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Biomedical subjects

A Macdonald

Publications and source records attributed to A Macdonald.

At least 73 records · Page 4Linked to original sources
PubMed1989

Controlled trial of heater probe treatment in bleeding peptic ulcers.

A prospective randomized controlled trial of endoscopic heater probe therapy in bleeding peptic ulcers was performed to determine whether probe therapy can reduce rebleeding rates. Of 630 patients endoscoped for suspected upper gastrointestinal haemorrhage over a 16-month period, 166 (26 per cent) were found to have a peptic ulcer. Either minor or no stigmata of recent haemorrhage were found in 115 patients at the time of endoscopy. A single peptic ulcer with either active haemorrhage or a visible vessel was found in 51 patients, 43 of whom were entered into the trial. There were eight exclusions: four were inaccessible, one was a torrential haemorrhage and three were excluded for non-technical reasons. Patients were randomized to receive either heater probe (n = 20) or sham (n = 23) therapy. In actively bleeding ulcers, immediate haemostasis was achieved following probe therapy in 14 of 18 patients (78 per cent) compared with none of 21 having sham treatment (P less than 0.002). No rebleeding occurred in the probe therapy group (n = 20) compared with rebleeding in five of 23 sham treated patients (P = 0.05). Urgent surgery for haemostasis was required in three of the five sham treated patients who rebled. It is concluded that heater probe therapy may be effective in reducing rebleeding rates in peptic ulcers accessible to the endoscope.

Clinical Trials as Topic↗
PubMed1989

Rebound nocturnal hypersecretion after four weeks treatment with an H2 receptor antagonist.

Daytime intragastric pH, fasting and meal stimulated serum gastrin and nocturnal acid output were studied in eight male duodenal ulcer patients before, during and two days after completing nizatidine 300 mg nocte (20:00 h) for four weeks. Median nocturnal acid output (mmol/10 h) decreased during treatment to 11.6 (range 0.4-26.7) compared with pretreatment value of 39.4 (9.8-91.2); median acid inhibition 77% (p less than 0.01) which was strongest between 24:00 and 04:00 h. Two days after discontinuing treatment, nocturnal acid output increased to 74.1 (11-181). Compared with the pretreatment value this represents median rebound hypersecretion of 77% (p less than 0.05), caused by increased H+ concentration and volume of secretion. Overall median daytime intragastric pH (09:00-21:00 h) was unchanged on the final day of treatment and two days after completing therapy, compared with the pretreatment values. Fasting serum gastrin measured between 09:30 and 10:00 h and the integrated gastrin response to an OXO breakfast taken out at 10:00 h were also similar during and after treatment, compared with pretreatment values. The rebound nocturnal hypersecretion may be relevant to the high ulcer relapse rates after stopping H2 receptor antagonists.

Adult↗
PubMed1988

Twin birth and adult psychiatric disorder. An examination of the case records of the Maudsley Hospital.

We compared the general distribution of diagnoses in 20,895 patients at the Maudsley Hospital with that of 504 patients born twins, including 117 twins where the co-twin had died before the age of 15. Significant differences in diagnostic distribution were found in the co-twin-dead compared with the co-twin-alive group; the former received diagnoses of schizophrenia, personality disorder, or substance abuse more often than the latter. While there were no overall differences between twins and non-twins, there were relatively more twins in the above three diagnostic groups. We suggest that the factors leading to the death of one twin are implicated in the later psychiatric morbidity of the survivor.

Adult↗
PubMed1986

The practical problems of nutritional support for children on continuous ambulatory peritoneal dialysis.

Data are presented from the results of 46 dietary assessments on 13 children on continuous ambulatory peritoneal dialysis (CAPD). The results demonstrate that even with dietary supplements, energy and protein intakes are generally inadequate. Nutritional requirements and possible reasons for suboptimal intake are discussed and potential methods for improving nutritional intake are suggested.

Adolescent↗
PubMed1985

Distribution of sodium valproate in normal whole blood and in blood from patients with renal or hepatic disease.

Sodium valproate at a concentration of 300 mumol/l in whole blood, partitioned between the red blood cell and plasma to produce a red blood cell/plasma partition ratio of 0.20. Red blood cell uptake was proportional to percent free drug in plasma and uptake was maximal when plasma was replaced by buffer, producing a red blood cell/buffer ratio of 0.87. Reduction of plasma protein binding by plasma dilution, by increasing the total sodium valproate plasma concentration, or by renal or hepatic disease in 24 patients, caused a predictable rise in red blood cell uptake of drug. The red blood cell represented a relatively small compartment for free sodium valproate in blood, however uptake of the drug into this compartment increased considerably in states of reduced plasma protein binding. Because the concentration of drug in the red blood cell reflects free drug concentration in plasma, the red blood cell may serve as an indicator of free drug changes in blood.

Adult↗
PubMed1984

Antibodies to liver-specific lipoprotein in children with chronic liver disease due to "autoimmune" chronic active hepatitis, cystic fibrosis, and alpha 1-antitrypsin deficiency.

Antibodies to a liver-specific lipoprotein complex (LSP) were determined by radioimmunoassay in the sera of 65 children with possible chronic liver disease. Thirteen had "autoimmune" chronic active hepatitis (CAH), 21 alpha 1-antitrypsin deficiency PiZ (alpha 1-ATD), all having significant liver disease, while 10 of 31 children with cystic fibrosis (CF) had abnormal biochemical tests of liver function, six having cirrhosis. Sera from 12 (92%) of 13 untreated CAH patients contained detectable anti-LSP antibodies, the highest titres occurring in those with anti-liver/kidney microsomal or smooth muscle antibodies. Titre of anti-LSP antibodies correlated with piecemeal necrosis of periportal hepatocytes in liver biopsies, but not with standard biochemical tests of liver function or serum immunoglobulin concentrations. The incidence of LSP antibodies fell as liver damage improved with immunosuppressant therapy, being positive in 18 of 26 sera from children in whom the transaminases were still above normal, but positive in only two of 20 in whom transaminase values were within the normal range (chi 2 = 16, p less than 0.001). Sera from two of 31 patients (6%) with CF contained anti-LSP antibodies as did sera from six of 21 patients with alpha 1-ATD. Antibody concentrations were lower than in CAH, and in alpha 1-ATD the presence of anti-LSP could not be correlated with the presence or absence of piecemeal necrosis on liver biopsy. Our data suggest that autoimmune mechanisms involving antibody to hepatocyte membrane components have a role in the pathogenesis of chronic liver disease in autoimmune CAH in children as in adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Intracranial tuberous sclerosis in infancy.

Transfontanelle sonograms and CT scans of the brain were obtained in 2 infants with tuberous sclerosis. Each modality showed typical subependymal nodules in both infants, as well as a large mass adjacent to the foramen of Monro in one of them; in the other, peripheral cortical tubers were clearly outlined with CT but not detected by ultrasound.

Humans↗
PubMed1983

Immune responses in patients with obstructive jaundice of infancy. Anti-LSP and Clq binding in sera.

To investigate possible involvement of immune responses in the pathogenesis of obstructive jaundice in infancy we measured antibody to liver specific lipoprotein (LSP) by radio immunoassay and immune complexes by their ability to bind C1q in sera from 16 patients with extrahepatic biliary atresia and 16 with neonatal hepatitis and 13 age matched controls. Anti-LSP was present in 6 of 16 with preoperative biliary atresia and 6 of 16 with hepatitis. Mean percentage C1q bound was higher in hepatitis (22 SD 15%) than preoperative biliary atresia (11.1 SD 2.3%). Nine of 16 hepatitis patients had elevated C1q binding as compared with 1 of 16 with biliary atresia. The highest value for anti-LSP and C1q binding were found in sera from patients with histologically severe hepatitis and hepatitis associated with specific viral or bacterial causes. Anti-LSP was significantly raised 5 months post-operatively in all of 6 patients with biliary atresia and poor biliary drainage but only 2 of 5 survivors. Elevated C1q binding was detected in 6 of 7 with poor drainage and 1 of 7 survivors at the same stage. Anti-LSP and C1q binding fell in 4 patients with neonatal hepatitis on recovery. These findings suggest that immunological mechanisms, possibly involving antibody to hepatocyte membrane components and immune complexes, may be involved in the pathogenesis of progressive liver disease in biliary atresia.

Antigen-Antibody Complex↗
PubMed1981

Correlation of intrahepatic pressure with collagen in the Disse space and hepatomegaly in humans and in the rat.

In 70 alcoholic patients the amount of collagen in the space of Disse was compared, using an electron microscopic graded score, to the height of the intrahepatic pressure. A highly significant correlation was found between the amount of collagen and intrahepatic pressure in the group as a whole (r = 0.84; p < 10(-6)), as well as in subgroups of 30 alcoholic patients with normal livers or steatosis (r = 0.83; p < 10(-6)), 9 patients with alcoholic hepatitis (r = 0.81; p < 0.01), and 31 with cirrhosis (r = 0.86; p < 10(-6)). A nonparametric correlational analysis for the complete group also showed a significant relationship (rho = 0.85; p < 10(-6)) between collagen scores and intrahepatic pressure. In 60 patients hepatocyte surface area was measured in the biopsies. In these, hepatocyte surface area significantly correlated with intrahepatic pressure (r = 0.68; p < 10(-7)). No correlation was found between intrahepatic pressure and fat, alcoholic hyalin, or terminal hepatic vein sclerosis. Only with necrosis (r = 0.38; p < 0.001) and inflammation (r = 0.29; p < 0.05) was there a significant relationship with intrahepatic pressure. Chronic ethanol administration for 4 wk in liquid diets to young Wistar rats produced a 50% hepatomegaly due to an increase in hepatocyte size. Intrahepatic pressure in the rats receiving alcohol (19.3 +/- 2.3 mmHg) was significantly higher than in the controls on sucrose (10.4 +/- 0.9 mmHg) (p < 0.01). A highly significant correlation was found between hepatocyte surface area and intrahepatic pressure (r = 0.70; p < 0.005). There was no increase in collagen in the Disse space in these animals. Therefore, hepatomegaly in the absence of an increase in collagen in the Disse space may result in increased intrahepatic pressure. These studies may indicate a sequence of events: hepatomegaly, portal hypertension, and collagenization in the Disse space, which could occur in alcoholic liver disease.

Alcoholism↗
PubMed1977

Effects of blood glucose levels on aspirin-induced gastric mucosal damage.

In female rats aspirin-induced gastrin mucosal damage was increased and glycoprotein synthesis decreased by fasting and by insulin administration. Glucose added to the drinking water during the fasting period reduced mucosal damage and increased glycoprotein synthesis to control levels. Alloxan diabetes did not affect mucosal damage or glycoprotein synthesis. Alloxan diabetes plus insulin restored blood glucose levels to normal, and susceptibility to aspirin damage and glycoprotein synthesis were also normal. Alloxan diabetes plus fasting restored blood glucose levels to normal but increased aspirin-induced mucosal damage and reduced glycoprotein synthesis. In vitro incubation of gastric mucosal homogenates showed that diburyryl cyclic AMP and theophylline inhibited glycoprotein synthesis but dibutyryl cyclic GMP had no significant effects. The importance of an adequate supply of glucose to the gastric mucosa and the effects of cyclic nucleotides on glycoprotein synthesis are discussed.

Adrenal Cortex Hormones↗
PubMed1975

Effects of fasting, stress and drugs on gastric glycoprotein synthesis in the rat.

1 The relationship between gastric mucosal damage and synthesis of gastric glycoproteins, as measured by the rate of incorporation of N-acetyl-[3H]glucosamine, was investigated in rats after fasting and restraint stress and a single administration of aspirin (200 mg/kg, orally), phenylbutazone (200 mg/kg, orally), prednisolone (200 mg/kg, orally), or adrenaline (2 mg/kg, i.p.). In one experiment, the effects of aspirin and phenylbutazone on carbohydrate content of the glycoproteins were also determined. 2 Restraint stress, phenylbutazone and aspirin resulted in acute gastric mucosal erosions in some of the rats. Adrenaline produced severe sub-mucosal haemorrhage, but no erosions or ulceration, while prednisolone and fasting gave no gross pathology. 3 The rate of incorporation of N-acetyl-[3H]glucosamine into glycoproteins was decreased after all treatments except adrenaline. In the groups receiving restraint stress, aspirin or phenylbutazone, the decreases were more marked in rats which developed erosions than in those with no gastric pathology. 4 Aspirin and phenylbutazone also produced changes in the carbohydrate content of the glycoproteins, the effects again being greater in the rats which developed erosions. 5 The results are discussed in the context of a possible association between erosion formation and glycoprotein synthesis and it is proposed that inhibition of mucus glycoprotein biosynthesis may be one mode of action of stress and drugs in causing gastric mucosal damage.

Animals↗