Severe aortic regurgitation in RF positive polyarticular JIA.
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Adolescent↗
Biomedical subjects
J Lindeman
Publications and source records attributed to J Lindeman.
Comparative analysis of human papillomavirus infections in cervical scrapes and biopsy specimens by general SPF(10) PCR and HPV genotyping.
Human papillomavirus (HPV) can be detected by DNA amplification from clinical samples. The aim of the present study was to compare the HPV status in both cervical scrape and biopsy specimens obtained from 174 patients, using the recently developed broad spectrum SPF(10) PCR-LiPA method. The detection rate of HPV in these materials was determined and the spectrum of HPV genotypes was compared. Cervical scrapes and biopsy specimens were obtained, either on the same day (group I), or with an interval of up to almost 2 years (group II, mean interval 97 days, range 1-469 days). HPV DNA was amplified by SPF(10) PCR and detected in a microtitre plate hybridization assay. Of the HPV-positive cases, the genotype was determined by reverse hybridization of the same SPF(10) amplimer on a line probe assay (LiPA), discriminating between HPV genotypes 6, 11, 16, 18, 31, 33-35, 39, 40, 42-45, 51-54, 56, 58, 59, 66, 68, 70, and 74. The results showed that the detection rate and the spectrum of HPV genotypes in cervical scrapes and the corresponding biopsy specimens were highly comparable in both patient groups, even when multiple genotypes were present. In both groups, multiple HPV genotypes were more frequently detected in cervical scrapes than in the corresponding biopsy specimens. In conclusion, HPV infection can be diagnosed in cervical scrapes and biopsy specimens using the SPF(10) PCR-LiPA system. Analysis of cervical scrapes accurately reflects the spectrum of HPV genotypes in the patient's cervical region, even with a sampling interval between the cervical scrape and the biopsy specimen.
Biopsy↗
Quantitative assessment of gastric corpus atrophy in subjects using omeprazole: a randomized follow-up study.
OBJECTIVES: Atrophy of the gastric mucosa most frequently results from chronic Helicobacter pylori infection and is a risk factor for the development of gastric cancer. Profound acid suppression has been suggested to accelerate the onset of gastric mucosal atrophy. The aim of the present study was to evaluate the effects of H. pylori eradication and acid inhibition by omeprazole on gastric atrophy by means of quantitative analysis of tissue morphology. METHODS: Corpus biopsy specimens were obtained during endoscopy in 71 gastroesophageal reflux disease (GERD) patients at baseline and after 3 and 12 months. A total of 48 subjects were H. pylori positive and 23 were H. pylori negative. All subjects received omeprazole 40 mg once daily after the first endoscopy for 12 months. After randomization, 27 of the 48 H. pylori-positive patients also received eradication therapy. In hematoxylin and eosin-stained slides the volume percentages of glands (VPGL), volume percentages of stroma (VPS), and volume percentages of infiltrate (VPI) were measured in the glandular zone of the mucosa. The results were evaluated by computerized morphometric analysis. RESULTS: In the eradication group, the mean VPGL increased from 63.0% to 67.7% and 71.5% after 3 and 12 months (p < 0.001), respectively. The mean VPS and VPI decreased from 33.1% and 4.0% to 29.3% and 3.0% and to 26.4% and 2.1% (p < 0.001 and p = 0.04), respectively. Patients with the lowest VPGL at baseline showed the largest increases of VPGL after eradication treatment as compared to patients with high a VPGL at baseline. In the H. pylori-persistent group the VPI showed a significant increase (p = 0.01), and in the H. pylori-negative group VPGL increased significantly from 71.9% to 75.2% (p = 0.03) after 12 months. CONCLUSIONS: Eradication of H. pylori leads to restitution of the volume percentage of glandular epithelium to normal levels, even during treatment with proton pump inhibitors. Whether this effect can also be seen in patients with marked atrophy needs further investigation.
Adult↗
Rapid quantitative assessment of gastric corpus atrophy in tissue sections.
BACKGROUND/AIMS: Grading of Helicobacter pylori induced atrophic gastritis using the updated Sydney system is severely limited by high interobserver variability. The aim of this study was to set up a quantitative test of gastric corpus mucosal atrophy in tissue sections and test its reproducibility and correlation with the Sydney scores of atrophy. METHOD: Mucosal atrophy was assessed in 124 haematoxylin and eosin stained corpus biopsy specimens by two experienced gastrointestinal pathologists (EB, JL) according to the updated Sydney system as none (n = 33), mild (n = 33), moderate (n = 33), or pronounced (n = 25). In each specimen, the proportions of glands, stroma, infiltrate, and intestinal metaplasia in the glandular zone were measured as volume percentages using a point counting method. The optimal point sample size, intra-observer and interobserver reproducibility, discriminative power for degrees of atrophy, and correlations with H pylori status were evaluated. RESULTS: Counting 400 points in 200 fields of vision provided the smallest sample size that still had excellent intra-observer and interobserver reproducibility (r > or = 0.96). Overall, the volume percentage of glands (VPGL), infiltrate (VPI), and stroma (VPS) correlated well with the Sydney scores for atrophy (p < or = 0.003). However, no differences were found between non-atrophic mucosa and mild atrophy. No correlation was found between age and either the Sydney grade of atrophy or the VPGL or VPS. In non-atrophic mucosa and mild atrophy, H pylori positive cases showed a significantly higher VPI than did H pylori negative cases. A lower VPGL was seen in H pylori positive cases than in H pylori negative cases in the mild atrophy group. VPS did not correlate with H pylori status within each grade of atrophy. CONCLUSION: Point counting is a powerful and reproducible tool for the quantitative analysis of mucosal corpus atrophy in tissue sections. These data favour the combination of "none" and "mild" atrophy into one category, resulting in a three class grading system for corpus atrophy, when using the updated Sydney system.
Adult↗
Helicobacter pylori-related and -non-related gastric cancers do not differ with respect to chromosomal aberrations.
Gastric carcinogenesis is strongly associated with Helicobacter pylori infection, but the underlying genetic mechanisms are largely unknown. The aim of this study was to correlate chromosomal aberrations in gastric cancer to H. pylori status and its different strains, as well as to histological type and other clinico-pathological variables. DNA from 46 gastric cancers (male/female 35/11, age 27-85 years) was extracted from formaldehyde-fixed, paraffin-embedded material and tested for chromosomal gains and losses by comparative genomic hybridization (CGH). Chromosomal aberrations with frequencies of 20% or higher were considered to be non-random changes associated with gastric cancer. The mean number of chromosomal events per tumour was 9.7 (range 0-27), with a mean of 3.2 gains (range 0-16) and 6.5 losses (range 0-15). Gains were most frequently found at chromosomes 8q and 13q (24% and 26%, respectively). Losses were predominantly found on chromosome arms 2q, 9p, 12q, 14q, 15q, 16p, 16q, 17p, 17q, 19p, 19q, and 22q (22%, 30%, 43%, 22%, 33%, 50%, 28%, 50%, 39%, 33%, 39%, and 37%, respectively). Common regions of overlap narrowed down to 2q11-14, 8q23, 9p21, 12q24, 13q21-22, 14q24 and 15q11-15. The mean number of gains was higher in tumours with metastases than in localized tumours (4.1 vs. 1.9, p=0.04). Tumours with a loss at 17p showed a higher number of losses than tumours without a 17p loss (9. 5 vs. 4.7 on average, p<0.001). Neither H. pylori status (+, n=25; -, n=21) nor H. pylori strain was correlated to the total number of events or to any specific chromosomal aberration, nor were there differences between intestinal (n=30) and diffuse (n=15) cancers or any other clinico-pathological variable tested. In conclusion, a complex of chromosomal aberrations is involved in gastric cancer, but their pattern does not depend on H. pylori status or strain, nor on the histological type of the tumour. The exact biological meaning of these aberrations in carcinogenesis needs further clarification.
Adult↗
Additive cytotoxic effect of cisplatin and X-irradiation on human glioma cell cultures derived from biopsy-tissue.
PURPOSE: Investigation of the in vitro cytotoxic effect of X-rays, either alone or combined with cisplatin on early passage cell cultures derived from human glioblastoma multiforme biopsy tissue. MATERIALS AND METHODS: Fresh tumour specimens from four patients were processed to cell cultures. The U373 glioma cell line was used as a reference. Early passage cell cultures were X-irradiated (0-8 Gy) either alone or in combination with cisplatin (0.5-1 microgram/ml). Cell survival was determined by either clonogenic assay or the colorimetric MTT assay. Survival curves were generated and mathematically analysed using the linear quadratic model, to obtain the radiosensitivity parameters alpha, beta, and SF2, i.e., the Surviving Fraction after 2 Gy. RESULTS: Two patient-derived glioma cell cultures and the U373 cell line showed rather high SF2 values of 0.61-0.72 in the clonogenic assay, indicating relative high radiation resistance. Cisplatin alone (1 microgram/ml) reduced cell survival by 10-30% (n = 4). When combined with irradiation, a clear additive cytotoxic effect of cisplatin was demonstrated by the unaltered value of the alpha-parameter for reproductive cell death. CONCLUSION: Cisplatin exerted an additive rather than radiosensitising cytotoxic effect in uncharacterised patient derived glioma cell cultures.
Adult↗
Prevalence of human papillomavirus DNA in different histological subtypes of cervical adenocarcinoma.
The prevalence of human papilloma virus (HPV) DNA in different histological subtypes of cervical adenocarcinoma and related tumors was examined using formalin-fixed, paraffin-embedded tissue samples from 105 primary cervical adenocarcinomas and adenosquamous carcinomas. Broad-spectrum HPV DNA amplification and genotyping was performed with the SPF10 primer set and line probe assay (LiPA), respectively. HPV DNA was detected in 82 of 90 (91%) mucinous adenocarcinomas, encompassing endocervical, intestinal, and endometrioid histological subtypes, and in nine of nine adenosquamous tumors (100%). HPV DNA was not detected in any nonmucinous adenocarcinomas including clear cell, serous, and mesonephric carcinomas (0/6). The most common viral types detected in adenocarcinoma were HPV 16 (50%) and HPV 18 (40%), followed by HPV 45 (10%), HPV52 (2%), and HPV 35 (1%). Multiple HPV types were detected in 9.7% of the cases. In conclusion, mucinous adenocarcinomas and adenosquamous carcinomas of the cervix demonstrate a very high prevalence of HPV DNA, similar to that reported for cervical squamous cell carcinoma. Only rare histological variants of cervical adenocarcinoma seem unrelated to HPV infection.
Adenocarcinoma↗
Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment.
Parietal cell protrusion (PCP), swelling and bulging of parietal cells, has been observed in the oxyntic mucosa of patients receiving omeprazole. The frequency of this event and the underlying mechanisms remain to be clarified. As such, it is unknown whether there is a relation with either serum gastrin or Helicobacter pylori infection, and whether PCP predisposes to the development of fundic gland cysts (FGC). We therefore investigated the development of PCP and FGC in gastroesophageal reflux disease (GERD) patients treated with omeprazole and correlated findings to duration of therapy, gastrin, and H pylori infection. In a randomized, double-blinded study, GERD patients were evaluated by endoscopy with biopsy sampling for histology and culture at baseline, and after 3 and 12 months' therapy with omeprazole 40 mg daily. H pylori-positive patients were randomized to additional eradication therapy or placebo antibiotics at baseline. All histological slides were scored blinded for time and outcome of culture for the presence of PCP and FGC. Fasting serum samples from all visits were used for gastrin measurements. The prevalence of PCP increased during omeprazole therapy from 18% at baseline to 79% and 86% at 3 and 12 months (P < .001, baseline v both 3 and 12 months). The prevalence of FGC increased from 8% to 17% and 35% (P < .05, baseline v 12 months). The prevalence of PCP and FGC did not differ among the H pylori-positive and H pylori-negative patients at baseline (PCP 16% v 20% and FGC 7% v 8%, respectively). Whereas H pylori eradication did not significantly affect development of PCP (P = .7), FGC developed significantly more often in the H pylori-eradicated patients when compared with persistent H pylori-positive patients (P < .05). PCP development was related to serum gastrin rise during therapy. In conclusion, PCP occurs in most patients within the first months of omeprazole treatment and is related to increased gastrin levels. FGC develops more gradually and is enhanced by H pylori eradication.
Adult↗
Effect of Helicobacter pylori eradication on chronic gastritis during omeprazole therapy.
BACKGROUND: We have previously observed that profound acid suppressive therapy in Helicobacter pylori positive patients with gastro-oesophageal reflux disease is associated with increased corpus inflammation and accelerated development of atrophic gastritis. AIM: To investigate if H pylori eradication at the start of acid suppressive therapy prevents the development of these histological changes. PATIENTS/METHODS: In a prospective randomised case control study, patients with reflux oesophagitis were treated with omeprazole 40 mg once daily for 12 months. H pylori positive patients were randomised to additional double blind treatment with omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg twice daily or placebo for one week. Biopsy sampling for histology, scored according to the updated Sydney classification, and culture were performed at baseline, and at three and 12 months. RESULTS: In the persistently H pylori positive group (n=24), active inflammation increased in the corpus and decreased in the antrum during therapy (p=0.032 and p=0.002, respectively). In contrast, in the H pylori positive group that became H pylori negative as a result of treatment (n=33), active and chronic inflammation in both the corpus and antrum decreased (p<or =0.0001). The decrease in active and chronic inflammation in the corpus differed significantly compared with the persistently H pylori positive group (both p=0.001). For atrophy scores, no significant differences were observed between H pylori eradicated and persistently H pylori positive patients within one year of follow up. No changes were observed in the H pylori negative control group (n=26). CONCLUSIONS: H pylori eradication prevents the increase in corpus gastritis associated with profound acid suppressive therapy. Longer follow up is needed to determine if H pylori eradication prevents the development of atrophic gastritis.
Adult↗
Fibroblast-like synoviocytes from rheumatoid arthritis patients have intrinsic properties of follicular dendritic cells.
The production of IgG rheumatoid factors in the inflamed synovium of many patients with rheumatoid arthritis (RA) implies that local sites exist where plasma cell precursors undergo isotype switching and affinity maturation by somatic mutation and selection. Lymphonodular infiltrates of the synovium-containing germinal centers (GCs), are candidates to fulfill such function in the rheumatoid patient. It has been suggested that these GCs are organized around, obviously ectopic, follicular dendritic cells (FDCs). The present study attempts to find out whether these putative FDCs 1) are specific for RA, 2) have the same phenotype and functional capacity as FDCs in lymphoid organs, and 3) may locally differentiate from fibroblast-like synoviocytes (FLS). Synovial biopsies from patients with RA versus non-RA, yet arthritic backgrounds, were compared. Cells with the FDC phenotype were found in both RA and non-RA tissues as well as in single cell suspensions thereof. When FLS were cultured in vitro, part of these cell lines could be induced with IL-1beta and TNF-alpha to express the FDC phenotype, irrespective of their RA or non-RA background. By contrast, the FDC function, i.e., stable binding of GC B cells and switching off the apoptotic machinery in B cells, appeared to be the prerogative of RA-derived FLS only. The present data indicate that FDC function of FLS in RA patients is intrinsic and support the idea that synovial fibroblast-like cells have undergone some differentiation process that is unique for this disease.
Adult↗
Trends in hospitalization and mortality from rotavirus disease in New Zealand infants.
BACKGROUND: Rotavirus illness is associated with significant morbidity and mortality worldwide. We have examined trends in diarrheal disease in New Zealand children to determine the disease burden attributable to rotavirus and to estimate the proportion of hospitalizations preventable by vaccination. METHODS: Hospital admissions data and laboratory records for 1994 to 1996, were obtained for children 0 to 4 years at four sites (serving -60% of the New Zealand population). Rotavirus disease burden was estimated using combined admissions and laboratory data. Severity of disease was estimated in a sample of 150 hospitalizations for rotavirus diarrhea, and the proportion of vaccine-preventable admissions was extrapolated. Mortality attributed to diarrheal causes was determined from national records for 1974 to 1993. RESULTS: Between 1994 and 1996, 4436 children <5 years of age were hospitalized with diarrhea (1047/100000 children per year). Admissions associated with rotavirus were estimated at 1522 to 1535 (315 to 362/100000 annually). Infants between 6 and 17 months were most commonly affected (42% of all cases). More male children than female children were hospitalized (P < 0.001) and mean length of stay was calculated as 1.51 days (SD 2.35). Disease severity scoring revealed that 61.3 and 38.0% of admissions reviewed were severe and very severe, respectively. Deaths from diarrheal causes numbered 138 among children 0 to 4 years old for the 20-year period 1974 to 1993, with 18 deaths occurring between 1984 and 1993 (10 years). CONCLUSION: Current vaccines control severe disease, suggesting that 72% of cases reviewed would be eligible for prevention. A full cost effectiveness analysis is required to demonstrate anticipated benefits of vaccination.
Child, Preschool↗
Development and clinical evaluation of a highly sensitive PCR-reverse hybridization line probe assay for detection and identification of anogenital human papillomavirus.
Human papillomavirus (HPV) can be detected by amplification of viral DNA. A novel PCR primer set generating a short PCR fragment (SPF PCR) was used for amplification of a fragment of only 65 bp from the L1 region and permitted ultrasensitive detection of a broad spectrum of HPV genotypes. The intra- and intertypic sequence variations of the 22-bp interprimer region of this amplimer were studied. Among 238 HPV sequences from GenBank and clinical specimens, HPV genotypes were correctly identified based on the 22-bp sequence in 232 cases (97.2%). Genotype-specific probes for HPV genotypes 6, 11, 16, 18, 31, 33 to 35, 39, 40, 42 to 45, 51 to 54, 56, 58, 59, 66, 68, 70, and 74 were selected, and a reverse hybridization line probe assay (LiPA) (the INNO-LiPA HPV prototype research assay) was developed. This LiPA permits the use of amplimers generated by the SPF as well as the MY 09/11 primers. The assay was evaluated with a total of 1, 354 clinical specimens, comprising cervical scrapes (classifications ranging from normal cytology to severe dyskaryosis) and formalin-fixed, paraffin-embedded cervical carcinoma samples. LiPA results were highly concordant with sequence analysis of the SPF amplimer, genotype-specific PCR, and sequence analysis of amplimers generated by MY 09/11 primers. The sensitivity of the SPF primers was higher than that of the GP5(+)/6(+) primers over a broad range of HPV types, especially when multiple HPV genotypes were present. In conclusion, the SPF LiPA method allows extremely sensitive detection of HPV DNA as well as reliable identification of HPV genotypes in both cervical smears and paraffin-embedded materials.
Base Sequence↗
Immunohistochemical localization of somatostatin receptor sst2A in human rheumatoid synovium.
OBJECTIVE: To identify the somatostatin receptor-expressing cells in rheumatoid synovium using a recently developed antiserum directed against the somatostatin receptor subtype 2A (sst2A). METHODS: We carried out immunohistochemical studies of synovial biopsies from 7 patients with rheumatoid arthritis (RA) and one non-RA patient, using a rabbit polyclonal antiserum directed against sst2A and monoclonal antibodies directed against phenotypic markers. RESULTS: SSt2A was expressed by the endothelial cells of the synovial venules but also by a subset of synovial macrophages. CONCLUSION: The identification of somatostatin receptors on macrophages, which are thought to be important effector cells in RA, may offer mechanistic insights into the potential therapeutic effect of somatostatin (analogs) in RA.
Animals↗
Monoclonal antibodies against the human mannose receptor as a specific marker in flow cytometry and immunohistochemistry for macrophages.
Recently we developed mouse monoclonal antibodies (mAb) against the isolated human 175-kDa mannose receptor. In the present study we tested whether these mAb are suitable for the detection of the mannose receptor on cultured macrophages using flow cytometry and on cells in human tissues using immunohistochemistry. Human monocytes did not react with the mAb in flow cytometry. Mannose receptor expression became detectable on monocytes cultured for 3 days (macrophages), and was maximal from 4 days onward. The mannose receptor was up-regulated on dexamethasone-treated (immunosuppressed) macrophages, and down-regulated on lipopolysaccharide-treated (activated) macrophages. Immunohistochemically the staining pattern of our mAb was compared with the marker of monocytes/macrophages KP1. In a bone marrow smear, only macrophages were stained with our mAb, whereas all myeloid cells were stained with KP1. In the thymus and lymph node, mannose receptor-positive branched cells (macrophages and dendritic cells) were detected in connective tissue, thymus cortex (not medulla), and in the T cell area (not the B cell area) of lymph nodes, whereas KP1 stained branched cells in all areas. It was concluded that the mAb are useful tools in flow cytometry and immunohistochemistry for the specific detection of cells expressing mannose receptor.
Antibodies, Monoclonal↗
Growth factor profiles of human gliomas. Do non-tumour cells contribute to tumour growth in glioma?
BACKGROUND: Growth factors play a role in proliferation and motility of malignant glial cells, through autocrine and paracrine mechanisms. Also, proliferation of non-tumour cells, e.g., endothelial cells, is likely to be controlled by growth factors. Several growth factors with their appropriate receptors can be involved, but studies on tissue specimens evaluating this in glioma are rare. MATERIALS AND METHODS: We evaluated the potential role of Transforming growth factor-alpha (TGF-alpha) and Epidermal growth factor receptor (EGF-R), the Platelet-derived growth factor A- and B-chain (PDGF-A and PDGF-B) and its receptors (PDGFR alpha and PDGFR beta, and basic fibroblast growth factor (bFGF) in gliomas by analysing 86 of these tumours on the single cell level for the presence of immunoreactive growth factors and receptors. In a few cases double-staining experiments were done to directly visualize co-expression of factor and receptor. RESULTS: Multiple growth factors and their receptors are present in astrocytic tumours; the higher the grade, the more growth factors and the more positive cells are found. Oligodendroglial tumours and pilocytic astrocytomas showed little expression. Autocrine and paracrine mechanisms were frequently possible in the astrocytic tumours, often more than one loop could be involved. Interestingly, it was also frequently possible that non-tumour cells produced a growth factor for which the tumour cells expressed the receptor. CONCLUSIONS: Multiple growth factors appear to be involved in astrocytic tumours, with frequent autocrine and paracrine loops. Expression of these molecules seems to increase with increasing grade. The results argue for a contribution of non-tumour cells to the growth of a tumour.
Astrocytoma↗
Polymerase chain reaction for the detection of Helicobacter pylori in formaldehyde-sublimate fixed, paraffin-embedded gastric biopsies.
To improve morphologic detail and immunohistochemical staining, mercuric chloride-containing fixatives such as formaldehyde-sublimate (FS) has been widely used as an alternative for neutral buffered formalin. FS-fixed, paraffin-embedded tissue, however, is considered to be an unreliable source of DNA. We used an adapted DNA-extraction method for FS-fixed, paraffin-embedded tissue. In all cases tested we obtained amplifiable DNA with polymerase chain reaction (PCR), after FS-fixation and after fixation in neutral buffered formalin as well. A PCR assay for the 16S-rRNA region of Helicobacter pylori was developed amplifying a fragment of 145 bp. The specificity of this PCR assay was tested on a range of different microorganisms. PCR was performed on 46 archival FS-fixed paraffin-embedded gastric biopsies. The results were compared with histologic examination and with immunohistochemical detection using a polyclonal antibody against H. pylori. Both PCR and immunohistochemistry are very sensitive methods for the detection of H. pylori. A PCR offers the possibility of additional subtyping in archival FS-fixed, paraffin-embedded tissue.
Biopsy↗
Malabsorption syndrome associated with ulceration of the stomach and small bowel caused by chronic intestinal ischemia in a patient with hyperhomocysteinemia.
We describe a 39-year-old woman with an 8-month history of abdominal pain, diarrhea, and weight loss. Clinical and laboratory evaluation indicated the presence of a malabsorption syndrome. Endoscopy revealed multiple gastric ulcerations and an abnormal "picture" of the duodenal mucosa. At duodenal biopsy, necrosis confined to the distal parts of the enteric villi and a polymorphonuclear leukocyte response were found. Further evaluation revealed intestinal ischemia as a result of mesenteric atherosclerosis. After a revascularization procedure was performed, the symptoms disappeared. The macroscopic and microscopic picture of the bowel normalized. In our search for risk factors of atherosclerosis, we found a substantially increased basal plasma homocysteine concentration. This case suggests that hyperhomocysteinemia may have a causal role in the development of symptomatic, premature atherosclerosis of the mesenteric circulation.
Adult↗
Serological parameters in assessment of degree of gastritis in healthy volunteers.
This study was undertaken in healthy volunteers to determine the relation between serum levels of pepsinogen A, pepsinogen C, pepsinogen A:C ratio, and gastrin on the one hand and histology of the gastric mucosa on the other. The grade of gastritis was scored separately for antral and fundic mucosa by three different classifications: Whitehead, activity, and the Sydney score. Among 48 healthy volunteers studied, 17 were found to have gastritis according to the criteria of Whitehead. Fourteen of these 17 subjects with gastritis had H. pylori in gastric biopsies. In all 48 subjects serum pepsinogen A (r = 0.298-0.506; P < 0.01-P < 0.05), pepsinogen A:C ratio (r between -0.377 and -0.495; P < 0.001-P < 0.05) and gastrin (r = 0.38-0.695; P = 0.007-P < 0.01) were significantly correlated to the severity of both antral and body gastritis as assessed by all three classifications. In contrast, there was no significant correlation between serum pepsinogen C and any of the gastritis scores. When the 17 subjects with gastritis were analyzed separately, there were no correlations between the parameters studied and gastritis of the antrum. Regarding the corpus mucosa, serum PgA correlated significantly with the activity score (r = 0.520; P = 0.03), weakly with the Sydney score (r = 0.465; P = 0.06), but not with the Whitehead score. Serum PgC correlated with the Whitehead (r = 0.555; P = 0.02) and Sydney score (r = 0.523; P = 0.03), but only weakly with the activity score (r = 0.441; P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗