This is a 35-year-old male, with no toxic habits or clinical history of interest, who came to the emergency department for dyspnea.
Two months before admission, the patient presented with progressive dyspnea on moderate exertion and mild cough.
Concomitantly, skin lesions appeared on the metaphalangeal and proximal interphalangeal zones that were diagnosed at first as contact eczema and later psoriasis, without improvement after treatment.
She also complained of pain and swelling in her hands knees and elbows.
Physical examination revealed marked desaturation with the auscultation, together with fine tidal crackles on auscultation.
He had diffuse erythematous scaly lesions "psoriasis-like" in both hands and elbows, as well as pain and swelling in the proximal interphalangeal area of several fingers of the hands.
In both eyelids a very striking violet erythema area was observed.
Absence of myalgia on examination and anamnesis.
No other relevant data were found.
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Among the complementary tests, a VSG of 49 mm stood out, with normal blood count.
Hepatic and renal profile, proteinogram, CRP and RF, CK and aldolase in normal range, ferritin 645 mg/dl. ANAs, Acs. anti-Ro, ant-iclNP and anti-r
Positive anti-Jo1 antibodies were detected.
Tumor markers were negative.
The chest X-ray showed a fine interstitial biphasic pattern, which was confirmed by tomographic images.
A restrictive pattern was observed in the mestizo with mild alteration in carbon monoxide diffusion.
Electromyogram was normal.
Our patient had clear cutaneous stigmas, such as "mechanical hands", "Gottron papules" and erythema heliotropase heliotropase signs in the middle echocardiography, all of which showed interstitial and radiological progressive dyspnea.
With these data we performed a clinical diagnosis of amyopathic dermatomyositis/antisynthetase syndrome.
Treatment was initiated with steroids (methylprednisolone) at a dose of 1 mg/kg, with significant functional improvement of the lesions and disappearance of the skin lesions.
Weeks after the beginning of treatment there was a rebound of the disease that progressed to worsening clinical manifestations of respiratory disease, so treatment was proposed with intravenous cyclophosphamide boluses and maintenance of corticosteroid therapy.
The patient underwent 6 cycles with significant clinical improvement, which at present allowed the decrease of corticoid therapy, finding the patient asymptomatic.
