It has been suggested that obliterative vasculitis in the lung might mimic pulmonary embolism on a ventilationperfusion scan. The combined scans of six patients with breast cancer who had undergone radiotherapy to the chest wall, which can induce pulmonary vasculitis, were therefore examined. Eleven of the 12 scans showed perfusion defects with ventilation-perfusion mismatch on the irradiated side. Special care is needed in interpreting the lung scans of patients who have received an appreciable tissue dose of radiation to the lungs; mismatch need not indicate pulmonary embolism.
Pulmonary permeability was assessed using the technique of 99mTc (technetium-99m) diethylene triamene pentacetic acid (DTPA) aerosol transfer in 10 patients who had antibodies to human immunodeficiency virus (HIV) and were non-smokers and in 20 HIV antibody positive smokers. Five patients had Pneumocystis carinii pneumonia (PCP) proved by transbronchial lung biopsy; four were non-smokers and one a smoker. Two findings emerged: patients with PCP had greater epithelial permeability than non-smokers and smokers; and the permeability curves were monophasic in smokers and non-smokers, but biphasic in patients with PCP. The biphasic curve observed is indicative of diffuse alveolar damage and might be useful to predict PCP in patients with antibodies to HIV who have normal chest radiographs. As the study was of only five patients with PCP, however, further studies are necessary to confirm this observation.
A 54 year old man presented with features of acute hepatitis and the nephrotic syndrome. A diagnosis of active syphilis was only made by chance after extensive investigation. Syphilis should be considered in the differential diagnosis of both acute hepatitis and the nephrotic syndrome occurring separately as well as together.
The case of a 42-year-old West Indian woman with meningococcal septicaemia and steroid-responsive immune complex disease is reported.
Out of 250 patients with renal failure, seven (2.8%) treated by regular haemodialysis alone (four) or given cadaveric allografts (three) later showed recovery of function of their own kidneys lasting from one to four years. In the patients receiving haemodialysis alone recovery was easily recognised from their serum creatinine concentrations, but in those with transplants recovery was discovered unexpectedly during radionuclide scanning. These findings suggest that recovery of renal function may be more common than generally recognised, which should be borne in mind when beginning renal replacement treatment and particularly when contemplating bilateral nephrectomy.
Solitary parathyroid adenomas were correctly located before surgery in 20 out of 21 cases by using 201mT1 and 99mTc in a subtraction technique. The technique was not useful in identifying hyperplastic parathyroid glands. The technique is recommended as a useful procedure before surgery for primary hyperparathyroidism.
Nine patients with stable angina (group 1) underwent maximal treadmill stress testing and thallium-201 (201T1) myocardial scintigraphy after intravenous propranolol hydrochloride, and after placebo. Though seven of the nine patients exercised longer after propranolol than after placebo, this difference did not reach statistical significance. Propranolol, however, significantly reduced the mean maximum rate pressure product. Comparison of the perfusion scans on and off propranolol showed that in 36 out of 90 of the myocardial segments recorded (nine patients, five segments scanned twice per patient), only one of the scans showed a defect. In 24 out of 36 of these the propranolol scan was negative, the defect appearing in the placebo scan. Defects present on both scans but differing significantly in size occurred in 22 out of 54 view pairs (nine patients, three views after exercise and three views after redistribution on propranolol and on placebo), and in 19 of these the smaller defect was seen in the propranolol scan. In one of the nine patients, the propranolol scan was normal (false negative), whereas defects corresponding to angiographically proven coronary artery lesions were seen on the placebo scan. Six patients (group 2) were maximally exercised after propranolol and then re-exercised to the same rate pressure product on placebo. Again 16 out of 60 of the segment pairs disagreed and in 10 of these the unmatched defect was present on the placebo scan. In 10 out of 14 discrepant view pairs, the smaller defect occurred on the propranolol scan. Thus in patients taking propranolol, negative results do not exclude coronary artery disease, and perfusion defects (if present) though accurately reflecting the presence of disease may underestimate its true extent.
Infarct size was estimated by cumulative creatine kinase MB isoenzyme (CKMB-r) release and by technetium 99m stannous pyrophosphate (TcPYP) scintigraphy in 27 patients with acute anterior myocardial infarction. In eight patients, scintigraphy showed a central area of reduced tracer uptake surrounded by a peripheral rim of increased TcPYP accumulation ("doughnut" pattern). This appearance occurred only in large infarcts and the maximal scintigraphic area (51.3 +/- 2.8 cm2, mean +/- SEM) in this group was significantly greater than that in the remainder (28.1 +/- 2.5 cm2). Correlation between CKMB-r and maximal scintigraphic infarct area was moderate in the whole group. Exclusion of patients, however, with "doughnut" scintigrams in which correlation was very poor, resulted in substantial improvement in the remainder. It is suggested that in the central regions of large "doughnut" infarcts, reduced blood flow hinders the efflux of CKMB from the centre causing an underestimate of infarct size. Pyrophosphate scintigraphy appears to be more accurate than CKMB release in measuring the size of these large anterior infarcts.
Nineteen healthy subjects were studied and 17 patients with gastric ulcer before and after ulcer healing with carbenoxolone. Gastric deoxytibonucleic acid (DNA) loss was measured as an index of epithelial cell turnover, and N-acetylneuraminic acid (NANA) content of gastric juice as an index of mucus secretion. In normal subjects there was a negative correlation (p less that 0-025) between gastric DNA loss and NANA secretion; the lower the cell turnover the higher the NANA production. In gastric ulcer patients DNA loss or turnover was significantly (p less than 0-01) higher than normal, and fell significantly (p less than 0-01) after four weeks' treatment with carbenoxolone when 16 of the 17 ulcers had healed. At the same time NANA output increased significantly (p less than 0-01). It is suggested that patients with gastric ulcer lose cells at a high rate, a state of affairs which is returned towards normal by carbenoxolone, thus allowing the epithelial cells to mature within the mucosa and produce more mucus.
The incidence of pulmonary embolism and deep vein thrombosis was measured in 50 matched pairs of patients undergoing common surgical procedures with preoperative and postoperative ventilation-perfusion lung scans and the fibrinogen uptake test. One patient in each pair was treated with intravenous dextran 70 and pneumatic leggings. The incidence of pulmonary embolism among the treated patients was significantly reduced from 24% to 8%, but the incidence of deep vein thrombosis was not significantly reduced (34% to 24%).
In a retrospective survey we found that five (8·5%) out of 59 women with giant-cell arteritis had a history of thyrotoxicosis. This was significantly higher than in a control group of patients. Giant-cell arteritis and thyrotoxicosis occurred simultaneously in two cases. Knowledge of this association is of clinical use and is further evidence for an immunological basis for giant-cell arteritis.
The conventional method of lung scanning detects defects of pulmonary artery perfusion. False positive results occur because regions of hypoventilation, such as are present in obstructive airways disease, also cause defects of perfusion. The converse is not true, however, as defects of perfusion continue to be ventilated. Thus in pulmonary embolism ventilation-perfusion discrepancy (normal ventilation and impaired perfusion) occurs.
We have assessed the clinical value of this discrepancy. Out of 18 patients with ventilation-perfusion discrepancy 14 had a final diagnosis of pulmonary emboli, whereas in none of the 34 patients without the discrepancy was this final diagnosis made. We conclude that combined ventilation-perfusion lung scanning distinguishes pulmonary emboli from other lung conditions such as asthma and bronchitis which cause impaired pulmonary perfusion. The false positive rate was only 4% overall and 7·7% in patients with perfusion defects.
Thrombosis in the deep veins of the legs commonly follows surgical operations but is often undiagnosed. The fibrinogen uptake test is an aid to its detection. Perfusion lung scanning after injection of labelled macroalbumin aggregates has advanced the diagnosis of pulmonary embolism.
Studies were carried out on 40 patients undergoing surgical operation to determine whether the results of the fibrinogen uptake test were correlated with those of ventilation-perfusion lung scanning. A statistically significant relationship was found: 18% of patients had small, clinically silent emboli.
Benorylate (4-acetamidophenyl 2-acetoxybenzoate) is a new esterified aspirin preparation whose antirheumatic properties are reported to be as good as those of aspirin. Gastrointestinal blood loss, measured with 51Cr-labelled red cells, during benorylate therapy was compared with that during therapy with soluble aspirin in 15 subjects, a simplified crossover procedure being used. Mean blood loss during benorylate therapy was 1·7 ml/day which was significantly less than that during therapy with soluble aspirin (5·1 ml/day; P <0·001). In 12 of the 15 patients blood loss with benorylate was less than 2·5 ml/day. Benorylate appears to be a definite improvement on current formulations of aspirin and should be a useful drug for the treatment of patients with chronic rheumatic disorders.
One hundred and two patients with clinical signs indicating a possible diagnosis of deep vein thrombosis were studied with the fibrinogen uptake test and phlebography to assess the reliability of the test as a means of diagnosing established venous thrombosis. The test gave a correct diagnosis in 78% of the 85 legs shown to contain thrombus by phlebography and only 19 (10%) false-negative results in the 195 legs examined. The duration of the symptoms, the administration of anticoagulants, and mild leg swelling did not affect the accuracy of the test. Very old thrombus, phlebographically more than 11 days old, was associated with an increased false-negative rate.
The fibrinogen uptake test is accurate enough to make it a valuable method of clinical investigation.
A hippuran renogram pattern of the type usually interpreted as indicating urinary tract obstruction was seen in acute tubular necrosis and was present both in the oliguric and in the diuretic phase. It seems that in acute renal failure the renogram does not distinguish urinary tract obstruction from intrinsic renal disease.
Total protein and deoxyribonucleic acid (dna) were measured in small-intestinal washings from rats with normal and high rates of dna (or cell) loss. There was a significant relationship between the loss of these two substances. Preparations of isolated viable epithelial cells contained much less protein in relation to dna than did the intestinal washings. It was calculated that only 8 to 15% of the protein lost by washing the rat small intestine arose from the intracellular protein of exfoliated epithelial cells. The rest was derived from extracellular sources.
Protein and dna loss from small-bowel mucosa was measured in six patients. The ratio of protein to dna was similar to that found in the rats. The mean protein loss from 5 cm of human upper small intestine was 956 μg per min or 1·4 g per 24 hours. By calculation, total protein loss from the whole small intestine of man was about 84 g per day, about 10 g coming from within exfoliated cells and the rest arising from extracellular sources. The normal intestine must reabsorb most of this material.
Large numbers of cells are shed from small intestinal mucosa but they are so rapidly destroyed that there is little direct information about their morphological types. Material obtained by washing the human and rat small intestine was immediately processed and examined by light and electron microscopy. Small intestinal epithelial cells could not be identified by light microscopy but were readily recognized—by the presence of brush borders—using the electron microscope. Eighty to 85% of the cells from both rats and patients with normal small intestinal mucosa were intestinal absorptive cells. This was also the case in four patients with the coeliac syndrome and flat intestinal mucosa. These findings provide further support for the view that measurements of cell loss using intestinal washing techniques and the DNA-loss method, reflect predominantly small intestinal epithelial cell loss and turnover.