A 38-year-old female smoker of 21 years/pack, type II diabetic and with a history of bronchial asthma for 4 years without any treatment or follow-up.
She had been working as an administrative professional in a dental clinic for nine months, presenting intermittent fever and dyspnea with the change of work and, as she referred in relation to it, she had suffered from daytime and nighttime wheezing.
The symptoms had worsened in the last weeks despite antipyretic treatment, so he came to the emergency room in July 2002, later admitted.
On admission, the patient had a regular general condition, fever of 38 oC, 20 vpm, 65 ppm, good hydration and coloration.
Cardiac auscultation was normal, and pulmonary auscultation revealed decreased breath sounds, bilateral wheezing.
The rest of the examination showed no relevant findings.
Chest X-ray at admission showed bilateral patchy alveolarinterstitial pattern, predominantly perihilar atelectasis.
Arterial blood gas analysis breathing room air showed: pH 7.45, PO2 54.7 mmHg, PCO2 35.6 mmHg, HCO3 24.3 mmol/l and SaO2 89%.
Laboratory tests showed 15700 leukocytes with 90% neutrophils and 0% eosinophils, as well as ESR 89 mm. Biochemistry showed glucose of 198 mg/dl being the rest of normal parameters except CRP of 17.29 mg/dl.
1.
An HRCT scan of the chest showed a bilateral ground-glass pattern predominantly in the upper lobes and a small area atelectasis in the middle lobe and consolidation patch; there were no findings of significance mediast level
The tests showed: FVC 2280 ml compatible with respiratory distress, FEV1 1770 ml restrictive, FEV1/FVC 78 (90%), DLCO 15.6 ml/min/volume (61%), alveolar alteration/VA 4.69.
Fiberoptic bronchoscopy was performed on the fourth day of admission, and no airway abnormalities were observed.
Bronchoalveolar lavage (BAL) showed 500 cells/μl, with 65% macrophages, 20% lymphocytes, 10% polymorphonuclear, 5% eosinophils with CD4+ lymphoid subpopulations 46.9% and CD8+ 29.
The microbiology of LAB, including bacteria, Zhiel-Nielsen and culture of Lowenstein, as well as weaken and illiteracy was negative.
Bronchoaspirate Zhiel and Lowenstein (BAS) were equally negative, and BAL and BAS cytology were negative for malignancy.
Transbronchial biopsy (TBB) was not performed because the technique had to be interrupted due to incoercible cough of the patient.
Upon admission he had started treatment with spirotherapy, amoxicillin-clavulanic 1 gr/IV/8h, remaining apyretic at 24 hours and on the 5th day of admission a radiological improvement was observed.
IgE was 327.3 IU/ml and PSA was requested, which was subsequently received, positive for grasses, pollen or gum epithelium, negative for mites and tapeworm.
Serum precipitins for Alternaria Tenuis, Aspergillus, avian proteins and Thermoactinomyces were also negative.
a Being on his vacation and his conditioning in the LAB and the rapid radiological improvement, he was questioned again to the patient, referring that the respiratory symptoms had begun to change his work apparatus, he found himself worse.
On the sixth day of hospitalization, prednisone 40 mg/day was added and the patient was discharged 10 days after admission with a descending pattern.
In a subsequent follow-up, one month later, the patient was asymptomatic showing a respiratory functional examination FVC 3,380 ml (105%), FEV1 2670 ml (96%), FEV1/FVC 79 (96%), non-exhaustive DLCO 19.8 ml/ ACT scan
Our patient did not attend the successive appointments because she was asymptomatic until January 2006 she was admitted again due to general malaise, arthromyalgias, shivering, and no feverish sputum.
For three months he had worked as an administrative and salesman in a gress store.
The symptoms had started when the hot air heating systems started in his office.
Upon auscultation, he had bilateral crackles, as well as a bilateral micronodular interstitial pattern on chest X-ray.
An HRCT scan of the chest revealed patchy ground-glass opacities predominantly in the upper lobes with thickening of the interlobular septa.
The laboratory tests showed an increase in ESR, IgE and CRP, as well as partial acute respiratory failure pH 7.51, PO2 49.7 mmHg, PCO2 35.9 mmHg, HCO3 28.3 mm/l and SaO2.
1.
A new fiberoptic bronchoscopy with LAB was performed, which showed 357 cells/μl, with 70% macrophages, 20% lymphocytes, 6% polymorphonuclear, 4% basophils, and 37% lymphocytic necrosis with subpopulations CD8
Respiratory function tests showed: FVC 2180 ml (62%), FEV1 1590 ml (57%), FEV1/FVC 73 (92%) DLCO 17 ml/min/mmHg, and abnormal bronchodilator intake 30 days later (96%).
