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Biomedical subjects

P Sipponen

Publications and source records attributed to P Sipponen.

At least 19 recordsLinked to original sources

Diagnostic value of decreasing IgG, IgA, and IgM antibody titres after eradication of Helicobacter pylori.

Titres of antibody to Helicobacter pylori are known to fall with eradication of bacteria. To find out what degree of fall would reliably indicate eradication, 144 patients with Helicobacter pylori infection were given antimicrobial therapy for 2 weeks and then followed up at 6 weeks, 6 months, and 12 months with serological tests, bacterial cultures, and histological studies of gastric specimens. 6 weeks after treatment IgG titres had fallen by 20-30% irrespective of the success of bacterial eradication. In the 121 bacteria-negative patients the decrease continued. 6 and 12 months after treatment the titre was 50% or less of pretreatment value in 97% of these patients. In the 23 patients who remained infected, the initial drop of IgG titres, if any, was followed by unchanged or slightly rising titres. IgA and IgM titres, initially raised in 64% and 4% of the patients, respectively, showed similar trends. The high sensitivity (97%) of the IgG antibody tests and a consistent fall within 6 months after eradication of H pylori infection made IgG the most useful immunoglobulin class for follow-up of antimicrobial therapy in individual patients. IgA antibodies were valuable in the 2% patients who had raised titres in this immunoglobulin class only. The few patients (5.5%) who had raised IgM titres also had high IgG titres. Serological tests thus are a cheap and reliable means of monitoring success of eradication of H pylori.

Adult

Natural history of gastritis and its relationship to peptic ulcer disease.

Chronic gastritis is a common inflammatory disease. In a number of patients, the inflamed gastric mucosa shows a gradual tendency to become atrophic (atrophic gastritis). Gastritis tends to be lifelong, and spontaneous healing is rare. With very few exceptions (e.g. in patients with autoimmune chronic corpus gastritis), gastritis is associated with the presence of the bacterium Helicobacter pylori. Inflammation and atrophy of the gastric mucosa result in impairment of gastric secretory functions (e.g. secretion of gastric acid, pepsin and gastrin). Such impairment is dependent on the topographic type of gastritis; i.e. whether the inflammation and atrophy occur in the antrum (chronic antral gastritis), corpus (chronic corpus gastritis) or in both the antrum and corpus simultaneously (chronic pangastritis). Gastritis of different topographic types associates with different gastric diseases. In patients with H. pylori-related antral or pangastritis, peptic ulcer disease, and in particular duodenal ulcer, is common (with an incidence exceeding 20% after 10 years' follow-up), as compared with peptic ulcer disease, which is very rare in patients with a normal stomach. Gastric ulcer may sometimes occur in patients with a rather atrophic stomach, but both gastric and duodenal ulcers are extremely rare in patients in whom the gastritis accompanies severe atrophic changes in the corpus mucosa. Routine biopsies from the antrum and corpus, and interpretation of the results in the light of the data on gastritis and its atrophic sequelae, allow the gastroenterologist to predict the risk and likelihood of peptic ulcer disease in patients with gastritis.

Adult

Gastric changes in coronary-operated patients with low-dose aspirin.

Low-dose aspirin is widely used in patients operated on for coronary disease as secondary prevention of coronary artery occlusion. The changes caused by aspirin in therapeutic doses to gastric mucosa are well documented, but the effect of long-term low-dose aspirin is not so well known. Forty-six volunteer coronary-operated patients with daily low-dose aspirin were interviewed postoperatively, and an upper gastrointestinal tract endoscopy was performed and biopsy specimens taken 3 months after the operation. The findings were compared with a normal population sample of 358 persons from a study previously published. There were significantly more erosions and ulcers or fresh scars in the study group than in the control population--11 of 46 patients and 24 of 358 patients, respectively. The presence of superficial gastritis was similar. Mostly, the lesions were asymptomatic. History of peptic ulcer disease, use of other ulcerogenic drugs, smoking, and alcohol consumption had no predictive value for acute lesions. In contrast, the lesions were associated with chronic superficial gastritis and Helicobacter pylori infection.

Adult

Gastric carcinoma: failed adaptation to Helicobacter pylori.

Helicobacter pylori is the major cause of chronic gastritis. Unlike bacterial infections in general, H. pylori acquisition causes a chronic, usually life-long infection. After acquisition, chronic inflammation (gastritis) appears and develops slowly into atrophic gastritis (with intestinal metaplasia) in a proportion of affected subjects. Inflammation and atrophy result from a failure of the immune system to eliminate the H. pylori infection. In infected stomach, several cascades of reactions are triggered which may result in impairments of structure and function of the gastric mucosa, some of which lesions also increase the risk of gastric carcinoma (CGA). A sequence of events from an early H. pylori infection into an atrophic gastritis has risen a theory that the H. pylori acquisition is a key issue in the development of GCA. Several aspects in the epidemiology and pathogenesis of GCA can be understood and explained by this infectious background. The H. pylori gastritis is unexpectedly common in patients with GCA of both intestinal or diffuse type, and the infection and gastritis precede the development of cancer. In Finland, 70-80% of the GCA cases seem to develop in connection with an H. pylori-positive gastritis or atrophy, 10-15% develop in a normal stomach (genetically determined GCA cases?), and 10-15% are associated with an H. pylori-negative corpus-limited (autoimmune) gastritis and atrophy. Case control studies suggest that the presence of H. pylori related inflammation raises the risk of GCA twofold, and the appearance of atrophic gastritis (and intestinal metaplasia) raises further this risk 2-3 times, as compared to the risk of GCA in subjects with a normal stomach.

Adaptation, Physiological

Histochemical reactions of gastrointestinal mucosubstances with orcein, high iron diamine and Alcian blue after prior oxidation of tissue sections.

The histochemical orcein reaction (orc) for mucosubstances in tissue samples from the human gastrointestinal tract was compared with PAS, high iron diamine (HID) and Alcian blue reactions at pH 1.0 or 2.5 (AB 1 and AB 2.5). Orc, HID and AB 1 reactions were performed also with prior oxidation of the tissue sections with potassium permanganate or performic acid (ox-orc, ox-HID and ox-AB reactions, respectively). Orc reaction stained mucosubstances similarly to HID and AB 1; only the brush border and goblet cells in the colon were stained. The reactions of the mucosubstances obtained with ox-orc differed from those with PAS, HID, AB 1 or AB 2.5 but were similar to those with ox-HID or ox-AB; the mucosubstances in the brush border and the goblet cells in the colon and small bowel and in the foveolar epithelium of the stomach were strongly stained. Pyloric and cardiac glands were stained faintly with ox-orc but not with ox-HID or ox-AB. Brunner's glands were negative with ox-orc, ox-HID and ox-AB reactions. It was assumed that the orc reaction stains, like HID or AB 1, sulphate groups in epithelial mucosubstances, and that sulphonic acid residues, resulting from oxidation of disulphide groups in the protein core of mucus glycoproteins, are responsible for the ox-orc as well as for the ox-HID and ox-AB reactions.

Alcian Blue

Histochemical reactions of gastrointestinal mucosubstances with high iron diamine after prior oxidation and methylation of tissue sections.

High iron diamine reactions after the prior methylation and oxidation of tissue sections with performic acid or potassium permanganate (metox-HID or ox-met-HID) in epithelial mucosubstances and in mucosal mast cells were studied in tissue samples from the human gastrointestinal tract and were compared with reactions with high iron diamine without any pretreatment (HID) and high iron diamine with the prior methylation (met-HID). High iron diamine reactions after the prior oxidation (met-ox-HID, ox-met-Hid and ox-Hid) demonstrated mucosubstances in a way which seemed to operate by the staining of acidic groups evoked by the oxidation of the tissue sections. These acidic groups were not blocked by the methylation. It was supposed that they are sulphonic acids resulting from sulphur groups (sulphydryls or disulphides) in some mucus glycoproteins. Met-ox-HID and ox-met-HID reactions seemed to stain mucosubstances and mast cells in a similar way but differed from the ox-HID reactions with the manner which could be interpretated to be due to the blocking of free sulphate ester groups in reactions of the former. Met-ox-HID (and ox-met-HID) positive and in goblet cells of small and large bowel.

Diamines

Detection of iodine, sulphur and phosphorus in histological thyroid sections by using electron probe microanalysis.

Electron probe microanalysis for iodine, sulphur and phosphorus was performed in histological frozen sections from thyroid tissue of 5 patients undergone thyroid surgery for benign disease. Iodine seemed to be localized in the colloid of the thyroid follicles. Phosphorus localized in areas which corresponded with the epithelium of the follicles. Sulphur showed a strong association with iodine both in localization and in relative amounts. It was suggested that iodine and sulphur reflect the presence of thyroglobulin in the colloid of thyroid follicles.

Electron Probe Microanalysis

Carcinoembryonic antigen in endoscopic brush specimens from benign and malignant gastric lesions.

The measurement of carcinoembryonic antigen (CEA) in serum and endoscopic brush specimens was evaluated for the differential diagnosis of malignant and nonmalignant gastric disease. Brush specimens were studied from 33 patients with gastric cancer and 36 patients with benign gastric lesions or apparently normal gastric mucosa. Demonstrable CEA immunoreactivity was found by radioimmunoassay in brush specimens from 24/33 cancer patients (73%) and from 23/36 patients with benign lesions (64%). Patients with CEA+ tissue in the immunoperoxidase test had somewhat higher CEA concentrations in the brush specimens than cases with CEA- biopsy tissue, although overlap was considerable. Thirty-five per cent of cancer patients had both a positive tissue CEA reaction and a CEA/DNA ratio greater than 10 ng/micrograms, whilst patients with benign lesions had only 15% of positives by these criteria (0.01 greater than P greater than 0.001). The serum CEA concentration was above the upper normal level of 5 ng/ml in 2/39 patients, both of whom had gastric cancer. The CEA immunoreactive material from benign and malignant lesions eluted in gel filtration on Sephadex G-200 in the same volume as CEA purified from liver metastases of cancer of the colon, showing that a glycoprotein sharing immunological and physicochemical properties with CEA is present both in malignant and nonmalignant lesions of the gastric mucosa, and that there is considerable overlapping in the amount of CEA. The estimation of CEA in gastric-brush specimens is therefore of limited value in the differential diagnosis of benign and malignant gastric lesions.

Adult

Alcoholic liver damage is provoked by 4-methylpyrazole, which prolongs the influence of ethanol but reduces acetaldehyde levels.

Rats chronically fed ethanol developed liver injury only if they also received low doses of the alcohol dehydrogenase inhibitor, 4-methylpyrazole, suggesting that the consistency of the influence of ethanol and its metabolism, rather than the level of acetaldehyde or the degree of the metabolic effects, contributes to the pathogenesis of alcoholic liver damage.

Acetaldehyde

Carcinoembryonic antigen (CEA) in the gastric mucosa after partial gastrectomy.

Carcinoembryonic antigen (CEA) was studied by the three-layer bridge immunoperoxidase technique in gastric biopsy specimens taken from 49 patients, 13--20 years after partial gastrectomy. Routine histological examination revealed various degrees of chronic atrophic gastritis in all patients. A positive CEA reaction was found in 6 out of 9 with malignant or premalignant mucosal changes and in 4 out of 40 without these changes. In two cases of carcinoma the biopsies revealed a positive CEA reaction. In 4 patients with carcinoma diagnosed 1--2 years after the first examination the initial nonmalignant biopsies were CEA-positive in one case. All biopsies from mucosa with severe dysplasia and adenomatous polyps were CEA-positive. Four patients without malignant or premalignant changes in the gastric mucosa had CEA-positive biopsies. No carcinoma has been found in these patients at re-examinations after 1 year. The results indicate that the occurrence of immunohistochemically detectable CEA may be associated with malignant transformation of the gastric mucosa. The value of this method in screening patients at increased risk of gastric carcinoma will be further explored.

Adolescent

Morphometric analysis of the loss of chief and parietal cells after partial gastrectomy for duodenal ulcer.

Relative chief and parietal cell volume densities were estimated morphometrically in the remnant mucosa of 98 male patients ("series"), operated on for duodenal ulcer by the Billroth II, and in the body mucosa of 55 subjects, age and sex matched, from a random series of a Finnish population ("controls"). The relative volumes of chief and parietal cells were significantly lower in the series than in the controls. The mean chief cell: parietal cell ratio was significantly higher in the series than in the controls. In the controls the ratio decreased with increasing loss of normal tubules. However, no such decrease was discernable in the series, owing to wide scatter of the individual ratios. High ratios (greater than or equal 2.0) were found in 17 cases of the series and in one of the controls. These 17 patients with high ratios had a significantly higher mean length of the foveoles and a significantly lower mean score of the round cell infiltration than the operated patients with lower ratios.

Adult

Familial syndrome with panhypopituitarism, hypoplasia of the hypophysis, and poorly developed sella turcica.

Two sisters who died at the age of 2.5 years and 5 weeks are described. Both showed signs of panhypopituitarism. At necropsy, no hypophysis could be found in the first child and a rudimentary and partly ectopic hypophysis was found in the other. Both children had a flat, poorly developed sella turcica, and the sellar anomaly could be seen in skull x-rays. These patients represent a hereditary syndrome characterised by neonatal panhypopituitarism, hypoplasia of the pituitary gland, and flat sella turcica.

Child, Preschool

Cystic "hamartomatous" epithelial polyps of the stomach.

Nine cases of cystic polyps were found among 15,000 routine gastroscopies. All but one of the subjects were women. The polyps were found only in the body of the stomach. They were less than 5 mm in size and in most cases multiple. Endoscopically they were verruca-like lesions and appeared to be loosely attached to the mucosal membrane. They consisted of mucosal cysts lined with normal but irregularly arranged epithelial cells of the body mucosa. No inflammatory reaction or metaplasia was seen in the polyps or outside them. These characteristics suggested the hamartomatous nature of these polyps.

Adult

Hereditary nephronophthisis with a life span of three decades. Light and electron microscopical, immunohistochemical, clinical and family studies.

Familial nephronophthisis was diagnosed in a son and two daughters of a mother who herself died in uraemia at the age of 29 years. The son died at 33 years, two daughters are alive at 30 and 33 years. Our cases suggest a dominant autosomal type of inheritance because the mother married twice; the affected son was from the first marriage and the affected daughters from the second marriage. There was no known consanguinity between the parents. The pathogenesis of the disease can be explained by a slowly progressive process that leads to complete or partial obstruction of the tubules in the corticomedullary area, and also, therefore, to cystic dilatations. Histological evidence for this is provided by the proliferation of fibroblasts around the collecting ducts and other tubules, prominent thickening of the tubular basement membrane, and fibroblasts and collagen fibrils in or inside the thickened basement membranes. An ultrastructural description of affected kidneys is given.

Adult