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Biomedical subjects

B Melgaard

Publications and source records attributed to B Melgaard.

At least 19 recordsLinked to original sources

Branched chain enriched amino acid versus glucose treatment of hepatic encephalopathy. A double-blind study of 65 patients with cirrhosis.

We studied the effects of infusion of a branched chain enriched amino acid mixture versus glucose on acute hepatic encephalopathy in patients with cirrhosis. Sixty-five patients were randomly treated with 1 g/kg per day of an amino acid mixture with 40% branched chain contents (32 patients), or isocaloric glucose (33 patients) for a maximum of 16 days. The regimens further included glucose infusion to a total of 26.5 kcal/kg per day and lactulose. The patients took part in the study for 5-6 days. In each group 17 patients woke up. In the amino acid group eleven died and four developed renal failure. In the glucose group ten died, three developed renal and two respiratory failure, and one remained encephalopathic. The coma score worsened in three of the patients who died in the amino acid group, but in all patients who died in the glucose group. The negative nitrogen balance on entry reversed in the amino acid group, but not in the glucose group. Thus, the branched chain enriched amino acid supplement did not change the prognosis for wake-up, but had other effects on the cerebral state and on nitrogen homeostasis.

Adult

Hypothalamic-pituitary and thyroid function in chronic alcoholics with neurological complications.

Endocrinological tests were performed in 14 chronic alcoholic men with signs of intellectual impairment and/or peripheral neuropathy. All had been abstinent from alcohol for at least 1 month. Basal serum growth hormone (GH) was consistently increased in only one patient whereas the GH responses to insulin hypoglycemia stimulation was normal in all patients. Thyroid function values (T4, T3, rT3, TSH) were normal in all patients whereas baseline serum prolactin values were significantly increased in alcoholics as compared with a control group. In a combined TRH- and GnRH-stimulation tests, GH-responses were also normal whereas TSH and prolactin responses were blunted or absent in about half of the patients, the responses correlating significantly (p less than 0.01). It is concluded that disturbances in the hypothalamic-pituitary axis may occur in chronic alcoholics with nervous impairment independently of the physical deterioration, which often is associated with chronic alcoholism.

Adult

Regional cerebral blood flow in chronic alcoholics measured by single photon emission computerized tomography.

Regional cerebral blood flow (CBF) was measured by single photon emission computerized tomography of inhaled 133-Xe in 20 chronic alcoholic men. Mean CBF was 51 ml/(100 g x min) compared with 53 ml/(100 g x min) in 20 normals. Reduced cerebellar blood flow correlated both to structural abnormalities seen on CT scan and to cognitive dysfunction. Slight abnormalities of the regional CBF was observed in the alcoholics. They had a higher incidence of regional low flow areas than a control group. Low flow areas were found in frontal and posterior parts of the brain not only in patients with atrophia, but also in patients without CT abnormalities, suggesting neuronal dysfunction. The occurrence of regional low flow areas was associated with the severity of alcoholism, cerebral atrophy and intellectual impairment.

Adult

Nervous system damage and nutritional factors in chronic alcoholics.

Dietary habits in 45 chronic alcoholics were assessed by the dietary history method, and plasma albumin and serum transferrin. These variables as well as clinical findings did not indicate general malnutrition, but a moderate deficiency in folate intake was found. There was no correlation between the nutritional variables and central and peripheral nervous system function investigated by neuroradiological, neuropsychological, and neurophysiological methods. Transketolase and thiamine-pyrophosphate effects were measured in a subgroup of alcoholics and compared to a control group. No differences were found and there was no correlation to central nervous system impairment. These findings do not support the hypothesis that nervous system damage found in chronic alcoholics is of nutritional etiology.

Adult

Vitamin B-12 and folate function in chronic alcoholic men with peripheral neuropathy and encephalopathy.

Forty-six male alcoholics hospitalized with polyneuropathy or intellectual impairment were studied after at least 2 wk of alcohol abstention. Neurological evaluation included neurophysiological examination of the sural nerve and tibial nerve, neurophysiological examinations, and CT-scanning of the brain. Alcohol and vitamin intakes were quantified by the interview method. Vitamin B-12 and folate status included examinations of peripheral blood and bone marrow aspirate, plasma vitamin B-12, plasma and erythrocyte folate, formiminoglutamic acid excretion test (FiGlu), methylmalonic acid excretion, and deoxyuridine suppression test (dU) on phytohemagglutinin-stimulated peripheral lymphocytes. The liver function was assessed by galactose elimination capacity and plasma clearance of antipyrine. There was no hematological sign of folate or vitamin B-12 deficiency. About 8% had low plasma folate, while neither erythrocyte folate nor plasma vitamin B-12 were decreased. However, half of the patients had functional folate deficiency as determined by abnormal FiGlu or dU. Compared to the remaining patients, those with abnormal FiGlu or dU had significantly more abnormal neurophysiological tests, and lower folate intake. There was no correlation between FiGlu or dU and the quantitative liver function tests. It is concluded that 1) folate deficiency may contribute to the development of alcoholic polyneuropathy, 2) the classical parameters for folate deficiency (blood concentrations, peripheral blood, and bone marrow examinations) are not reliable in diagnosing folate deficiency and 3) functional tests like FiGlu and dU are necessary to diagnose folate deficiency in alcoholics.

Adult

Misonidazole neuropathy. A prospective study.

The frequency with which polyneuropathy developed was investigated in patients with cancer of the larynx and pharynx who participated in a double-blind trial of the radiosensitizing drug misonidazole. Fourteen of 36 patients receiving misonidazole (total dose of about 11 g/m2) developed neuropathy, while this occurred in only 2 of 34 patients in the placebo group. Vibration perception threshold increased in all patients who developed neuropathy, but also in 12 (5 misonidazole and 7 placebo treated) without other symptoms or signs of neuropathy. Pharmacokinetic studies of misonidazole revealed a correlation between development of neuropathy and a high 'peak plasma concentration/g misonidazole in each fraction' and especially a high 'area under plasma concentration curve/g misonidazole in each fraction'.

Adult

A cluster survey of mortality due to neonatal tetanus in Kenya.

Three house-to-house surveys were conducted in three different districts in Kenya, using a cluster survey technique for estimation of neonatal tetanus death rates. The results showed neonatal death rates of 10, 16 and 23 per 1000 livebirths and neonatal tetanus death rates of 6, 11 and 16 per 1000 livebirths respectively. A recall method based on interviews with women attending antenatal clinics gave much lower rates. The community surveys indicate a total neonatal tetanus death rate of 8 per 1000 livebirths and it is estimated that each year between 8000 and 12,000 children die in Kenya from this preventable disease.

Epidemiologic Methods

Creatine kinase BB release into cerebrospinal fluid after lateral ventricle cannulation.

Creatine kinase (CK) and creatine kinase BB isoenzyme (CK-BB) activities were measured in ventricular CSF obtained by lateral ventricle cannulation in patients suspected of normal pressure hydrocephalus. Lateral ventricle cannulation resulted in highly and variably elevated CK and CK-BB levels. The results emphasise the interference of these CK and CK-BB elevations in studies on the prognostic value of CSF CK and CK-BB levels in head trauma patients with respect to outcome.

Catheterization

Discordance between the cortisol response to insulin-hypoglycemia and 30-minute ACTH stimulation test in chronic alcoholic men.

An insulin hypoglycemia test and a 30-min ACTH stimulation test was performed in 10 chronic alcoholic men, who had been abstinent from alcohol for at least one month. Attenuated serum cortisol responses were found in six of the patients despite a normal ACTH test. Four patients showed normal responses to both the insulin hypoglycemia test and the short ACTH test. No correlation was demonstrated between the cortisol response and the severity of alcoholism, cerebral atrophy, and peripheral neuropathy. It is concluded that in chronic alcoholism the short ACTH test may fail in disclosing hypofunction of the integrated hypothalamic-pituitary-adrenocortical (HPA) axis as assessed with the insulin hypoglycemia test.

Adrenocorticotropic Hormone

Ataxia and cerebellar atrophy in chronic alcoholics.

Forty-five alcoholics were examined clinically and by CT scanning in order to evaluate the relationship between ataxia, cerebellar atrophy and peripheral neuropathy. A significant relationship was found between ataxia and cerebellar atrophy as well as between ataxia and peripheral neuropathy.

Alcohol Withdrawal Delirium

Symptoms and signs of polyneuropathy and their relation to alcohol intake in a normal male population.

In a normal population of 468 45-year-old males symptoms and signs of polyneuropathy were investigated and related to self-reported alcohol consumption and associated problems. Sensory disturbances in the feet were claimed by 3.4%, 5.8% had abolished Achilles tendon reflexes, and 7.7% increased vibratory perception thresholds. Significant correlations were found between persons with signs of neuropathy and persons with physical or social consequences of alcohol abuse.

Alcohol Drinking

Frequency, diagnosis, and prognosis of spinal cord compression in small cell bronchogenic carcinoma. A review of 817 consecutive patients.

A retrospective review of 817 consecutive patients with small cell bronchogenic carcinoma disclosed 29 cases of spinal cord compression (frequency, 3.5%). Twelve patients (group 1) presented with symptom of cord compression, whereas the remaining 17 patients (group 2) developed this complication during therapy. Clinical features differed in the two groups: pain was present in 83% of the patients in group 1 and in 47% of those in group 2. Pain preceded motor dysfunction in 75% and 12% of the two groups, respectively. Radiologic bone destruction of the spine was found in 11 of 12 patients in group 1 and in 3 of 16 patients in group 2. Myelography was performed in 8 patients in group 1 and in 14 patients from group 2. A complete block was found in seven and none of the patients in each of the two groups, respectively. Treatment with irradiation and/or laminectomy rarely resulted in a significant improvement of preexisting neurologic impairment but it frequently prevented the progression of symptoms, leading to preservation of sphincter control and ambulatory function in eight of nine and seven of eight patients, respectively. Careful evaluation is mandatory for patients presenting with back pain and radiographic evidence of bone destruction, as 11 of 26 such patients were found to have spinal cord compression. It is concluded that spinal cord compression presents in two distinct ways. One with early onset, pain, evidence of bone destruction, and complete myelographic block. The second is characterized by motor impairment with no evidence of bone destruction and only partial myelographic block. Treatment rarely ameliorates symptoms but prevents deterioration, making early diagnosis important.

Carcinoma, Bronchogenic