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Biomedical subjects

O K Refvem

Publications and source records attributed to O K Refvem.

8 recordsLinked to original sources

Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2,438 m (8,000 ft) altitude.

The arterial oxygen tensions (Pa,02) in chronic obstructive pulmonary disease (COPD) patients travelling by air, should, according to two different guidelines, not be lower than 7.3 kPa (55 mmHg) and 6.7 kPa (50 mmHg), respectively, at a cabin pressure altitude of 2,438 m (8,000 ft). These minimum in-flight Pa,O2 values are claimed to correspond to a minimum Pa,O2 of 9.3 kPa (70 mmHg) at sea-level. The authors have tested whether this limit is a safe criterion for predicting severe in-flight hypoxaemia. The authors measured arterial blood gases at sea-level, at 2,438 m and at 3,048 m (10,000 ft) in an altitude chamber at rest and during light exercise in 15 COPD patients with forced expiratory volume in one second (FEV1) <50% of predicted, and with sea-level Pa,O2 >9.3 kPa. Resting Pa,O2 decreased below 7.3 kPa and 6.7 kPa in 53% and 33% of the patients, respectively, at 2,438 m, and in 86% and 66% of the patients at 3,048 m. During light exercise, Pa,O2 dropped below 6.7 kPa in 86% of the patients at 2,438 m, and in 100% of the patients at 3,048 m. There was no correlation between Pa,O2 at 2,438 m and pre-flight values of Pa,O2, FEV1 or transfer factor of the lung for carbon monoxide. In contrast to current medical guidelines, it has been found that resting arterial oxygen tension >9.3 kPa at sea-level does not exclude development of severe hypoxaemia in chronic obstructive pulmonary disease patients travelling by air. Light exercise, equivalent to slow walking along the aisle, may provoke a pronounced aggravation of the hypoxaemia.

Aged↗

Acute sarcoid arthritis: occurrence, seasonal onset, clinical features and outcome.

In a 2-yr prospective follow-up study of patients presenting clinically with possible reactive arthritis (ReA), 17 (9%) of the patients turned out to have acute sarcoid arthritis (SA). The number of new cases of SA per year was 2.9/100,000 persons in the city of Oslo between 18 and 60 yr of age. The onset of SA clustered in the spring. All the SA patients presented with bilateral ankle joint involvement and bilateral hilar lymphadenopathy, and ten (59%) presented with the triad of erythema nodosum, arthritis and lung involvement. A prospective follow-up after 104 weeks showed complete remission of arthritis in all 17 cases of SA. The total duration of arthritis [median (range)] was 11 (2-107) weeks. Erythema nodosum was mild and transient in all cases. At week 104, the lung and hilar manifestations had resolved. We conclude that the outcome of SA appeared favourable. Bilateral ankle joint involvement, erythema nodosum and bilateral hilar lymphadenopathy found at the routine chest X-ray examination are important clues for the diagnosis of SA.

Adult↗

[Sudden unexpected death and near death among children with asthma].

During four winter months 1989-90, two children died suddenly from asthma, and one suffered a life threatening attack. A 20 months old boy with moderately severe asthma, just recovered from an adenovirus infection, was symptom free at a routine consultation less than 12 hours before death. He died suddenly after a spell of coughing. A six year old girl with severe but well controlled asthma received unknown quantities of inhaled nebulized salbutamol during a three day exacerbation. She died at home due to respiratory arrest. A 16 year old boy who attended the clinic sporadically had a severe uncontrolled attack of asthma. He inhaled at least 400 doses of salbutamol via a metered dose inhaler during the two days prior to a sudden respiratory arrest. He was successfully resuscitated. This paper addresses possible mechanisms underlying different types of severe attacks of asthma.

Adolescent↗

A scoring system on respiratory symptoms.

A method for quantitative recording of psychiatric symptoms has been modified for application to respiratory symptoms such as cough, attacks of breathlessness, wheezing and dyspnoea. The method was evaluated in a survey of 193 subjects without pulmonary disorders and 186 patients with pulmonary disorders. The average time taken to obtain scores for four symptoms was six minutes. Inconsistencies were few when the subjects selected statements about symptoms. Cough score discriminated between groups of healthy persons with various smoking habits. Wheezing score distinguished healthy persons from patients with obstructive lung disease more accurately than cough, attacks of breathlessness and dyspnoea score. Regression analyses showed that per score point of dyspnoea and cough the peak expiratory flow rate decreased by almost 12 and 7% of predicted, respectively.

Cough↗

Monoarthritis due to Mycobacterium chelonei.

A 48-year-old woman with infection of the tendon sheaths and proximal interphalangeal joint by Mycobacterium chelonei is described. Antibiotic therapy was not administered, and the patient recovered spontaneously.

Arthritis, Infectious↗

Altered prednisolone pharmacokinetics in patients treated with rifampicin.

The pharmacokinetics and protein binding of prednisolone were studied in 7 patients before and after 3 weeks of rifampicin therapy. The elimination half-time for prednisolone decreased by 45 +/- 8.1% (p less than 0.01), and the total body clearance of prednisolone increased by 91 +/- 26% (p less than 0.01). The area under the time-concentration curve (AUC) of total (free plus protein-bound) prednisolone decreased by 48 +/- 7.3% (p less than 0.01) and of free, unbound prednisolone by 57 +/- 9.8% (p less than 0.01). The reduction in AUC was greater for free than for total prednisolone (p less than 0.05) mainly due to the non-linear nature of prednisolone protein binding. There was no significant change in the volume of distribution. Because of the marked reduction in total and especially free prednisolone, the dosage should be adjusted accordingly if prednisolone and rifampicin are prescribed concomitantly.

Adult↗

Changes in prednisolone pharmacokinetics and protein binding during treatment with rifampicin.

Prednisolone pharmacokinetics and protein binding were studied after i.v. injection before and after three weeks of rifampicin therapy. The elimination half-time for prednisolone fell by 44.8% +/- 8.1% (p less than 0.01) and the area under the time-concentration curve by 47.5% +/- 7.3% (p less than 0.01). The reduction in area under the time concentration curve of free, non-protein bound prednisolone was 56.5% +/- 9.8% (p less than 0.01). The reduction in AUC was greater (p less than 0.05) for free prednisolone than for total prednisolone because of non-linear protein binding of prednisolone. The total body clearance of prednisolone increased from 73.5 +/- 14.6ml/min to 142.7 +/- 35.8ml/min (p less than 0.01). There was no change in the volume of distribution of prednisolone. Because of the marked reduction in the extent of bioavailability of total, and especially free, prednisolone, dosage adjustments should be made accordingly if prednisolone and rifampicin are prescribed concomitantly.

Adult↗