A 72-year-old male, diagnosed with type 2 diabetes mellitus in treatment with glizipide for 5 years and a stage C2 colon adenocarcinoma Astler-Coller in March 2003, underwent adjuvant chemotherapy with MayLV clinical regimen.
He was admitted in November 2003 with a picture of constitutional syndrome and persistent hemoptoic sputum for a month although in small quantity.
Physical examination revealed mucocutaneous discomfort and dry crackles in both lung bases.
Laboratory tests showed iron deficiency anemia (Hb 6.1 g/dL, MCV 73, HCM 21, sideremia 15, ferritin 3, transferrin 285), increased ESR (89 mm), polyclomnal CRP and fibrinogen.
ANA and anti-DNA antibodies were negative.
Sputum acid-fast bacilli (BAAR) were negative.
Tumor markers showed CA19.9 of 8 U/mi (< 37 U/ml) and CEA of 3 U/mi (<5 U/ml).
Chest X-rays showed a predominantly alveolar-interstitial pattern in both bases.
Bronchoscopy showed no endobronchial lesions or signs of bleeding.
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Abdominal ultrasound, gastroscopy, and direct fibrolaryngoscopy were normal.
She was discharged with oral iron and outpatient follow-up due to suspicion of a tumor process unrelated to both the admission clinic and the analytical results.
He was readmitted in February 2004 for acute respiratory failure (pH 7.36; pCO2 44 mmHg; pO2 56 mmHg; O2 saturation 66.6%) requiring high flow therapy.
The chest X-ray revealed a bilateral alveolar-interstitial pattern, affecting both bases and the right midfield. The patient was diagnosed with bilateral pneumonia and received antibiotic treatment ceftriaxone and erectum.
Laboratory tests revealed leukocytosis with left shift, hypochromic and microcytic anemia, increased ESR and LDH.
The elemental urine analysis was normal.
Blood cultures were repeatedly negative; AFB in urine and negative sputum; serology HCV, HBV, CMV, HIV, Legionella, Q fever, Mycoplasma and Clamydias negative.
Angiotensin converting enzyme was within the normal range.
Tumor markers were normal (ECA 3 U/ml and CA19.9 20 U/ml).
Abdominal CT showed diffuse interstitial reticular pattern at the pulmonary level with interlobular thickening, more marked in the posterior segments and a golden glass pattern in both bases.
Bronchoscopy showed no endobronchial tree lesions and segmental bronchi with negative cytology.
Transbronchial biopsy was not representative.
Given the clinical situation of the patient, a bronchioalveolar lavage was performed, which showed a neutrophilic infiltrate with abundant macrophages containing hemosiderin.
Culture and cytology were negative for germs and tumor cells.
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The patient remained without clinical or radiological improvement. Upon suspicion, due to the findings in the bronchial lavage, diffuse pulmonary haemorrhage, an immunological study was requested, which showed negative antinuclear antibody titers (1plasma / 650) and antinuclear antibody titers (AN).
Treatment was initiated with methylprednisolone (initial dose of 1 mg/kg/day for 20 days, with progressive reduction in the following weeks).
From the beginning of the steroid treatment the patient achieved favorable clinical manifestations, as well as by gas.
Radiologically, the presence of bilateral pulmonary infiltrates was maintained, and a diffuse pattern of pulmonary fibrosis was observed in the last follow-up.
Three months after discharge, the patient did not require prednisone and remained on a descending oral regimen.
Subsequently, the patient was periodically reviewed in the outpatient clinic of the hospital.
Currently, after one year of evolution, she is in a good clinical situation, without anemia (Hb 13 g/dL), normalization of SGV, acute phase reactants and negativization of p-ANCA antibodies.
Pathologic confirmation, CT scan and tumor markers were performed again, but no tumor recurrence was observed.
