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Biomedical subjects

T Johnsen

Publications and source records attributed to T Johnsen.

34 records · Page 2Linked to original sources
PubMed1981

Infectious mononucleosis and peritonsillar abscess.

A 10-year material of infectious mononucleosis and concomitant peritonsillar abscess from an ENT department has been analysed retrospectively. The incidence of this combination was one per cent among all patients admitted for infectious mononucleosis. Only one patient showed signs of relative upper airway obstruction. All four patients improved shortly after stab incision. In diagnostic considerations and treatment it is important to bear in mind the rare combination of infectious mononucleosis and peritonsillar abscess.

Adolescent↗
PubMed1980

Bromocriptine concentration in saliva plasma after long-term treatment of patients with Parkinson's disease.

Salivary and plasma concentrations of bromocriptine (BCT), a dopamine agonist, were measured by gas chromatography in four patients with Parkinson's disease. All the patients had been on mono-therapy with BCT for years, and during the 3 weeks prior to the investigation they received constant but individually different dosage regimens. Paired samples of pure, parotid, serous saliva and of blood were collected hourly during one eight hour dose interval. The concentrations of BCT in saliva were very low and there was a ten-fold range in the areas under the salivary and plasma concentration/time curves. It is concluded that in clinical practice measurement of BCT in saliva is not suitable for exact estimation of the plasma concentration of BCT. Using the measured salivary pH and the plasma BCT concentration, calculations based on the Henderson-Hasselbalch equation showed that the assumption of about 99% plasma protein binding of BCT best fited the observed concentrations of BCT in saliva.

Aged↗
PubMed1980

Paramyotonia congenita (von Eulenburg) in Denmark.

Paramyotonia congenita (von Eulenburg) (PMC) is described in a Danish family in seven generations and 39 persons. PMC has not previously been described in Denmark and an epidemiological description of the family is given. The diagnostic difficulties versus hyperkalemic familial periodic paralysis with myotonia, adynamia episodica hereditaria and myotonia congenita (Thomsen) are discussed.

Adolescent↗
PubMed1979

Insulin receptors, insulin secretion, and glucose disappearance rate in patients with periodic hypokalaemic paralysis.

In a study of 6 male patients with periodic hypokalaemic paralysis (PHP), we found reduced insulin binding to monocytes as compared with a group of 25 normal subjects (P less than 0.1). The decreased insulin binding was caused by the decreased binding affinity. During induction of paralysis by a prolonged oral glucose load, one patient showed 24-h variations in the insulin binding to monocytes not differing from those observed in normals. After iv administration of glucose, these patients showed an elevated initial insulin response compared with the normals (P less than 0.1). However, the iv glucose tolerance tests revealed normal glucose disappearance rates. We conclude that changes in insulin receptor binding do not appear to be of pathophysiological significance for eliciting the parese attacks in PHP. However, the increased insulin response, following carbohydrate intake, might be of significance in the generation of paralytic attacks in patients with PHP.

Adolescent↗
PubMed1978

Skeletal muscle characteristics and carbohydrate metabolism after glucose loading in hypokalaemic periodic paralysis.

A prolonged glucose load was administered to four patients with hypokalaemic periodic paralysis and four healthy control sujbects. Muscle ATP and CP concentrations as well as lactate dehydrogenase, hexokinase and phosphorylase activities were similar in those two groups, but succinate dehydrogenase was approximately 50% higher in the control muscles. Muscles fibre composition was almost identical in the two groups, whereas patients had a higher degree of capillarization. Complete muscle weakness was produced in all patients, accompanied by hypokalaemia. Glucose loading resulted in elevated insulin levels and a minor rise in blood glucose level was seen in the patients compared to the control subjects. Glucose loading decreased hexokinase activity in controls, but increased this in the patients. At similar times, muscle and blood lactate levels and blood pyruvate values were generally higher in the patients over the course of the experiment. Initial glycogen concentrations were higher in patients, but glucose loading did not result in greatly increased glycogen values. These data suggest that patients with hypokalaemic periodic paralysis have an enhanced metabolism of carbohydrates and that insulin seems to be an important factor leading to the onset of muscle weakness.

Adenosine Triphosphate↗
PubMed1977

Endogenous insulin fluctuations during glucose-induced paralysis in patients with familial periodic hypokalemia.

Endogenous insulin production in patients with familial periodic hypokalemia has not previously been studied during induced attacks. The serum insulin, serum potassium, and blood glucose concentrations were measured in six patients with familial periodic hypokalemia during six attacks of paralysis induced by long-lasting glucose stimulation. The same parameters were measured in four normal subjects under the same conditions. There was no difference in insulin response or in blood glucose between the two groups. Basal insulin levels showed no difference. There was no correlation between the occurrence of the attack and the serum insulin level in the patients. All the patients responded by severe paralysis and hypokalemia.

Adult↗
PubMed1977

Trial of the prophylactic effect of diazoxide in the treatment of familial periodic hypokalemia.

Five patients suffering from familial periodic paralysis with hypokalemia (FPP) were exposed to standard paralysis induction trials which elicited total paralyysis and hypokalemia. In all cases the serum potassium fell to or below 2.6 mmol/1. After being pre-treated with diazoxide for 72 h, the same five patients were exposed to the same standardized paralysis induction procedure. None of them developed any demonstrable symptoms or signs of paralysis. In one the serum potassium dropped to 3.2 mmol/1, but in all the others the levels were higher. The serum glucose level was significant higher (P less than 0.01), the serum insulin level was significant lower (P less than 0.01) when induction of paralysis was attempted under diazoxide cover than during the untreated stimulation phase. Three patients were put on prophylactic diazoxide medication. After a few months, without paralytic episodes or other prophylactic drugs, adaptation to the diazoxide occurred and the previous, frequent paralytic episodes returned in unchanged severity. This experimental prophylactic effect of diazoxide supports the hypothesis that the glucose deposition in muscles is a major step in eliciting the parese attacks in FPP.

Acute Disease↗
PubMed1977

Effect upon serum insulin, glucose and potassium concentrations of acetazolamide during attacks of familial periodic hypokalemic paralysis.

In four patients with periodic hypokalemic paralysis paralytic attacks were induced in the untreated state and later, after the patients had been treated with acetazolamide. There was a distinct, clinically favourable effect of acetazolamide upon the length as well as the severity of paralysis. The maximum fall in serum potassium was less marked during acetazolamide therapy. After treatment all four patients showed significantly reduced serum levels of glucose and insulin during induced attacks of paralysis as compared with the levels obtained during paretic attacks in the untreated state. These findings indicate that the prophylactic effect of this drug does not relate merely to metabolic acidosis. The hypothesis is advanced that the lower serum insulin and glucose levels might represent reduced absorption which would amount to an indirect prophylactic action.

Acetazolamide↗
PubMed1976

A new standardized and effective method of inducing paralysis without administration of exogenous hormone in patients with familial periodic paralysis.

A prolonged glucose loading test is described. When used in five patients with familial periodic paralysis it brought them into a state of massive hypopotassaemic paralysis at the first attempt, without the use of exogenous hormone. Three normal persons were subjected to the same glucose loading without exhibiting hypopotassaemia or muscular weakness. There were no essential differences in serum glucose levels between the two groups of individuals. The efficacy of previous methods of inducing paralysis, hormonal as well as non-hormonal, is reviewed, and the advantages of this new method are pointed out.

Blood Glucose↗
PubMedDate not supplied

Mondini cochlea in Pendred's syndrome. A histological study.

In the past the Mondini malformation of the cochlea has been described histologically on the basis of findings in one temporal bone from a patient with confirmed Pendred's syndrome. The present study presents the histological examination of six temporal bones from 5 patients with confirmed Pendred syndrome. The characteristic Mondini cochlea was found in all preparations. It is concluded that the inner ear malformation in Pendred's syndrome is more in accordance with Mondini's original description than in other syndromes in which a Mondini-like cochlea has been described.

Aged↗