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Biomedical subjects

M Hillbom

Publications and source records attributed to M Hillbom.

At least 55 records · Page 3Linked to original sources
PubMed1990

Alcohol abuse and brain infarction.

Recent findings on the relation between alcohol abuse and ischaemic brain infarction are reviewed. Much of the association has hitherto been explained by the effects of confounding factors such as smoking. Alcohol increases blood pressure in both hypertensive and normotensive subjects and alcohol induced hypertension enhances the risk of both hemorrhagic and ischaemic strokes. Analysis of case histories shows that alcohol abuse has precipitated cerebral embolism in conjunction with cardiac diseases including alcoholic cardiomyopathy and paradoxical embolism due to deep vein thrombosis via atrial septal defect. Among young adults, falling when intoxicated with alcohol has caused traumatic dissection of the carotid artery and consequent brain infarction. Alcohol may predispose individuals to cerebral embolism, thrombosis and ischaemia via its effects on the coagulation cascade, platelet count and function and contractility of the cerebral vessels. Further studies are needed to prove that these mechanisms are significant and to identify any other mechanisms which may mediate the risk associated with alcohol abuse. On the basis of current data, alcohol should be considered as an independent risk factor for ischaemic cerebral infarction in young adults.

Alcohol Drinking↗
PubMed1989

The effects of earlier surgery and shorter bedrest on the outcome in patients with subarachnoid haemorrhage.

The effects of earlier surgery and shorter bedrest on the outcome in 338 consecutive patients with subarachnoid haemorrhage admitted within five years to a primary emergency hospital were evaluated. Mortality from rebleeds diminished more than surgical mortality increased. Shortened bedrest did not increase the number of rebleeds in patients not operated on. The combined mortality from rebleed and surgery decreased by 32% and the overall mortality by 21%.

Activities of Daily Living↗
PubMed1988

Fatal encephalitis caused by a bat-borne rabies-related virus. Clinical findings.

The clinical findings are described in the first reported European case of fatal encephalitis of bat origin caused by a rabies-related virus. A bat zoologist developed the symptoms of rabies 51 days after his last exposure to a bat bite. The clinical disease of 23 days duration was a combination of the paralytic and 'furious' forms of rabies. Serial BAEP and EEG recordings, CT and MR scans of the brain, as well as CSF findings, demonstrated severe ascending destruction of the brain. An unusual progression from isolated brainstem death to cortical brain death occurred. Neuropathologically, the brain showed severe lytic changes. The presence of rabies-related virus antigens in brain smears was shown using a panel of fluorescent antibodies. The virus was inoculated into and isolated from suckling mice. The virus had a close resemblance to European bat rabies isolates, which belong to the group of rabies-related viruses. Of particular concern is whether the virus can spread from bats to terrestrial animals and whether the European type of bat rabies constitutes a danger to man.

Adult↗
PubMed1988

Concentration-time profiles of ethanol and acetaldehyde in human volunteers treated with the alcohol-sensitizing drug, calcium carbimide.

1. The disposition kinetics of ethanol and its toxic metabolite acetaldehyde were investigated in 10 healthy male volunteers who ingested 0.25 g kg-1 ethanol after an overnight fast. This dose of ethanol was given 2 h after they swallowed a tablet of either calcium carbimide CC (50 mg), a potent inhibitor of low Km aldehyde dehydrogenase (ALDH), or placebo according to a single-blind crossover design. 2. The pulmonary blood concentrations of ethanol and acetaldehyde were estimated indirectly by means of a gas chromatographic method modified for analysis of end-expired breath. This non-invasive sampling technique allowed replicate determinations at 15 min intervals. 3. The distribution volume of ethanol (V) was 0.64 +/- 0.023 1 kg-1 after CC and 0.68 +/- 0.026 l kg-1 after placebo treatment (P greater than 0.05). The zero order slope of the blood-ethanol decay profile (ko) decreased by about 5% when low Km ALDH was inhibited. The elimination of ethanol from the body (V X ko) was 1.9 +/- 0.051 mmol kg-1 h-1 after CC compared with 2.11 +/- 0.056 mmol kg-1 h-1 in placebo control experiments (P less than 0.001). The area under the ethanol concentration time curve (0----180 min) increased after CC treatment implying a change in clearance. 4. The disposition of acetaldehyde was markedly different in subjects pretreated with CC. The peak blood-concentrations, estimated by analysis of breath, ranged from 40-242 mumol l-1 compared with 1.7-6.5 mumol l-1 after placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1988

Platelet thromboxane formation capacity after ethanol withdrawal in chronic alcoholics.

Collagen-, arachidonate- and ADP-stimulated platelet thromboxane B2 (TXB2) formation was studied in platelet-rich plasma (PRP) of 14 alcoholics, 7 of whom had a biopsy-verified alcoholic fatty liver. On admission for detoxication, the alcoholics showed decreased platelet count and aggregability (p less than 0.001) as compared to nonalcoholic healthy controls. Platelet TXB2 formation was decreased (p less than 0.01), if PRP was stimulated by arachidonate, but not if it was stimulated by ADP or collagen. In contrast, 9-14 days after ethanol withdrawal platelet TXB2 formation had increased to markedly higher levels than those seen in nonalcoholic controls (p less than 0.01), if PRP was stimulated by ADP, but not if it was stimulated by arachidonate or collagen. Skin bleeding time was found to be prolonged (p less than 0.05) on admission in alcoholics having fatty liver, but it normalized within 2 weeks after ethanol withdrawal. We conclude that the effect of ethanol withdrawal in alcoholics on platelet TXB2 formation is influenced by platelet count, aggregability and the agonist used to induce platelet aggregation.

Adenosine Diphosphate↗
PubMed1987

Effects of vitamin E therapy on ethanol-induced changes in platelet aggregation, thromboxane formation, factor VIII levels and serum lipids.

A transient increase in platelet thromboxane formation has been observed in non-alcoholics during acute ethanol intoxication and in alcoholics shortly after ethanol withdrawal. Whether these effects are related to the generation of free radicals and lipid peroxidation was investigated by using vitamin E as a free radical scavenger and inhibitor of lipid peroxide formation. The results demonstrate that a high dose of vitamin E (1800 IU) taken daily by non-alcoholic men slightly (P less than 0.05) decreases aggregation-associated platelet thromboxane formation during ethanol oxidation. Likewise, vitamin E prevents the ethanol-induced increase (P less than 0.01) in factor VIII coagulant activity. These observations suggest that the enhancement of platelet thromboxane formation and factor VIII coagulant activity by acute ethanol ingestion may be related to stimulated lipid peroxidation. By contrast, similar effects of vitamin E were not found in alcoholics shortly after ethanol withdrawal suggesting other mechanisms for their platelet hyperreactivity.

Adult↗
PubMed1987

High-dose estrogen-progestagen oral contraceptives: a risk factor for aneurysmal subarachnoid hemorrhage?

A 10-year follow-up (1970-79) of a defined general population (n = 159 200) of middle-aged (born in 1911-40), urban, native Swedes, revealed that the prevalence rate of subarachnoid hemorrhage was 2.8 times higher in females than in males. This was mainly due to an accumulation of non-hypertensive aneurysmal subarachnoid bleeds in women born in the period 1932-40. The cases were significantly (P less than 0.001) overrepresented among divorced women, with relative risks of 1.89, 0.98 and 0.63 for divorced women, married women and spinsters (never married), respectively. Since high-dose estrogen-progestagen oral contraceptives have largely been used by the younger members of this study cohort, it may be speculated whether the observed substantial excess prevalence rate of subarachnoid hemorrhage with saccular aneurysm, not reported previously, represents a cohort effect unexpected after the introduction of low-dose oral contraceptives.

Adult↗
PubMed1987

Associations between brain infarction, diabetes and alcoholism: observations from the Gothenburg population cohort study.

The relationship of brain infarction to diabetes and alcoholism was studied in a 10-year follow-up of a defined general population (n = 159,200) of native, urban Swedes. Confounding bias due to high age and lower socioeconomic conditions was reduced with a new epidemiological technique which was used instead of conventional mathematical multivariate procedures. We observed 6-13-fold and 4-6-fold excess rates of subjects with brain infarction among diabetics (P less than 0.001) and alcoholics (P less than 0.001), respectively. In addition, diabetes and alcoholism were often found to be associated. The distribution of these diseases varied with the topography of the city and demography of the population. Hence, in future studies into the pathogenesis of brain infarction, study samples should be made homogeneous not only from a clinical, but also from an epidemiological point of view. We conclude that diabetes, alcoholism and both in combination, associate with brain infarction.

Adult↗
PubMed1987

Urinary excretion of 2, 3-dinor-6-keto prostaglandin F1 alpha and platelet thromboxane formation during ethanol withdrawal in alcoholics.

The excretion of 2,3-dinor-6-keto prostaglandin F1 alpha, a major urinary metabolite of prostacyclin, and the formation of thromboxane B2, a stable metabolite of thromboxane A2, by platelets stimulated by adenosine diphosphate, were studied in alcoholics, who had been admitted for detoxification. Once prolonged heavy drinking had stopped, platelet count and thromboxane formation, calculated either per 10(7) platelets or per litre of blood, significantly increased (p less than 0.05), while the skin bleeding time and urinary excretion of the metabolite of prostacyclin decreased (p less than 0.05). The balance between prostacyclin and thromboxane therefore seemed to favour the excretion of prostacyclin while it shifted to favour thromboxane formation about a week later.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effects of a small dose of ethanol and calcium carbimide-induced acetaldehyde intoxication on human platelet aggregation, associated thromboxane formation and urinary excretion of 2,3-dinor-6-keto prostaglandin F1 alpha.

We studied ADP-induced platelet aggregation, associated thromboxane B2 (TXB2) formation, urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto prostaglandin F1 alpha (2,3-dinor-6-keto PGF1 alpha) and formation of malondialdehyde in 10 healthy volunteers after ingestion of a small dose of ethanol (0.25 g per kg of body weight) and calcium carbimide (50 mg). Platelet aggregation in platelet-rich plasma (PRP) was suppressed (p less than 0.05) by ethanol, but no change occurred in platelet TXB2 formation. Ingestion of calcium carbimide caused significant elevations in blood acetaldehyde (p less than 0.001) and ethanol (p less than 0.05) levels, but acetaldehyde did not influence platelet aggregability or the aggregation-associated TXB2 formation. However, calcium carbimide per se significantly (p less than 0.05) elevated TXB2 formation. No effects were found on plasma malondialdehyde levels and urinary excretion of 2,3-dinor-6-keto PGF1 alpha. These observations indicate that a small dose of ethanol attenuates platelet aggregation without any significant effect on aggregation-associated TXB2 formation. By contrast, ingestion of calcium carbimide per se may enhance TXB2 formation.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Elimination kinetics of ethanol and acetaldehyde in healthy men during the calcium carbimide-alcohol flush reaction.

In a crossover design experiment, we investigated the elimination kinetics of ethanol and acetaldehyde during the calcium carbimide (CC)-alcohol flush reaction. Ten healthy men swallowed a tablet of calcium carbimide (50 mg) or placebo and about 2 hours later drank 0.25 g/kg ethanol within 5 min. The pulmonary blood concentrations of ethanol and acetaldehyde were estimated indirectly by analysis of end-expired alveolar air. The onset of facial flushing and associated cardiovascular response coincided with the peak concentrations of ethanol and acetaldehyde in blood. The speed of absorption of alcohol was faster in subjects treated with CC. A smaller volume of distribution of ethanol was evident after pretreatment with CC; 0.636 L/kg compared with 0.675 L/kg after placebo. The rate of elimination of ethanol from blood was about 5% slower in subjects given the CC tablet. The disposition kinetics of acetaldehyde were markedly different when aldehyde dehydrogenase (ALDH) was inhibited. The maximum blood-levels of acetaldehyde ranged from 40-242 microM compared with 1.7-6.5 microM in the placebo control experiments. The elimination half-life of acetaldehyde after CC treatment ranged from 18-31 min. Our results do not support a significant role of acetaldehyde in regulating in-vivo metabolism of ethanol in humans.

Acetaldehyde↗
PubMed1987

Platelet function during acetaldehyde intoxication in healthy male volunteers.

ADP-induced platelet aggregation, associated thromboxane B2 (TXB2) formation and urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto prostaglandin F1 alpha (PGI2-M) were studied in healthy male volunteers after ingestion of ethanol (0.25 g per kg of body weight) and calcium carbimide (50 mg). Platelet aggregation was suppressed (p less than 0.05) by ethanol, but no changes were observed in platelet TXB2 formation. Ingestion of calcium carbimide caused a significant elevation in blood acetaldehyde (p less than 0.001) and ethanol (p less than 0.05) levels, but acetaldehyde did not influence platelet aggregation or TXB2 formation. However, calcium carbimide per se elevated TXB2 production (p less than 0.05). Ethanol and acetaldehyde appeared not to have any significant effect on urinary excretion of PGI2-M.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Combined effect of a small dose of ethanol and 36 hr fasting on blood-glucose response, breath-acetone profiles and platelet function in healthy men.

Six healthy men drank 0.25 g/kg ethanol after an overnight fast (12 hr) and the same dose was consumed again after a further 24 hr fasting. The concentration of ethanol and acetone in end-expired alveolar air was determined at 15 min intervals for 3 hr after ethanol intake by a gas chromatographic method. Before drinking and 30 and 90 min thereafter blood samples were taken for determination of glucose, ADP-induced platelet aggregation and associated thromboxane (TXB2) formation. The breath-ethanol time course was virtually identical after 12 and 36 hr fasting and the peak concentration occurred 30 min after drinking. Fasting for 36 hr caused a 20-fold increase in breath-acetone levels. Under these conditions, i.e. after 12 and 36 hr fasting, the hypoglycemic response to ethanol intake was 10 and 25%, while the antiketogenic response was 38 and 16%, respectively. ADP-induced platelet aggregation and associated TXB2 formation showed wide interindividual variations, but no definite effects of ethanol, hypoglycemia or metabolic acidosis were observed. Platelet function was not significantly influenced by ingestion of a small dose of ethanol after prolonged fasting.

Acetone↗