| 1. |
- Edshage Hallberg, Karin, 1958
(författare)
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Gastroduodenal epithelial transport in patients with cystic fibrosis
- 2000
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Cystic fibrosis (CF) is an inherited disease where respiratory failure due to chronic lung infection is the major cause of death. A defective protein, cystic fibrosis transmembrane conductance regulator (CFTR) alters chloride epithelial transport. Exocrine pancreatic insufficiency is found in 90% of the patients, but in spite of pancreatic enzyme supplements, gastrointestinal problems are common. CF patients have evidence of a disturbed intestinal motility and epithelial transport. The aim of this work was to give new insights to the altered function of the CF gut and thereby to improve the understanding of the coupling between the clinical expression and pathology of the disease and the basic defect. We used gastroduodenal manometri combined with intragastric perfusion to investigate fasting motility and motility secretion in 10 CF patients with different genotypes and 12 healthy controls. Eight CF patients showed a normal migrating motor complex. Motility related gastric secretion of acid and bicarbonate did not differ from healthy subjects while gastric net fluid secretion was significantly decreased and bilirubin reflux was significantly increased in the CF patients. Motility related secretion of gastric IgA was studied in ten CF patients and seven healthy controls. The CF patients had significantly lower levels of gastric IgA compared to healthy subjects during phase II and III of the migrating motor complex. Chloride secretion in duodenal biopsies from nine CF patients with different genotypes where investigated in an Ussing chamber. Prostaglandin E2 and acetylcholine induced no changes in chloride secretion in the DF508 homozygotes. In heterozygotes, the induced change in chloride secretion corresponded to the severity of the known mutations. The urinary excretion of orally given lactulose, L-rhamnose and xylose was studied in 19 CF patients and nine healthy controls. Patients who were homozygous or heterozygous for ?F508 had significantly higher lactulose/L-rhamnose excretion ratios, than patients with unidentified genotypes who had excretion ratios in the same range as in healthy controls.Conclusions: Our studies suggest that patients with CF have a normal fasting motility pattern in the upper gastrointestinal tract. Despite this, there were abnormalities in epithelial transport related to genotype, thus indicating a role of CFTR in the transport of fluid, IgA and small molecules. We also found that patients with CF with impaired pancreatic bicarbonate secretion had normal gastric bicarbonate secretion in fasting.
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| 2. |
- Öberg, Åke, 1954-, et al.
(författare)
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Limited value of preoperative serum analyses of matrix metalloproteinases (MMP-2, MMP-9) and tissue inhibitors of matrix metalloproteinases (TIMP-1, TIMP-2) in colorectal cancer
- 2000
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 20:2B, s. 1085-1091
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: We studied whether preoperative serum levels of free MMP-2, the MMP-2/TIMP-2 complex, and total amounts of MMP-9, TIMP-1 and TIMP-2 correlated to the tumor stage and prognosis in colorectal cancer.METHODS: Samples from 158 patients operated on for colorectal cancer (100 colon, 58 rectum) and samples from 80 healthy blood donors were analyzed using an ELISA technique. One hundred and thirty-three patients were resected for cure, (31, 61, and 41 in Dukes' stages A, B, and C, respectively). At follow-up in January 1998, 44 patients had died from their cancer after a median time 14 months (range 2-55). Fifteen patients died without tumor relapse. Ninety-nine patients were alive after, a median time of 46 months (range 17-68).RESULTS: Wide, overlapping ranges were observed for all factors both in the patients and in the control group. The patients as compared to the control group had significantly higher levels of free MMP-2 and total amounts of MMP-9, TIMP-1 and TIMP-2, whereas the level of the MMP-2/TIMP-2 complex was significantly lower. TIMP-1 was significantly higher in Dukes' D compared to Dukes' A-C cases; the other factors did not correlate to tumor stage. Elevated TIMP-2 levels (median cut-off limit), only, correlated to worse prognosis when analysed in all patients (p < 0.05). None of the factors (median cut-off limit) correlated to survival in Dukes' A-C patients; analyses based on the upper quartile cut-off limit demonstrated that elevated MMP-2 levels correlated to shorter survival time (p < 0.05).CONCLUSION: Serum analyses of free MMP-2 the MMP-2/TIMP-2 complex and total amounts of MMP-9, TIMP-1 and TIMP-2 are of limited value for tumor staging and prognosis in colorectal cancer.
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| 3. |
- Anan, Intissar, et al.
(författare)
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Liver transplantation restores endocrine cells in patients with familial amyloidotic polyneuropathy.
- 2000
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Ingår i: Transplantation. - 0041-1337 .- 1534-6080. ; 70:5, s. 794-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of this study was to investigate familial amyloidotic polyneuropathy, Portuguese type patients' endocrine cell content in the stomach and duodenum before and after liver transplantation, and to relate the findings to the patients' gastrointestinal disturbances.METHODS: Ten liver-transplanted familial amyloidotic polyneuropathy, Portuguese type patients and 10 healthy controls were seen. Endocrine cells were identified by immunohistochemistry and quantified with computerized image analysis. The activity of the cells was appraised by measurements of the cell secretory index and nuclear area. Clinical symptoms were obtained from the patients' medical records.RESULTS: After transplantation, a significant increase of several endocrine cell types were noted, and the pretransplant depletion of several types of endocrine cells disappeared. For no type of endocrine cell was any difference compared with controls noted after transplantation. There was no significant decrease of the amount of amyloid in the biopsies after liver transplantation. The patients' symptoms remained generally unchanged after transplantation, although a substantial time lapse between pretransplant evaluation and transplantation was present.CONCLUSIONS: Liver transplantation restores the endocrine cells in the upper part of the gastrointestinal tract. The restoration was not correlated with an improvement of the patients' symptoms. No decrease of the amyloid deposits was noted.
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| 4. |
- Andersson, Amelie, et al.
(författare)
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Expression and motor effects of secretin in small and large intestine of the rat
- 2000
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Ingår i: Peptides. - : Elsevier BV. - 0196-9781. ; 21:11, s. 94-1687
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Tidskriftsartikel (refereegranskat)abstract
- Immunocytochemistry and in situ hybridization revealed abundant secretin expressing cells on duodenal villi with a gradual decrease throughout the small intestines of the rat. They were absent in pancreas, stomach and colon. Secretin caused relaxation of rat intestinal longitudinal muscle in vitro. Studies on colon revealed that the secretin-evoked response was unaffected by apamin, tetrodotoxin, L-NAME, VIP or PACAP pretreatment; secretin itself caused desensitization. Addition of VIP or PACAP when the secretin-evoked relaxation was maximal evoked a further relaxation suggesting the presence of distinct receptors. Secretin causes relaxation via activation of secretin receptors located on the smooth muscle and not via any of the related VIP/PACAP receptors.
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| 5. |
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| 6. |
- Bergenfelz, A, et al.
(författare)
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Pancreastatin plasma levels in patients with primary hyperparathyroidism
- 2000
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Ingår i: World Journal of Surgery. - : Springer Science and Business Media LLC. - 0364-2313 .- 1432-2323. ; 24:12, s. 83-1579
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Tidskriftsartikel (refereegranskat)abstract
- Pancreastatin, a C-terminally amidated peptide derived from chromogranin A, is known to inhibit insulin secretion, pancreatic enzyme release, and gastric acid secretion. It also inhibits parathyroid hormone (PTH) secretion in animals. The physiologic and clinical relevance of pancreastatin in humans, however, is not known. Because pancreastatin has been found in parathyroid adenomas, we investigated the plasma levels in patients with primary hyperparathyroidism (pHPT). Thirteen patients operated on for solitary parathyroid adenoma were investigated. Plasma levels of pancreastatin and serum levels of ionized calcium and intact PTH were measured before and 6 weeks after operation. In 10 patients the levels were also monitored before and 60 minutes after adenoma excision. The adenomas were investigated for pancreastatin immunoreactivity by immunocytochemistry. The median weight of the excised parathyroid adenoma was 0.64 g (range 0.07-2.00 g). Cells displaying pancreastatin immunoreactivity were present in all adenomas examined and varied in number and immunostaining intensity among and within the adenomas. Intraoperatively, after adenoma excision the levels of PTH and pancreastatin declined (p < 0.01), whereas the levels of ionized calcium did not change (p = 0.96). At the 6-week follow-up the levels of ionized calcium and PTH had decreased compared to the preoperative levels (p < 0.01), and all patients were normocalcemic. In contrast, the pancreastatin levels were not changed (14.5 +/- 6.1 pmol/L preoperatively vs. 12.8 +/- 11.2 pmol/L 6 weeks postoperatively; p = 0.12). In patients with pHPT, pancreastatin is likely to be produced by the parathyroid adenoma. The changes in pancreastatin levels immediately after surgery warrant further investigation.
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| 7. |
- Bläckberg, Jonas, et al.
(författare)
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Occult hepatitis B virus after acute self-limited infection persisting for 30 years without sequence variation
- 2000
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Ingår i: Journal of Hepatology. - 0168-8278. ; 33:6, s. 992-997
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND/AIMS: After acute self-limited hepatitis B virus (HBV) infection, serological loss of viral antigens and appearance of anti-HBs is generally believed to signify viral clearance. Latent and occult HBV infection appearing decades after self-limited hepatitis B has not been reported, nor has the evolutionary rate of HBV DNA over the same observation period. METHODS: DNA from serum and leukocytes from 16 patients with acute self-limited hepatitis B 30 years earlier was tested by polymerase chain reaction and positive samples were sequenced. Liver tissue from four patients was also tested. Additionally, another 10 HBV strains isolated from acute HBV cases in 1969-72 were compared to 11 strains isolated from acute cases in 1998-99 in the same community. RESULTS: HBV DNA was detected in liver from two patients, but not in serum or leukocytes. The HBV strains detected in liver showed complete homology, in the sequences analyzed, to the strains originally infecting these patients. Ten strains from 1998-99 were identical in pre-S and core promoter/precore regions to strains from the same community isolated 30 years earlier. CONCLUSIONS: HBV can persist as an occult infection three decades after acute, apparently self-limited hepatitis B, and both the mutation and evolutionary rates of HBV DNA are low.
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| 8. |
- Börjesson, Lars, 1963
(författare)
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Neuromuscular function in the normal and inflamed colon. An experimental study in rat
- 2000
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Neuromuscular function of the longitudinal muscle layer of distal colon was investigated in segments from normal rats and from rats with colitis induced by dextran sulphate sodium (DSS) at 3% for 3 or 7 days or 5% for 7 days. The study was performed in vitro, on spontaneous tone, or after precontraction. Guanethedine was present to block noradrenergic neurotransmission.Intrinsic nerves were activated by DMPP, an agonist at ganglionic, nicotinic receptors, K+, or McN-A-343, an agonist at preferentially muscarinic, neuronal receptors. The pharmacological analysis of the neurogenic response to the respective compound revealed that DMPP and K+ elicited relaxations being dependent on purinergic and nitrergic neurotransmission, and possibly also on vasoactive intestinal peptide (VIP). In contrast, the relaxation to McN-A-343 was seemingly dependent solely on ATP. While the response to K+ utilized the cGMP and the cAMP transduction systems for relaxation, that to McN-A-343 was independent of these two intracellular pathways. DSS induced dose-dependent inflammation in the distal colon. Tissue weight, optimal preload, response to carbachol, tone and phasic contractile activity was increased in segments from rats treated with 5% DSS. The adaptive relaxatory response to preload was abolished in DSS treated animals, possibly due to impaired nitrergic neurotransmission. In animals treated with 5% DSS, some results indicate prevailing inhibition of the colon muscle mediated by (non-neurogenic) nitric oxide, which could be an effect of the inflammation.It is concluded that non-adrenerig, inhibitory neurotransmission in rat distal colon depend on ATP, nitric oxide and VIP and that activation of muscarinic, neuronal receptors may selectivly release ATP. DSS colitis induce myogenic, neuronal, and possibly also paracrine alterations of the neuromuscular function in rat distal colon
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| 9. |
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| 10. |
- Elzuki, A, et al.
(författare)
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Alpha1-antitrypsin deficiency (PiZ) may be a risk factor for duodenal ulcer in patients with Helicobacter pylori infection
- 2000
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Ingår i: Scandinavian Journal of Gastroenterology. - 0036-5521. ; 35:1, s. 32-35
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Tidskriftsartikel (refereegranskat)abstract
- Abstract BACKGROUND: Most individuals with Helicobacter pylori infection in Western countries have no evidence of peptic ulcer disease (PUD). We therefore assessed the PiZ deficiency variant of the major plasma protease inhibitor alpha1-antitrypsin (alpha1AT) as a risk factor for PUD in H. pylori-infected individuals. METHODS: The cohort comprised 100 patients with endoscopically or surgically proven PUD (30 patients with duodenal ulcer (DU) and 70 patients with gastric ulcer (GU)) and 162 age- and sex-matched controls with PUD-negative endoscopic findings and no history of PUD. Plasma samples were screened for alpha1AT deficiency (PiZ) with an enzyme-linked immunosorbent assay (ELISA) and phenotyped by isoelectric focusing. H. pylori infection was evaluated with an IgG ELISA technique. RESULTS: Among the 262 patients 17 (6.5%) were positive for the PiZ alpha1AT deficiency, a frequency of the same magnitude as in the Swedish general population (4.7%). Of the PiZ carriers 76% (13 of 17) had H. pylori antibodies compared with 61% (151 of 245) of the non-PiZ carriers (NS). The prevalence of DU tended to be higher in H. pylori-positive PiZ carriers than in non-PiZ carriers (15.4%, 4 of 26 versus 0 of 4). Furthermore, among patients with DU a high PiZ allele frequency (13.3%, 4 of 30) was found compared with the general population (4.7%) (odds ratio (OR), 3.2; 95% confidence interval (CI), 1.09-8.94; P = 0.02). All DU patients carrying the PiZ allele were positive for H. pylori. In addition, four of five PiZ carriers with H. pylori infection and PUD had DU. CONCLUSIONS: The PiZ allele may be a contributing factor in the development of DU in H. pylori-positive individuals.
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