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Biomedical subjects

F E Preston

Publications and source records attributed to F E Preston.

At least 235 records · Page 13Linked to original sources

Cellular hyperviscosity as a cause of neurological symptoms in leukaemia.

Six patients with various forms of leukaemia had neurological signs and symptoms associated with an extremely high white blood cell count and increased whole blood (but not plasma) viscosity. All were treated by leucapheresis with an Aminco Celltrifuge. Rapid and complete reversal of all symptoms occurred in three patients and partial recovery in one. One patient died shortly after leucapheresis and another (from cerebral intravascular coagulation) two days later. It is concluded that a cellular hyperviscosity syndrome may cause neurological dysfunction in patients with extremely high white cell counts, and that leucapheresis, in carefully selected patients, can be an effective method of treatment.

Adult↗

Elevated beta-thromboglobulin levels and circulating platelet aggregates in diabetic microangiopathy.

beta-Thromboglobulin levels and platelet-aggregate ratios were determined in blood-samples from healthy control subjects and from diabetic patients with and without microangiopathic complications. Patients with diabetic microangiopathy had significantly elevated beta-thromboglobulin levels and also reversible platelet aggregates. In nine newly treated diabetics blood-glucose control was associated with a significant fall in plasma beta-thromboglobulin. Since beta-thromboglobulin is a platelet-specific protein the results indicate that diabetic microangiopathy is associated with evidence of platelet activation and that this may be influenced by the degree of biochemical control.

Aged↗

Platelet aggregation in patients with peripheral vascular disease.

Platelet aggregation has been studied in 28 control subjects and 46 patients with peripheral vascular disease. The platelets from the patients with peripheral vascular disease were significantly more sensitive to the aggregating effects of adenosine diphosphate and adrenaline than those from the control group (P less than 0.001). In addition, spontaneous platelet aggregation was observed in vitro in several of the vascular patients; this response was not apparent in the control group. Increased platelet aggregation could add to the vascular impairment in the unoperated subject and might also play a part in premature graft failure. Platelet function studies should perhaps be included as a routine in the assessment of patients with peripheral vascular disease.

Adenosine Diphosphate↗

Myelomatosis and the hyperviscosity syndrome.

Eleven patients are described in whom myelomatosis was complicated by the laboratory and clinical features of the hyperviscosity syndrome (HVS). The myeloma type was IgA in nine and IgG3 in two. In those patients with IgA myeloma the HVS was related to the presence of high molecular weight complexes in the serum. Remission of clinical features was obtained in all patients by plasma exchange. Clinical improvement coincided with reduction of whole blood viscosity and in those patients with IgA myeloma, with a parallel reduction of the high molecular weight complexes. The relationship between the IgA complexes and blood viscosity has been examined by physicochemical analysis of purified IgA monomer and polymers and evidence is presented to show that the IgA polymer has a higher intrinsic viscosity and axial ratio than the larger IgM molecule. The significance of these observations is discussed.

Blood Viscosity↗

Characterization of serum fibrinogen and fibrin fragments produced during disseminated intravascular coagulation.

The fibrinogen and fibrin degradation products (FDP) in serum samples taken from nine patients with suspected disseminated intravascular coagulation have been characterized using a method of immunoprecipitation followed by sodium dodecyl sulphate polyacrylamide gel electrophoresis. Aall of the serum samples contained a fragment with the same electrophoretic mobility as fibrinogen fragment X, while the majority also had evidence of fragments with similar mobility to fibrinogen fragments Y and D. In eight of the nine serum samples there was strong evidence of the D-dimer fragment that is released by plasmin lysis of crosslinked fibrin. Also present in all but one of the samples were fragments of higher molecular weight than fibrinogen which were probably soluble, non-clottable, factor XIIIa induced crosslinked derivatives of fibrinogen. These results suggest that during disseminated intravascular coagulation thrombin and activated factor XIII act upon fibrin(ogen) to form complexes that are subsequently lysed by plasmin to produce soluble crosslinked derivatives of fibrin.

Blood Coagulation Tests↗

Hyposplenism in inflammatory bowel disease.

Splenic function was assessed in 35 patients with ulcerative colitis and 20 patients with Crohn's disease. Hyposplenism was diagnosed if there were Howell-Jolly bodies in the peripheral blood film or if there was prolongation of clearance from the peripheral blood of injected 51-Cr-labelled heat-damaged red blood cells. Thirteen of the patients with ulcerative colitis had hyposplenism as compared with only one patient with Crohn's disease. Conversely, heat-damaged red cell clearance values faster than the normal range were found in six out of the 20 patients with Crohn's disease. Four patients with hyposplenism and ulcerative colitis developed life-threatening septicaemia in the early postcolectomy period, two of these being further complicated by disseminated intravascular coagulation.

Colectomy↗

Relationship between splenic size and splenic function.

The rate of clearance of 51Cr labelled heat-damaged red cells from the circulation has been compared with the dimensions of the posterior scan of the spleen in 79 cases including nine controls. A strong negative correlation was found between the clearance half-time and the parameters of the scan but, as there was a large variation about the regression line, in the assessment of hyposplenism determination of the rate of clearance of heat-damaged red cells cannot be replaced by the easier determination of spleen size by scanning.

Erythrocyte Aging↗

Oral methionine loading as a cause of acute serum folate deficiency: its relevance to parenteral nutrition.

Oral methionine supplements (8.0 g daily for 4 days) were given to five normal volunteers who continued to eat their usual diet. This treatment resulted in a significant fall in serum folate concentration. Three days after the end of treatment concentrations had not completely returned to control values. The fall in concentration was prevented by giving oral folic acid supplements. It is suggested that folic acid supplements should be given to patients who are receiving intravenous infusions of amino acid mixtures.

Administration, Oral↗

Heparinised clotting factor concentrates in patients with Christmas disease and liver disease.

Evidence has been sought of activation of the coagulation system in two groups of patients following the infusion of two heparinised clotting factor concentrates. No changes were detected in 13 patients with mild hepatic dysfunction. In six studies on patients with Christmas disease induced abnormalities occurred in only one. Activation of the coagulation mechanism did not occur in another individual who had received the same batch of material.

Blood Cell Count↗

A simple technique for studying immunoglobulin synthesis by normal and malignant plasma cells in vitro.

Plasma cells from human marrows are saturated with C-14 labelled amino acids, harvested and recultured in unlabelled growth medium. The appearance of radioactivity in the growth medium then provides a simple and rapid measure of protein synthesis. The secreted radio-labelled material is characterized by isoelectric focusing and autoradiography in acrylamide gels, a technique which has advantages over established serological methods.

Autoradiography↗

Cerebral involvement with disseminated intravascular coagulation in intestinal disease.

Over a two-and-a-half-year period at the Sheffield Royal Infirmary, six patients developed disseminated intravascular coagulation as a serious complication of intestinal disease. There was clinical evidence of cerebral involvement in all six patients, and small vessel thrombi were demonstrated in the brains of all three cases examined post mortem. Where the true significance of the cerebral disorder was not recognised, this led to delay in the diagnosis with serious risk to the patient. In the single case in which the diagnosis was made early, the intravascular coagulation was completely reversed with heparin therapy.

Adult↗

A reassessment of vascular factors in relation to intravascular coagulation.

Sural nerve biopsy was performed in twenty-four diabetic patients, with clinical and electrophysiological evidence of diabetic neuropathy. Material from an autopsy case was also examined. Vessels plugged with fibrin were seen within nerve in nine cases. In three cases fibrin was observed tracking into the vessel wall and in four, older thrombus was observed in vessels. Areas of necrosis in nerve bundles were seen in two of the latter. In two patients there had been a preceding episode of intravascular coagulation. Fibrin deposition within small vessels could well play a part in damaging the diabetic nerve and a disturbance of the balance between deposition and removal by fibrinolysis could explain phasic variation in the symptoms of neuropathy.

Adult↗

Platelet abnormalities in diabetic peripheral neuropathy.

Abnormal platelet function has been demonstrated in 20 patients with diabetic peripheral neuropathy. The results are compared to those obtained from 19 matched diabetic patients with no clinical evidence of complications and 20 matched normal control subjects. Platelets from patients with diabetic neuropathy showed an increased sensitivity to the aggregating agents adenosine diphosphate and adrenaline. Spontaneous platelet aggregation was demonstrated in both groups of diabetic patients.

Adenosine Diphosphate↗

Serial changes in the coagulation system following clotting factor concentrate infusion.

Various parameters of the coagulation system have been monitored in patients with Christmas disease following the infusion of clotting factor concentrates. Significant reduction of clotting factor VIII and serum antithrombin III were observed in each of the five studies, whilst the plasma fibrinogen level fell in four subjects. The induced abnormalities were shortlived and there were no clinical sequelae. Further studies are required to assess the effects of similar concentrates in patients with liver disease.

Antithrombins↗