Corticosteroid-induced Myopathy and...

Corticosteroid-induced Myopathy and the Respiratory Muscles

Report of brace Cases

Systemic corticosteroid therapy is known to cause many unwanted side results among which muscular weakness and wasting have been observ since its earliest days. [12] Experimental steroid myopathy [3-5] was shown to share many of the features of its clinical counterpart, which was extensively described through Afifi et al. [6] A more precise definition of the biochemical abnormalities of this myopathy, a better correlation between clinical and laboratory findings, and a useful approach for early detection, differential diagnosis, and management were provided through Askari et al. [7]

Steroid-induced myopathy in the respiratory muscles, to our knowledge, has not been reported. We were fortunate to make observations forward respiratory muscle strength in sum of two units patients with steroid myopathy and complaints of dyspnea and in succession the changes caused by progressive tapering of the steroid therapy.

CASE REPORT

CASE 1

In January 1978 this 58-year-old woman disentangleed typical skin lesions of dermatomyositis and was followed up as an outpatient in the dermatology department. Clinical and biochemical investigation was negative, and spirometric example results were within normal limits.

Corticosteroid treatment (50 mg of prednisone daily) was started in March 1978 and across the following years continuously adjusted and tapered.

In March 1986 however, steadily worsening disease activity (reappearance of pathognomonic dermatologic features) necessitated an increase in prednisone dose, up to 60 mg daily. For the first time the patient unraveled rapidly progressing muscle weakness and was referr to us because of prominent dyspnea. Her nutritional status was normal. Muscle enzyme values remained normal, however 24-h creatine excretions were clearly elevated (Fig 1) Pulmonary function proof results revealed both notably decreased maximal inspiratory constraining force PImax, being 52 percent predicted and maximal expiratory compressing PEmax, being 40 percent predicted. After gradual reduction of the prednisone dose to 75 mg daily, the creatinuria substantially decreased, and the couple PImax and Pemax increased according to 33 percent.

CASE 2

In May 1986 the diagnosis of "unidentified connective tissue disease" was established in this 50-year-old woman with chronic pyelonephritis and secondary hypertension. Spirometric touchstone results were normal. Prednisone treatment (50 mg daily for four weeks, gradually tapered to 30 mg) be the effected in rapid regression of skin lesions and she was followed up as an outpatient in the division of nephrology

After ten weeks of treatment, she complained of general fatigue, dyspnea onward exertion, and muscle weakness. Serun enzyme values remained normal, nevertheless spirometric study results now showed clearly reduc bodys (VC, 74 percent; [FEV.sub.1], 70 percent) Physical disability considerably journey of stateed with distinct facial mooning, harsh girdle muscle wasting, osteoporosis, and lumbar vertebral collapse. The nutritional status, however, remained normal.

She was then seen in our outpatient clinic because of prominent dyspnea. Maximal transrespiratory constraining forces were clearly reduced, PImax and PEmax being 35 percent and 41 percent predicted, respectively. The 24-h creatinuria was sixfold increased and showed a gin decrease during prednisone dose reduction (Fig 1) This was associated with pronounced clinical improvement, normalization of spirometric values, and increased respiratory muscle vigor the PImax increasing by 70 percent and PEmax remaining relatively constant.

DISCUSSION

This report provides, to the best of our knowledge, for the first time consistent evidence of reduc respiratory muscle power caused by corticosteriod treatment.

Indeed, in the couple patients, diagnosis of steroid myopathy was firmly documented. First, in the same patient, typical complaints of muscle weakness occurr concomitant with the increased prednisone dosage. The other patient gradually expanded steroid myopathy during seven month of high-dose prednisone treatment. In as well-as; not only-but also; not only-but; not alone-but patients, greatly increased creatinuria appeared in the air of normal serum muscle enzyme of the same heights Second, underlying disease was in partial or integral remission, and especially in the next to the first patient muscle weakness appeared simultaneously with other disabling nonmyopathic side general intents of corticosteroid therapy. At the time of diagnosis, the couple patients were in a normal nutritional status and did not be stirred sick. Finally, in the two patients muscle strength improved and creatinuria decreased after steroid dosage reduction, which confirms the diagnosis of steroid myopathy. [7]

These cases also clearly indicate that considerable reductions in respiratory muscle hardness may be present with normal or no other than moderately reduced lung volumes forward spirometric study. [8] At the time of diagnosis in our patients, PImax were simply 52, respectively, and 35 percent predicted, and PEmax averaged about 40 percent predicted, indicating censorious muscle weakness. The vital capacity, however, was normal in the first patient and slightly reduc in the other After steroid dosage reduction, PImax improved to 70 (59 percent predicted), whereas PEmax showed a 33 percent improvement in individual patient and remained relatively unchanged in the second