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Morphometric measurements of nuclear area, nuclear concentration and nucleolar dimensions in defined tissue zones of orientated oesophageal biopsy sections were compared between three patient groups--asymptomatic/normal endoscopy (n = 8); symptomatic reflux/normal endoscopy (n = 17); and symptomatic/endoscopic oesophagitis (n = 15). No significant differences could be shown for any mean parameter between clinical groups. In a further group of 16 patients, identical morphometric measurements were made in non-orientated grasp biopsies and correlated with prolonged ambulatory pH data. No significant correlations could be shown between nuclear parameters and acid reflux measurements. These results suggest that morphometric measurement cannot be recommended as a diagnostic tool in the diagnosis of oesophagitis, although it may be useful in the assessment of individual therapeutic response in clinical trials.

To determine the effect of varying degrees of gastritis on the distribution of immuno-reactive gastrin cells 38 partial gastrectomy specimens have been studied. Routinely stained histological sections of mucosa were compared with serial and adjacent sections stained by specific immunohistochemistry using peroxidase and fluorescent techniques. While chronic superficial gastritis had no obvious effect, mild atrophic gastritis was associated with an uneven distribution of gastrin cells which became more marked with increasing severity of gastritis. In the region of intestinal metaplasia gastrin cells were almost totally absent. Small numbers of gastrin cells were found within areas of pseudopyloric metaplasia in the fundus, a region where those cells are not normally seen. Similarly, gastrin cells were detected within regenerative gastric polypi in both antrum and fundus.

Viral lymphadenitis may lead to a histological appearance that can simulate malignancy. The histological features of herpes simplex lymphadenitis have not previously been described in detail. We report a case of proved herpes simplex lymphadenitis in a 30 year old man which was characterised by a pronounced proliferation of immunoblasts. The microscopical findings are described and the published work is reviewed.

Jejunal biopsy specimens from 10 children with acute lymphoblastic leukaemia on methotrexate treatment were compared with 10 from children being investigated for diarrhoea or failure to thrive. In association with methotrexate treatment on both light and electron microscopy, there were marked morphological abnormalities in the villus enterocytes. These consisted of a striking distention of the lateral basal intercellular spaces, cell vacuolation and patchy necrosis and was most marked when methotrexate treatment was given between 24 and 72 h before biopsy. Two mechanisms may be involved: an early direct toxic effect on the mature enterocyte coupled with interference with crypt cell generation, possibly causing ageing and loss of cells proximal to the normal extrusion zone. These pathological changes may account for the malabsorption in association with methotrexate treatment.

A young male patient demonstrated unusual features of Cushing's syndrome, atrial myxomas and freckled skin pigmentation. At 4.5 years of age he presented with intermittent swelling of his face and abdomen associated with weight gain and mild hypertension. A left atrial myxoma, suspected from routine physical examination, was surgically removed at 6.1 years of age. The initial mild symptoms clinically thought to be due to Cushing's syndrome, persisted intermittently without any consistent biochemical abnormality. At 10 years of age height velocity decreased and at 12 years early osteoporosis was observed radiologically. Repeated dexamethasone tests revealed a paradoxical increase in cortisol and corticotrophin from normal basal levels. Further investigation showed a cyclical pattern of hypercortisolism. The removal of a pituitary microadenoma failed to correct the features of Cushing's syndrome or prevent intermittent hypercortisolism. At 15.3 years a second left atrial myxoma was removed. This was followed by bilateral adrenalectomy. Histologically the features were consistent with primary pigmented nodular adrenocortical disease. This is the first patient described with cyclical Cushing's syndrome as part of this unusual complex of disorders.

Morphometry of 31 pancreatic islet cell tumors was examined to determine the value of this technique in assessing tumor behavior. Patients were followed for a mean period of 5.1 years (range, 1 month-14 years) after diagnosis. Initially 17 localized and nine metastatic tumors were studied. Discriminant analysis was carried out on these cases and identified nuclear/cytoplasmic ratio and number of nuclei/mm2 as the significant discriminatory features. These were combined to derive a classification rule which was capable of correctly identifying localized and metastatic tumors in 92% of cases. The classification rule was applied subsequently to an additional five test cases, all of which were classified successfully. The failure of increased nuclear size and pleomorphism to correlate with malignancy in these tumors was confirmed. Tumors which metastasized had significantly greater gross diameters than localized lesions, but overlap existed. Mitotic counts were not a helpful discriminatory feature. Morphometry may be useful in improving histologic assessment of pancreatic islet cell tumor behavior.

Endothelial cells from porcine aorta and inferior vena cava have been harvested, using trypsin, EDTA or collagenase, and grown in tissue culture. Growth-behaviour, cytology, scanning and electronmicroscopy findings are reported. It is hoped that this technique will prove useful in the investigation of atherosclerosis.

Tumor tissue from a heterogeneous group of patients with clinically and histologically diagnosed islet cell tumors has been assessed for pancreatic polypeptide (PP) content using radioimmunoassay. Immunoreactive forms of PP, obtained by gel filtration of tissue extracts, were detected using antisera with different regional specificities. Normal pancreatic tissue contained one form of PP coeluting with human PP whereas, tumor tissue from patients with insulinoma, Zollinger-Ellison, and WDHA (watery diarrhea hypokalemic achlorhydric) syndromes contained, in addition, higher molecular weight forms of immunoreactive PP. Furthermore, a lower molecular weight form was detected in tumor tissue from a Zollinger-Ellison syndrome patient. The high molecular weight forms of immunoreactive PP were not recognized using a C-terminal-specific antiserum, whereas the smaller form was only detected using this antiserum. The variation in cross-reactivity observed with two antisera in this study emphasizes the limitations of using a single antiserum to detect molecular forms of peptide hormones, particularly those in islet cell tumors.

Thirty-one oesophageal rings from patients undergoing transection for varices were examined histologically for oesophagitis. Four cases showed neutrophil infiltration but all had recent oesophageal intubation. Fifteen patients had significant morphological epithelial changes of oesophagitis assessed by two sets of criteria. Only 4 of these patients (13 per cent) had no other likely causative factor such as recent sclerotherapy or recent insertion of a Sengstaken tube. Therefore there appears little evidence for oesophagitis as a major aetiological factor in bleeding oesophageal varices.

The nature of xenopsin immunoreactivity in mammalian antral G-cells has been reassessed. Xenopsin immunostaining was most intense in human antral G-cells, present in those of the dog and pig and not detected in guinea pig or rat tissues. Rigorous specificity controls for ionic binding of immunoglobulins to antral G-cell granules indicated that this mechanism was not responsible for xenopsin immunostaining. Preincubation of the xenopsin antiserum with xenopsin, human gastrin 1-13 and gastrin 2-17 completely abolished immunostaining at similar molar concentrations. Gastrin 34 was ineffective at much higher concentrations. These results infer that xenopsin-immunoreactivity in antral G-cells resides in the N-terminal region of gastrin 17. Examination of the primary structures of xenopsin and the N-terminal regions of some mammalian gastrins reveals a hitherto unrecognized homology.

Oral glucose tolerance tests were carried out on 51 men with atherosclerotic peripheral vascular disease, none of whom were known diabetics or had suffered recent myocardial infarction. The plasma insulin and blood sugar responses were compared with 47 age and sex-matched controls. There was no significant difference in obesity between the two groups. The patient group showed an increased plasma insulin response with a delay in return to fasting levels, and the blood sugar response was similar. These results suggest that hyperinsulinaemia and hyperglycaemia are often associated with atherosclerosis, and may have a role in its aetiology.