A 55-year-old woman, former smoker of 10 paq/year, with type 2 diabetes mellitus and chronic hypertension treated with regime, metformin, glibenclamide dyspnea and atenol 2005 presented progressive dryness in May.
He did not report general malaise, weight loss, fever, chills, chest pain, arthralgia, photosensitivity, or skin lesions.
He had no exposure to birds or substances and had not traveled.
On physical examination, the patient was in good general condition, obese, BMI: 31 kg/m2, HR: 78 beat/min, BP: 135/90 mmHg, RR: 20 breaths/min, cardiac auscultation:
He had no adenopathy, muscle weakness, digital clubbing, arthritis, or skin or eye lesions.
The chest X-ray showed multiple opacities of alveolar filling, especially in the lower lobes and the respiratory functional study showed restricted muscle strength and reduced carbon monoxide diffusion capacity (DLCO).
Chest computed tomography showed multiple ground glass foci of peripheral and subpleural distribution, especially in the lower lobes.
Laboratory tests (general platelet count, renal and hepatic function tests, lipid profile, urine sediment) were normal, and immunological tests (antinuclear antibodies and anti-DNA antibodies, rheumatoid factor antibodies) were negative.
1.
In June 2005, lung biopsy by videothoracoscopy was performed, which was compatible with the diagnosis of organizing pneumonia. The diagnosis of primary COP was raised and treatment with prednisone 1 mg/kg/day was initiated.
The patient progressively developed dyspnea and partial improvement in respiratory compromise, resuming steroid doses over a one-year period.
Table 1 describes the evolution of respiratory functional tests.
1.
In June 2006, after lowering the prednisone dose to 10 mg daily, the patient reported fever, myalgia, arthralgias, proximal muscle weakness, and then the appearance of a redness heliotrope, erythematous, respiratory opacity
Fiberoptic bronchoscopy with bronchoalveolar lavage was performed to rule out opportunistic infection, increasing the dose of prednisone to 1 mg/kg/day due to suspicion of COP reactivation.
The tests requested showed positive anti Ro and anti Jo-1 antibodies, elevated muscle enzymes (crea-tinphosphokinase: 2,910 defective U/L, LDH: 512 U/L) and increased spontaneous myopic shift (myogram).
Evaluated in conjunction with the rheumatology team, the diagnosis of dermatomyositis with interstitial lung involvement is proposed, adding to the therapy infusion of immunoglobulins 400 mg/kg/day intravenous cyclophosphamide for five days, pulses.
The patient presented with progressive deterioration of functional capacity, vestine fever, myalgia, arthralgia, arthralgia, deterioration of functional capacity, DLCO and proximal muscle weakness in six minutes.
The lack of clinical response and progression of respiratory compromise occurred within months of seeking alternative therapies, receiving two doses of rituximab of 1 g every 14 days, which showed a significant improvement in the clinical and functional parameters mentioned above (AU)
At six months, systemic symptoms, evening fever, arthralgias, myalgias and proximal muscle weakness reappeared, indicating a new cycle of rituximab in November 2007 (1 g lobule CT scans showed significant improvement).
