Functional and histologic picture of steroid-induced myopathy in chronic obstructive pulmonary disease.

Decramer, Marc; Bock, V. de; Dom, René

doi:10.1164/ajrccm.153.6.8665061

Cited by 246 publications

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“…In agreement with FERNANDEZ-SOLA et al [11], but in contrast to DECRAMER et al [12], no differences in parameters of qualitative muscle morphology were found between CORT-and CORT+ patients in the present study. Although comparable qualitative morphological features were assessed, the current study cannot readily be compared with the latter study, in which a higher dose of corticosteroids was used (14.2 mg methylprednisolone) and a predominantly type II muscle was analysed.…”

Section: Discussionsupporting

confidence: 93%

“…Although comparable qualitative morphological features were assessed, the current study cannot readily be compared with the latter study, in which a higher dose of corticosteroids was used (14.2 mg methylprednisolone) and a predominantly type II muscle was analysed. Furthermore, the subgroup of patients in the study by DE-CRAMER et al [12] that showed myopathic morphological features in the muscle biopsy, suffered from severe skeletal and respiratory muscle weakness. Unfortunately, in the present study, skeletal muscle function was not assessed.…”

Section: Discussionmentioning

confidence: 97%

“…In a recent human study histological abnormalities were observed in biopsies of the quadriceps femoris muscle of COPD patients with severe steroid-induced myopathy [12]. Alterations in qualitative morphology were found, including increased variation of fibre diameters, increased numbers of central nuclei and increased amounts of connective tissue in between muscle fibres.…”

mentioning

confidence: 97%

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Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Pouw¹,

Lang²,

Gosker³

et al. 2000

Eur Respir J

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Both abnormalities in high energy phosphate metabolism and a decreased oxidative enzyme capacity have been reported in skeletal muscle of stable chronic obstructive pulmonary disease (COPD) patients. The first aim of this study was to investigate whether these findings are present in anterior tibialis muscle and whether or not they are associated. Abnormalities in mitochondrial structure and function as well as signs of myopathy have been found during corticosteroid treatment. The second aim of this study, therefore, was to investigate whether in COPD patients prolonged use of low dose prednisolone has effects on muscle energy metabolism and qualitative morphology.In a cross-sectional study 15 COPD patients (forced expiratory volume in one second (FEV1) 33 9 (mean SD) % predicted) who were steroid-naive (CORT-) were compared with 10 healthy control subjects (HC) and with 14 COPD patients (FEV1 30 11 % pred), who had been using oral prednisolone for at least 1 yr (CORT+).It was found that adenosine triphosphate (ATP)/adenosine diphosphate was lower in CORT-compared to HC (5.7 versus 6.2, p=0.03). Inosine monophosphate was detected in 13 of 15 CORT-compared to 3 of 10 HC (p=0.004). However, although indications were found for an imbalance in production and utilization of ATP, comparing CORT-and HC, no differences in oxidative (citrate synthase and 3-hydroxy-acylcoenzyme A dehydrogenase) and glycolytic (hexokinase, lactate dehydrogenase and phosphofructokinase) enzyme capacities were found.When, comparing steroid-treated and steroid-naive patient subgroups, no differences in the above mentioned parameters of muscle energy metabolism and of muscle qualitative morphology were found. Eur Respir J 2000; 16: 247±252. Supported by a scholarship from ASTRA BV, the Netherlands.Exercise intolerance and dyspnoea are the most frequently occurring complaints in patients with severe chronic obstructive pulmonary disease (COPD). Weakness of both skeletal and respiratory muscles contributes significantly to these complaints [1]. Recently it has been shown that muscle weakness in COPD patients can predominantly be explained by muscle atrophy [2]. However, several studies suggested that exercise tolerance might also be impaired by alterations in muscle energy metabolism [3±5].Experimental evidence is accumulating that in COPD patients muscle energy metabolism is already disturbed at rest. JAKOBSSON et al. [6] found a decreased oxidative capacity and an increased glycolytic capacity in quadriceps femoris muscle. MALTAIS et al.[3] reported a decreased oxidative capacity in quadriceps femoris muscle. In another recent study [4], in tibialis anterior muscle, indications for an imbalance in adenosine triphosphate (ATP) utilization and resynthesis were found, as suggested by increased inosine monophosphate (IMP) levels, which were negatively related with ATP/adenosine diphosphate (ADP) ratios. However, in that study oxidative and glycolytic enzyme capacities were not investigated.In view of the above mentioned findings in skel...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 97%

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Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Pouw¹,

Lang²,

Gosker³

et al. 2000

Eur Respir J

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“…However, these effects do not necessarily lead to early death. During the last 10 yrs, several studies have pointed towards myopathy as a potentially dangerous complication of long-term systemic use of corticosteroids [16], especially as a result of the observed deleterious effects of muscle weakness on functional status of patients with COPD [17,18]. In addition, in a recent study it was found that peripheral muscle weakness, represented by reduced quadriceps force, was an independent contributor of health care costs and preliminary data by the same group even suggest an adverse influence on mortality [19].…”

Section: Discussionmentioning

confidence: 99%

Dose dependent increased mortality risk in COPD patients treated with oral glucocorticoids

et al. 2001

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Systemic corticosteroids are often administered in COPD patients. The relationship between systemic glucocorticoids and mortality in patients with moderate to severe chronic obstructive pulmonary disease (COPD) was retrospectively analysed. Baseline characteristics of the patients, in stable clinical condition, were collected on admission to a pulmonary rehabilitation centre. Overall mortality was asessed at the end of follow-up. The Cox proportional hazards model was used to quantify the relationship between glucocorticoid use, distinguishing administration route (oral/inhalation) and oral dose, and overall mortality, adjusted for the influence of age, sex, smoking, lung function, resting arterial blood gases and body mass index.On multivariate analysis, oral glucocorticoid use at a (prednisone equivalent) dose of 10 mg . day -1 without inhaled glucocorticoids, was associated with an increased risk (RR~2.34, 95% confidence interval (CI) 1.24 -4.44) while 15 mg . day -1 carried a relative risk of 4.03, CI~1.99 -8.15). A significant interaction was observed between inhaled and oral glucocorticoid use. Combined with inhaled glucocorticoids, the relative risk of oral glucocorticoid use appeared to be significantly smaller.It is concluded that in severe chronic obstructive pulmonary disease, maintenance treatment with oral glucocorticoids is associated with increased mortality in a dosedependent manner. Since the present study design cannot exclude the possibility of bias by indication, further prospective studies are indicated using a broader patient characterization.

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“…Die systemische Kortikosteroidtherapie des Patienten mit stabiler COPD führt zu einer Verschlechterung des Krankheitsbildes [35]. Systemische Kortikosteroide sind daher nur für den begrenzten Zeitraum einer Exazerbation indiziert [36].…”

Section: Antiinflammatorische Therapie Der Copdunclassified

COPD: Eine entzündliche Erkrankung der Atemwege?

Magnussen

2004

Pneumologie

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EinleitungDie chronisch obstruktive Bronchitis und das Lungenemphysem werden aufgrund der Schwierigkeiten der Abgrenzung der bronchitischen und emphysematösen Komponente nach dem Vorschlag der Global Initiative for Chronic Obstructive Lung Disease (GOLD) mit COPD (chronic obstructive pulmonary disease) abgekürzt [1].Die COPD ist durch eine nicht vollständig reversible Begrenzung des Atemflusses charakterisiert. Die Limitation des Atemflusses ist meist fortschreitend und mit einer abnormen entzündlichen Reaktion der Lungen vergesellschaftet [1, 2].Die Pharmakotherapie der COPD beruht überwiegend auf den Substanzen, die bei der Behandlung des Asthma bronchiale eingesetzt werden. Die Atemwegsobstruktion kann erfolgreich mit Bronchodilatatoren behandelt werden, während für die Beeinflussung der abnormen entzündlichen Reaktion bislang vorwiegend Kortikosteroide zur Verfügung stehen. Die hervorragende Effektivität der Kortikosteroide beim Asthma bronchiale hat zu zahlreichen Studien geführt, die den Einsatz insbesondere von inhalativen Kortikosteroiden bei der COPD rechtfertigen sollen.Ich möchte mich in dem folgenden Beitrag mit einigen Aspekten auseinandersetzen, die den Zusammenhang zwischen den funktionellen Konsequenzen der COPD, der abnormen Entzündungs-reaktion und den therapeutischen Möglichkeiten betreffen. Funktionelle Konsequenzen der COPDDie COPD ist durch eine meist progressive Limitation der Strö-mung innerhalb der Atemwege gekennzeichnet. Dieses funktionelle Merkmal wird üblicherweise mit Hilfe der Spirometrie gemessen, die aufgrund der internationalen Übereinkommen nur das exspiratorische Manöver berücksichtigt [3]. Die forciert exspirierte Vitalkapazität, FVC, das forciert exspirierte Volumen in der ersten Sekunde der Ausatmung, FEV 1.0 und deren Verhältnis beschreiben die Atemwegsobstruktion in qualitativer und quantitativer Weise. Die Stadieneinteilung der COPD beruht auf dem Nachweis einer obstruktiven Ventilationsstörung durch eine Erniedrigung von FEV 1.0 /FVC < 70 % sowie einer definierten Erniedrigung von FEV 1.0 . Während die spirometrischen Parameter von den verschiedenen Expertengremien in gleicher Weise eingesetzt werden, unterscheiden sich die quantitativen Angaben, die zur Abschätzung der Schweregrade führen. Dieser Umstand erschwert unter anderem den Vergleich epidemiologischer Erhebungen zur Häufigkeit und Schwere der COPD in verschiedenen Ländern [4,5].Die Objektivierung der obstruktiven Ventilationsstörung durch die alleinige Auswertung der forcierten Exspiration stellt einen

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Functional and histologic picture of steroid-induced myopathy in chronic obstructive pulmonary disease.

Cited by 246 publications

References 0 publications

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Dose dependent increased mortality risk in COPD patients treated with oral glucocorticoids

COPD: Eine entzündliche Erkrankung der Atemwege?

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