; in 12 patients extension was underestimated. The diagnostic accuracy of the assessment of lymph node involvement was 71% with ELU, and 72% with MRI. CONCLUSION: These findings indicate that MRI seems to underestimate the extension of rectal tumours, but both ELU and MRI can be helpful in selecting patients with advanced tumours for whom preoperative adjuvant treatment is being considered. ELU is superior in staging tumours confined to the rectal wall, and could be of value in the selection of patients whose tumours were suitable for local excision. None of these techniques, however, can reliably identify the extent of lymph node involvement.
Coeliac disease (CD) is associated with the presence of gliadin antibodies (GA) (IgG and IgA), often used as a screening test for CD. Using a modified micro-enzyme-linked immunosorbent assay for GA, we studied the prevalence of GA in three healthy groups: children (mean age, 12 years), adult blood donors (mean age, 38 years), and healthy women (mean age, 57 years). We also studied the clinical characteristics of the blood donors. On the basis of findings in 27 untreated CD patients, cut-off levels of IgG and IgA antibody titres were chosen to yield a test with relatively low sensitivity (56%) but high specificity (100%). Analysis of IgM antibodies did not improve the sensitivity. Of the 384 12-year-old children, both IgG and IgA GA positivity was found in 15 (3.91%), a rate significantly greater than that in the blood donors (22 of 1537, 1.43%; p < 0.001) or in the middle-aged women (11 of 944, 1.17%; p < 0.0001). Of the 22 GA-positive healthy blood donors, 13 underwent small-bowel biopsy, but only 1 of the specimens manifested histologic changes compatible with CD. The other 12 had normal specimens, including a normal intraepithelial lymphocyte count. The estimated frequency of CD among the blood donors was thus 1 of 1500, a figure consistent with those previously published. We conclude that GA occur frequently in the Swedish population but that their prevalence decreases with increasing age. As a screening test for CD in healthy individuals, the GA titre is of poor predictive value.
Cytogenetic analysis of short-term cultures from 52 colorectal carcinomas revealed a normal karyotype in 13 and clonal chromosome aberrations in 39 tumors. In the abnormal group, 13 tumors had simple numerical changes only, whereas 26 had at least one structural rearrangement with or without concomitant numerical changes. The most common numerical abnormalities were, in order of decreasing frequency, +7, -18, -Y, +8, +13 and -14. The most common structural rearrangements affected, again in order of decreasing frequency, chromosomes 8, 1, 6, 7, 17, 3, 11, 13, 14, 16, 2 and 10. The chromosome bands most frequently involved in the structural changes were 8q10, 17p11, 11q13, 8p11, 6q21, 7p15, 7q36, 12q13, 13q10, and 16q13. The most frequent genomic imbalances brought about by the structural rearrangements were losses from chromosome arms 8p, 1p, 6q, 17p, 7p, and 16q, as well as gains of 7q, 8q, 13q, and 11q. A statistically significant (p < 0.05) correlation between the karyotypic pattern and tumor grade was found, with the poorly differentiated carcinomas generally having more massive chromosomal abnormalities.
AIMS: To measure the content of immunoreactive human pancreatic secretory trypsin inhibitor (irPSTI) in colonic carcinoma and adjacent normal colonic mucosa. METHODS: From a stable hybridoma cell line producing monoclonal antibodies specific for human PSTI, a specific enzyme linked immunosorbent assay (ELISA) for human PSTI was developed. In a precipitation assay system these antibodies bound human PSTI in a dose-dependent manner. The specimens were obtained from resectional surgery. RESULTS: The content of irPSTI was 19.9 micrograms/g protein (0.55 micrograms/g tissue wet weight) in colonic carcinoma. In adjacent normal colonic mucosa 43.6 micrograms/g protein (1.12 micrograms/g tissue wet weight) was shown. CONCLUSIONS: The enzymatic degradation of surrounding tissue necessary for tumour cell invasion could be facilitated by this relative deficit of the inhibitor in infiltrative carcinoma.
Operative specimens from normal, inflammatory and neoplastic gallbladders were analyzed for immunoreactive pancreatic secretory trypsin inhibitor (irPSTI) using a peroxidase-antiperoxidase method. In normal and inflammatory gallbladders no irPSTI was demonstrated, while irPSTI was found in neoplastic gallbladders.
Specimens of normal and neoplastic colonic mucosa from 52 patients were analysed by immunohistochemistry using a monospecific polyclonal antiserum against human pancreatic secretory trypsin inhibitor (PSTI). In normal colonic mucosa PSTI was found in the goblet cells in the basal parts of the crypts. In adenomas of tubular, villous, and tubulo-villous types PSTI was also found in the upper parts of the polyps, usually occurring in the regeneration zone. There was a more intense staining reaction in polyps with increased atypia. Carcinomas of different types and of various grades of differentiation and of in situ type did not contain PSTI. These findings indicate that PSTI could be a marker for adenomatous rather than carcinomatous epithelium in the colon. Furthermore, the absence of the inhibitor in malignant cells might facilitate tissue invasion by malignant cells because of deficient protease inhibition.
Beta microseminoprotein (beta inhibin, PSP94), an unglycosylated protein of 94 amino acids with unknown function, is one of the predominating proteins in the secretion of the human prostate gland. In this work the authors have demonstrated that the expression of beta microseminoprotein is not restricted to the prostate and that the protein has a previously unrecognized widespread occurrence in the human body. According to radioimmunoassay, beta microseminoprotein immunoreactivity is present in many nonprostatic body fluids. The highest concentrations were found in secretions from the respiratory tract; in tracheobronchial fluid sometimes even at concentrations comparable to that in seminal plasma (about 1 g/l). Intermediate concentrations were found in gastric juice and some samples of secretion from the uterine cervix, whereas tears, saliva, pancreatic juice, bile, and mucus from the colon had low concentrations. According to gel chromatography, the molecular size of the beta microseminoprotein immunoreactivity present in tracheal fluid, gastric juice, and secretion from the uterine cervix did not differ from that of beta microseminoprotein in seminal plasma. The beta microseminoprotein immunoreactive component present in gastric juice had the same amino-terminal amino acid sequence as prostatic beta microseminoprotein (14 residues identified in material purified from gastric juice), providing further evidence for chemical identity of a nonprostatic beta microseminoprotein with the prostatic protein. Immunohistochemical staining with affinity-purified antibodies demonstrated the presence of beta microseminoprotein in many tissues, including the goblet cells in the tracheobronchial epithelium, tracheobronchial submucosal glands, certain mucosal cells in the antrum of the stomach, some glands of Brunner in the duodenum, and in parts of the mucosa of the colon. At least in the respiratory tract, the staining was localized to mucus-containing cells. beta microseminoprotein immunoreactivity also was localized to the cilia of the ciliated epithelium in the respiratory tract, the fallopian tubes, and the Gartner ducts of the uterine cervix. The pattern of tissue distribution of beta microseminoprotein found in this work indicates a connection of beta microseminoprotein with mucous secretions.