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Biomedical subjects

A M Peters

Publications and source records attributed to A M Peters.

At least 235 records · Page 13Linked to original sources
PubMed1986

Clinical experience with 99mTc-hexamethylpropylene-amineoxime for labelling leucocytes and imaging inflammation.

Hexamethylpropylene-amineoxime (HMPAO) forms a lipid-soluble neutral complex with 99mTc which is rapidly incorporated into leucocytes in vitro. In six patients with suspected or known inflammatory disease, a "mixed" leucocyte suspension isolated from 85 ml blood anticoagulated with acid-citrate-dextrose was labelled by 99mTc-HMPAO with a mean efficiency of 47% (SE2%), of which 78% (3) was taken up by granulocytes. Activity eluted more rapidly from other cell types in vitro than from granulocytes, which remained firmly labelled. Mean initial biodistribution of the label and granulocyte recovery in blood of 32% (8) at 30-40 min showed that the granulocytes were not significantly activated during labelling. All six patients were positive for inflammatory disease, as early as 30 min in five patients and at 3 h in the sixth; they all remained positive at 20-24 h. Four patients also received 111In-labelled "pure" granulocytes. In terms of detail, the 99mTc images were comparable or superior to the 111In images.

Adult↗
PubMed1986

Indium-111-labeled autologous leukocyte scanning in gastrointestinal graft versus host disease (GVHD).

The technique of scanning with indium-111 autologous leukocytes has been used to assess gastrointestinal graft-versus-host disease (GVHD) following allogenic marrow transplantation. In patients with active disease, abdominal scans showed extensive abnormal localization in the bowel, while in those whose disease was quiescent after responding to treatment, scans showed localized ileocecal involvement. Rectal histology showed excellent agreement with scanning in the diagnosis of GVHD, but in three of six cases with active disease underestimated disease severity. Indium-111 leukocyte scanning is a useful noninvasive technique for the diagnosis and assessment of gut GVHD.

Acute Disease↗
PubMed1986

Erythrocyte radiolabelling: in vitro comparison of chromium, technetium, and indium in undamaged and heat damaged cells.

The stability of the commonly used red cell radio labels chromium-51, indium-(111 or 113m), and technetium-99m, within intact red cells and stroma and their distribution within the cell were compared in undamaged and heat damaged red cells in relation to the clinical use of heat damaged cells in the assessment of splenic function. Chromium-51 labelled haemoglobin both in undamaged and heat damaged cells; indium predominantly labelled haemoglobin in undamaged cells but labelled stroma in heat damaged cells, even when the cells were labelled before heating; technetium-99m predominantly labelled haemoglobin in undamaged cells but only labelled stroma in heat damaged cells if these were heated before labelling. Indium was more firmly bound by stroma prepared from heat damaged cells, and technetium-99m showed a high rate of elution both from cells and stroma, although this rate was lower for heat damaged cells.

Chromium Radioisotopes↗
PubMed1985

Intrahepatic kinetics of indium-111-labelled platelets.

The intrahepatic kinetics of 111indium-labelled platelets have been studied using dynamic gamma camera scintigraphy immediately following injection. Platelets labelled in saline with 111In-oxine or 111In-acetylacetonate underwent rapidly reversible hepatic sequestration, indicating that they were "activated". Platelets labelled in plasma with 111In-tropolonate, however, did not display this phenomenon. On the assumption that plasma-labelled platelets display a normal initial bio-distribution, mean intrahepatic platelet transit time, as a factor of the transit time of 99m-Tc labelled red cells, was 1.45 +/- SE 0.12 (n = 6), implying the normal presence of a small intrahepatic platelet pool. Unlike the liver, transit through the spleen was not sensitive to the labelling medium; thus the mean intrasplenic transit time of plasma-labelled platelets was 9.3 +/- SE 0.7 min (n = 10), and of saline-labelled platelets 9.5 +/- SE 0.3 min (n = 8).

Blood Platelets↗
PubMed1985

The effects of thromboxane antagonism on the transit time of platelets through the spleen.

The spleen is well-known as a site for platelet pooling, although the mechanisms controlling intrasplenic platelet transit are essentially unknown. We tested the possibility that thromboxane A2 might be involved in this control by measuring intrasplenic platelet transit time in 10 subjects receiving a specific thromboxane A2 receptor antagonist (AH23848B; 70 mg; Glaxo Group Research Ltd), in 10 receiving aspirin (300 mg) plus dipyridamole (75 mg), and in 9 receiving placebo. All doses were administered 3 times daily commencing 4 days prior to transit time measurement. Mean intrasplenic platelet transit time was measured by monitoring the kinetics of equilibration of 111In radiolabelled platelets between blood and spleen following intravenous injection. There was no difference between the mean transit time in the 3 groups of subjects, lending no support to the hypothesis that thromboxane A2 is involved in the control of platelet traffic through the spleen.

Aged↗
PubMed1985

Clinical importance of enteric communication with abdominal abscesses.

The dynamics of leucocytes in abdominal abscesses were studied using indium-111 autologous leucocyte scanning in 30 patients. Thirteen patients showing enteric drainage of leucocytes on delayed scans were characterised by a lack of abdominal localising signs and a low detection rate by ultrasound (25%). By contrast, 16 of 17 patients without enteric drainage had abdominal signs, and in these patients ultrasound was associated with a higher detection rate (58%). Despite the presence of an enteric route of drainage for the abscess 10 of the 13 patients needed surgical intervention. These results help explain the wide variation in clinical presentation of abdominal abscesses; suggest that 111In leucocyte scanning should be the initial investigation in those patients without focal signs; and show that formal surgical drainage is needed in patients recognised as having enteric communication with abscesses.

Abdomen↗
PubMed1985

Specificity of indium-111 granulocyte scanning and fecal excretion measurement in inflammatory bowel disease--an autoradiographic study.

The validity of 111In granulocyte scanning and fecal excretion measurement, as a reflection of loss of cells into the gastrointestinal tract, was studied using an autoradiographic technique in 11 patients in whom 111In granulocyte scan and colonoscopy were carried out simultaneously. 111In granulocytes were injected 1.5-4 hr prior to colonoscopy, and intraluminal fluid, mucosal brushings, and colonic biopsies were collected during the colonoscopy. In two patients with no histological evidence of inflammatory bowel disease, and four patients with clinically and histologically inactive inflammatory bowel disease, no 111Indium was detected in fluid, brushing, or biopsies. In five patients with active disease, 85% of the 111In activity in colonic fluid was precipitated by low-speed centrifugation. Autoradiography confirmed that the label remained attached to whole granulocytes in colonic fluid and mucosal brushings. Studies on biopsies, at intervals up to 4 1/2 hr following labeled granulocyte injection, demonstrated labeled polymorphonuclear neutrophils (PMNs) on the inflamed epithelial surface, with occasional cells in crypt abscesses by 110 min. We conclude that the techniques of 111In granulocyte scanning and fecal counting in patients with IBD are specifically measuring cell loss; labeled PMNs are capable of migrating through the gastrointestinal mucosa, in active disease, within 2 hr of administration.

Autoradiography↗
PubMed1985

Splenic pooling of granulocytes.

The intrasplenic kinetics of granulocytes, isolated in plasma and labelled in plasma with 111In-tropolonate, have been studied in normal subjects, patients with negative studies for inflammatory disease and patients with positive studies, with the aim of identifying the nature of splenic activity seen after 111In-labelled granulocyte administration. Up to 40 min after injection, 111In activity was visible only in major blood vessels, liver and spleen, with slight, abnormal activity visible in most of those with positive scans. The time courses of uptake of hepatic and splenic activity were different, with liver activity rapidly reaching a plateau and splenic activity increasing mono-exponentially to a plateau achieved between 20 and 40 min. The clear difference between the shapes of the hepatic and splenic uptake curves and the magnitude of the splenic uptake rate constant indicated that splenic activity represented reversible uptake. The application of deconvolution analysis to the blood and splenic time-activity curves generated a splenic retention (or washout) curve consistent with dynamic exchange of granulocytes between blood and spleen. The slope of this curve indicated an intrasplenic granulocyte transit time of 9.3 (+/- SE 0.6) min. Taking splenic activity to be reversible, comparison of the 111In signal from the spleen 40 min after injection of 111In-labelled granulocytes with that given from the spleen after the injection of 111In-labelled erythrocytes (relative to their respective blood levels) indicated that intrasplenic granulocyte transit time was 14.4 (+/- SE 1.1) times that of erythrocytes. Based on actual erythrocyte time, this corresponds to a granulocyte transit time of 8.6-11.5 min, in close agreement with the estimate based on deconvolution analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Colitis↗
PubMed1985

The kinetics of 111indium distribution following injection of 111indium labelled autologous granulocytes in man.

The kinetics of human autologous granulocytes, separated and labelled with 111In without isolation from plasma, have been studied in subjects with and without sepsis with the aim of identifying the fate and sites of destruction of granulocytes in man. In subjects without inflammatory disease, 111In granulocyte recovery in faeces, urine and saliva over 4 d was less than 1% of the dose, so that the activity visualized by the gamma camera represented almost 100% of the dose. On images taken at 24 and 48 h, this activity was distributed between spleen, bone marrow and liver, with foci of additional abnormal activity in subjects with inflammatory disease. Splenic activity fell between 40 min and 24 h, consistent with the presence of a splenic granulocyte pool, but remained constant after 24 h. Since granulocyte clearance from the blood was predominantly completed by 24 h, the residual splenic activity at that time reflected splenic granulocyte destruction. In patients with sepsis, the fall in splenic activity was greater than in those without, implying diversion of granulocytes from splenic destruction to tissue utilization when inflammation is present. Bone marrow activity increased between 40 min and 24 h and then remained stable. Granulocytes that were extensively manipulated in saline prior to labelling failed to localize in marrow, suggesting that visualization of the latter reflected destruction of intact, normal granulocytes. Although the changes in splenic and marrow activities terminated at 24 h, at which time granulocyte clearance from blood was at least 80% completed, plasma 111In remained essentially unchanged between 40 min and 48 h at less than 5% of the dose, discounting it as the source of splenic and marrow activities.

Bone Marrow↗
PubMed1985

The kinetics of unmatched and HLA-matched 111in-labelled homologous platelets in recipients with chronic marrow hypoplasia and anti-platelet immunity.

The kinetics of homologous platelets, labelled in plasma with 111In-tropolonate, have been studied in five recipients with chronic marrow hypoplasia and severe thrombocytopenia, who were refractory to platelet transfusions as a result of alloimmunization. Mean platelet life span (MPLS), recovery, plasma 111In level and splenic and hepatic uptake kinetics were studied on two occasions, one using HLA-matched platelets and the other unmatched platelets. In each case, recovery of labelled platelets at 1 h post-injection and MPLS improved with HLA matching, although this improvement was highly variable. Only two of the five subjects would have derived any significant benefit from HLA-matched as compared with unmatched platelet transfusions. It was concluded that the need exists for additional cross-matching procedures, possibly related to platelet specific antigens, in patients who remain refractory to platelet transfusion.

Adolescent↗
PubMed1985

Quantification of the distribution of the marginating granulocyte pool in man.

The kinetics of autologous granulocytes, separated from whole blood and labelled with 111In-tropolonate with continuous maintenance in plasma, have been studied in man, using a gamma camera and computer, with the aim of quantifying the distribution of the marginating granulocyte pool (MGP). We have used 3 approaches: dynamic gamma camera imaging immediately following i.v. injection of labelled cells, comparison of the activity signal from 111In-granulocytes with that from previously injected 111In-labelled red cells and absolute quantification of 111In present in liver, spleen and blood. Deconvolution analysis of the hepatic and peripheral blood time activity curves indicated that hepatic granulocyte transit time was 2.5 +/- SE 0.14 min. By comparison with 111In red cells, hepatic transit time was calculated to be 7.4 +/- SE 0.82 that of red cells, which, assuming an hepatic red cell content of 6% that of the total red cell mass, is equivalent to a transit time of 1.8 min. By comparison with 111In red cells, lung granulocyte transit time as a factor of red cel transit time was 5.4 +/- SE 0.7 at 5 min and 2.5 +/- SE 0.13 at 40 min after granulocyte injection. Using these kinetic data, in combination with previously published values for splenic granulocyte transit time, it was calculated that, 5 min after injection, the MGP accounted for 54% of the total blood granulocyte pool (TBGP), was 90% filled, and was distributed between spleen (19%), liver (26%), lung (33%) and the remainder of the body (22%). At 40 min, the MGP accounted for 60% of the TBGP, had equilibrated with the circulating granulocyte pool (CGP), and was distributed between the spleen, liver, lung and remainder of the body according to the following respective percentages: 35, 25, 10 and 30. The total granulocyte contents of the spleen and liver calculated on the basis of the kinetic data were 21% and 22% respectively and in broad agreement with the values, 34 and 23% respectively, calculated from quantitative scanning. It was concluded that about 70% of the body's MGP was present in the spleen, liver and lung. If the MGP is itself 60% of the TBGP then only about 18% of the TBGP marginates in extra-hepatosplenopulmonary sites.

Cell Adhesion↗
PubMed1985

The kinetics of short-lived indium-111 radiolabelled platelets.

We have studied the kinetics of autologous 111In-labelled platelets in patients with reduced platelet life span (less than 4.5 d), most of whom were thrombocytopenic, and of homologous 111In-labelled platelets in patients with severe thrombocytopenia. Intrasplenic platelet transit time (t) was calculated by compartmental and deconvolution analysis. In patients with a mean platelet life span of less than a few h, compartmental analysis may not be valid and so only deconvolution analysis was applied. There was a close correlation between values of t given by the two approaches (r = 0.88, n = 18, P less than 0.001). In some patients with severely reduced mean platelet life span (MPLS), the deconvolved splenic platelet clearance curves appeared to approach an asymptote, the relative magnitude of which was indicative of the irreversible extraction fraction by the spleen of incoming platelets. In other patients with severely reduced MPLS resulting from abnormal intra-hepatic platelet destruction, the deconvolved splenic curves resembled the normal. The intrasplenic platelet transit time showed no clear relationship with other parameters. It was concluded that platelet pooling within the spleen is normal in patients with reduced platelet life span, including idiopathic thrombocytopenic purpura, even when the predominant site of destruction is the spleen, and that platelets are not delayed in transit through the spleen in preparation for their removal from the circulation and ultimate destruction.

Blood Platelets↗
PubMed1985

In vivo assessment of granulocyte migration to diseased bowel in Crohn's disease.

It has been suggested, on the basis of impaired granulocyte migration to skin windows, that there is a fundamental granulocyte defect in Crohn's disease. In vitro tests of granulocyte function have, however, failed to confirm this. We have studied granulocyte migration to inflamed bowel in Crohn's disease using a new approach which utilises dynamic gamma camera imaging after injection of 111In labelled autologous granulocytes. In 20 of 22 studies there was rapid migration to diseased bowel, compatible with no migration delay. Only two patients showed delays in migration of 12 and 15 minutes respectively, but neither had any clinical characteristics to distinguish them from the other 20 patients. This study shows that the majority of patients with Crohn's disease in relapse have rapid granulocyte migration to diseased bowel and provides evidence against a significant migration defect in this condition.

Cell Movement↗
PubMed1985

111Indium autologous granulocytes in the detection of inflammatory bowel disease.

Indium leucocyte scanning and measurement of faecal Indium leucocyte excretion are techniques which have recently been introduced for assessing patients with inflammatory bowel disease. The methodology has recently been made more specific for acute inflammation by labelling pure granulocytes rather than the mixed leucocyte preparation. To determine the accuracy of this modified technique in detecting inflammatory bowel disease, we have prospectively compared Indium granulocyte scanning and faecal In granulocyte excretion with rectal histology and contrast bowel radiology as screening procedures in 100 patients with suspected inflammatory bowel disease. Thirty three patients were shown to have inflammatory bowel disease - 24 with Crohn's disease and nine with ulcerative colitis or indeterminate colitis. Overall the respective sensitivities for detecting inflammatory bowel disease were 97% for faecal Indium granulocyte excretion, 94% for Indium granulocyte scanning, 79% for radiology and 70% for rectal histology. The superiority of In granulocytes over radiology and rectal histology in detecting inflammatory bowel disease was, in the main, due to the difficulty in diagnosing Crohn's with conventional techniques. Although three of the patients with ulcerative colitis and indeterminate colitis had normal sigmoidoscopic appearances - all had abnormal rectal histology. No patient with a non-inflammatory bowel disorder had a positive In granulocyte scan or a raised faecal excretion. These results show that investigations using In granulocytes are accurate in identifying inflammatory bowel disease and offer important advantages over conventional procedures for detecting Crohn's disease.

Colitis, Ulcerative↗
PubMed1985

Indium 111 autologous leucocyte scanning in lobar pneumonia and lung abscesses.

Indium 111 leucocyte scanning was used to examine the kinetics of granulocyte localisation in five patients with lobar pneumonia and four patients with lung abscess. Lung abscesses showed dense accumulation of labelled granulocytes within four hours of injection. In contrast, in all cases of lobar pneumonia granulocytes failed to accumulate over a period of up to 24 hours despite evidence of adequate perfusion and of uptake in inflammation elsewhere. These results suggest that the recruitment of granulocytes to lobar pneumonia may be terminated early in its clinical course.

Cell Movement↗
PubMed1985

Pulmonary platelet kinetics in asthma.

Platelets produce a range of bronchoconstrictor mediators. Measurements of plasma factors have implicated platelet activation in allergic asthma, and sensitised guinea pigs challenged with ovalbumin show pulmonary platelet aggregation accompanying bronchoconstriction. To investigate this further we injected autologous platelets labelled with indium 111 and red cells labelled with technetium 99m into three young volunteers with atopic asthma and three non-asthmatic volunteers and, after equilibration of platelets between blood and splenic pool, monitored lung 99mTc and 111In activities continuously. Comparison with the corresponding activities in blood samples allowed calculation of pulmonary platelet to red cell transit time ratio (tp/tr). This ratio was 0.9, 1.02, and 0.98 in the non-asthmatic subjects compared with 1.04, 0.97, and 1.17 in the asthmatic subjects. This argues against the existence of an intrapulmonary platelet pool in normal subjects; transpulmonary transit time was slightly prolonged in one asthmatic subject. Bronchial challenge with Dermatophagoides pteronyssinus was performed in the asthmatic subjects and monitoring continued for a further 30 minutes. Antigen induced falls in FEV1 of 20-50% were accompanied by small decreases in the 111In but not in the 99mTc lung signal. In line with this tp/tr fell to 0.89, 0.89, and 1.05. Antigen induced bronchoconstriction was therefore not accompanied by intrapulmonary platelet accumulation. Platelet survival was normal at 10.2 days in both groups of subjects.

Adult↗
PubMed1985

The splenic extraction ratio of antibody-coated erythrocytes and its response to plasma exchange and pulse methylprednisolone.

Splenic blood flow was measured in a series of normal subjects and patients with connective tissue diseases by measuring the rate of equilibration and the partition of 111In-labelled autologous platelets between blood and spleen. These data were used to quantify the role of splenic blood flow in determining the splenic clearance of IgG coated erythrocytes (IgG-RBC) from the circulation. Previous studies have interpreted the clearance rates of IgG-RBC only in terms of splenic reticuloendothelial function. Splenic blood flow was increased in seven of eight patients with systemic lupus erythematosus (SLE), six of 10 patients with rheumatoid arthritis (RA) and in all five patients with essential mixed cryoglobulinaemia (EMC) compared with a series of thirteen normal subjects. Expressing the rate constant of clearance of IgG-RBC as a fraction of splenic blood flow gave a value for the 'extraction ratio' of IgG-RBC (a specific measurement of reticuloendothelial function, corrected for splenic blood flow). Normal splenic extraction ratio of IgG-RBC was calculated to be 32%. All the patients with SLE and with EMC had reduced extraction ratios (in seven out of 13 patients less than 10%). In RA the extraction ratio tended to be normal (average 27.3%) but variable (9-59%). Following plasma exchange in nine patients, a significant increase in IgG-RBC extraction ratio (average of 39% with respect to pre-exchange values, P less than 0.05) was found. In contrast there was no significant change in extraction ratio following pulse methylprednisolone therapy in a further nine patients. Although the rate constant of clearance of IgG-RBC decreased by an average of 33% (P less than 0.01) in the latter group, it was matched by an equal decrease of splenic blood flow (average 37%, P less than 0.01) and so extraction ratio showed no change. These data indicate that quantification of splenic reticuloendothelial function requires measurement of both IgG-RBC clearance and of splenic blood flow.

Adolescent↗