The inflammatory diseases of muscle are a group of disorders characterized by proximal muscle weakness. Most cases fall into three major diagnostic categories, polymyositis (PM), dermatomyositis and inclusion body myositis. Respiratory complications are a common feature and are an important cause of morbidity and mortality. The three main types of pulmonary involvement are interstitial lung disease, aspiration pneumonia and ventilatory incapacity (VI) due to muscle weakness. There are few reported cases in which mechanical ventilation has been used in patients with PM and VI in absense of lung disease. We present a patient with PM and VI due to muscle weakness who underwent therapy maintenance with mechanical ventilator and was weaned 4 months later.

Las miopatías inflamatorias son un grupo de enfermedades caracterizadas por debilidad muscular proximal y las causas mayores incluyen la polimiositis (PM), dermatomiositis y miositis por cuerpos de inclusión. Las complicaciones respiratorias son comunes y adquieren importancia por la incidencia sobre el pronóstico. Las tres formas de compromiso frecuentes son la enfermedad pulmonar intersticial, la neumopatía aspirativa y la incapacidad ventilatoria (IV) por debilidad de los músculos respiratorios, que en su forma severa es de ocurrencia excepcional. Se presenta una paciente con IV sin compromiso del parénquima pulmonar, que requirió asistencia respiratoria mecánica por 4 meses con «destete» exitoso.

We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9% NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 µg of Evans blue/g dry tissue in the basal condition and 1750 µg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.