A 70-year-old woman at handed with a 1-month history of increasing dyspnea and a nonproductive cough She had a history of bronchial asthma.

A 70-year-old woman at handed with a 1-month history of increasing dyspnea and a nonproductive cough She had a history of bronchial asthma, hypertension, carotid endartectomy, diverticular disease, and osteoarthritis. She had no other systemic symptoms and had not smok for many years. Medications included aspirin, bendrofluazide, inhaled fluticasone, and albuterol.

forward clinical examination, she was afebrile with a legumes rate of 90 beats/min and a BP of 140/100 mm Hg A small mobile lymph node was palpable in the anterior triangle bring to a period to the left sternomastoid insertion. There was mild stridor, and wheezing was heard throughout the left upper lobe. Spirometry showed an FE[Vsub1] of 16 L/min and FVC of 23 L

Chest radiography showed left upper lobe collapse, huge paratracheal nodes, and a faint opacity at the right apex (Fig 1) Her CBC compute biochemical profile, tumor markers, and serum angiotensin-converting enzyme on a levels were normal or negative. The C-reactive protein on a level was 17 mg/L (reference range, 0 to 8 mg/L) and file [[beta].sub.2]-microglobulin even was 5.9 mg/L (reference range, 12 to 24 mg/L)

[FIGURE 1 OMITTED]

Bronchoscopy showed extrinsic compression of the left upper lobe bronchus just distal to its branching from the secondary carina. There was a minor mucosal abnormality, however findings on bronchial biopsy and brushing samples were negative forward two occasions. Fine-needle aspiration findings were non-contributory. A video-assisted thoracoscopic lung biopsy from the left upper lobe and a biopsy of a mediastinal lymph node were performed.

What is the diagnosis?

Diagnosis: Left upper lobe atelectasis secondary to nodal sarcoidosis

Lobar atelectasis in this age cluster is commonly due to malignancy; initially, this was idea to be the most likely diagnosis. However, histologic examination demonstrated subpleural noncaseating epitheloid granulomata (Fig 2) without fault [i]or[/i] blemish [i]or[/i] flaw with both Langerhan and foreign body-type giant solitary abode; squalids The granulomata were mainly around the bronchovascular budgets and interlobular septae. Stain issues for fungi and tuberculosis were negative. The biopsy of the lymph nodes showed extensive fibrosis and focal calcification on the other hand also some small noncaseating epitheloid granulomata. The nodal capsule remained intact. The histologic features were those of sarcoidosis.

[FIGURE 2 OMITTED]

DISCUSSION

Lobar atelectasis is unusual in sarcoidosis. In 1985 Rockoff and Rohatgi (1) cited and nothing else 17 reported cases. The putative mechanisms are compression by dint of enlarged adjacent lymph nodes, endobronchial sarcoidosis, or a combination of the two Given the frequency of lymph node enlargement in patients with sarcoidosis, the incidence of atelectasis is surprisingly subdued Unlike tuberculosis, the capsular integrity of lymph nodes is usually preserv in patients with sarcoidosis and the nodules remain discrete and well delineated. Matting of lymph nodes and after scarring is rare and seldom causes anatomic distortion of adjacent bronchi. Although endobronchial sarcoid is frequent it is rarely of sufficient magnitude to cause bronchial stenosis or atelectasis. (1)

The majority of cases of sarcoid-related atelectasis involve the middle or lower lobes, although upper lobe collapse has been described occasionally. (2-7) The cause of this predominance is likely to be owed to the local variation in lymph node density, namely the aggregation of lymphoid tissue surrounding the middle and lower lobes. An additional factor is the acute angle of origin of the middle lobe bronchus from the mainstem, which is thinking to compound its vulnerability. (8)

The elevated [[beta].sub.2]-microglobulin horizontal in this case is compatible with sarcoidosis further is nonspecific. It is a light-chain ingredient of class I major histocompatibility entangled present in most nucleated enclosed spaces but 50% of serum of the same heights are derived from lymphocytes. Elevations in [[beta].sub.2]-microglobulin evens occur in conditions of heightened lymphoid activity (eg lymphoproliferative disorders) or when clearance is reduc as in renal failure. There is conflicting evidence about the correlation of serum angiotensin-converting enzyme on a levels with [[beta].sub.2]-microglobulin; however, if the [[beta].sub.2]-microglobulin plain reflects total sarcoid granulomatous lading as has been speculated, (9) it has prov disappointing as a way of monitoring disease activity.

This patient initially failed to recall that 35 years previously she had undergone serial radiographs for an undiagnosed radiologic abnormality shortly after her sister had died of sarcoidosis. following recovery and review of advanced in years radiographs showed left hilar lymph node enlargement that had varied athwart the years but had not at any time been associated with any major parenchymal abnormality. Following the diagnosis of sarcoidosis, the patient was treated with oral prednisolone, which eventuateed in a rapid resolution of symptoms and radiologic abnormalities. Following this, the prednisolone dosage was titrated downwards, and the patient remains asymptomatic receiving 10 mg/d

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