Departments of 1 Internal Medicine, 2 Pathology and Laboratory Medicine, American University of Beirut-Medical Center, PO Box; 1136044 Beirut, Lebanon (E-mail: bazarbac{at}aub.edu.lb)
We report a 66-year-old male patient, heavy smoker, diagnosed 5 years earlier with asymptomatic chronic lymphocytic leukemia (CLL) CD5+/CD23+, Binet stage A, with lymphocytosis and cervical lymph node enlargement. Recently, he presented with a few days history of dizziness, loud snoring, excessive diurnal somnolence, and many episodes of nocturnal apnea and nocturia with no evidence of cataplexy or hypnogogic hallucinations. Physical examination was unremarkable, except for marked obesity and cervical lymph node enlargement. Complete blood cell count showed isolated lymphocytosis with no evidence of anemia or thrombocytopenia. Arterial blood gases, liver function tests, renal function, urine analysis and thyroid function tests were normal. Electrocardiogram was unremarkable. Computed tomography scan of the chest revealed enlarged axillary and mediastinal lymph nodes. Magnetic resonance imaging of the brain and neck revealed multiple enlarged cervical lymph nodes with hypertrophy of the adenoids and lingual tonsils causing narrowing of the upper airways. Polysomnography revealed severe obstructive sleep apnea (OSA) that was completely relieved by Bi-pap application. The patient was started on CHOP chemotherapy (cyclophosphamide, adriamycin, oncovin, prednisone). After the third cycle, excellent clinical response was noted with disappearance of sleep apnea symptoms and a normal polysomnography.
The pathogenesis of OSA includes hypoxemia, hypercapnea and acidosis (reviewed in Fogel and White [1]). Obstruction is caused by periodic apposition of the tongue with the posterior pharynx. This phenomenon may be an exaggeration of a normal physiologic occurrence during sleep, leading to a purely obstructive event despite the persistence of diaphragmatic effort and accessory respiratory muscles. Symptoms can vary from mild hyper-somnolence, insomnia, headache, cardiac arrhythmia, intellectual impairment, memory loss, behavioral changes, to apparent mental retardation, and overt hypercapneic respiratory failure with cor pulmonale. This disorder can be secondary to obesity, alcohol intake, micrognathia or macroglossia (reviewed in Fogel and White [1]). OSA has also been described in benign or malignant lymphoid hyperplasia [2], plasmacytoma [3], amyloidosis [4], pharyngeal tumors or any other diseases that can involve the nasopharyngeal structures. OSA syndrome secondary to adenotonsillar hypertrophy has been reported in only one patient with CLL [5].
This case gives another insight into OSA as a mechanical life-threatening complication of lymphoproliferative diseases, hence representing an additional indication for therapy. In this setting, OSA can be resolved simply by treatment of the underlying disease. We suggest thorough investigation for any change in sleep habits or related complaints in patients with lymphoproliferative disorders.
A. Chehal1, J. H. Haidar2, R. Jabbour1, B. Yammout1 & A. Bazarbachi1
Departments of 1Internal Medicine, 2Pathology and Laboratory Medicine, American University of Beirut-Medical Center, PO Box; 1136044 Beirut, Lebanon (E-mail: bazarbac{at}aub.edu.lb)
References
1. Fogel RB, White DP. Obstructive sleep apnea. Adv Intern Med 2000; 45: 351389.[Medline]
2. Carbone JE, Barker D, Stauffer JL. Sleep apnea in amyloidosis. Chest 1985; 87: 401403.[Abstract]
3. Zorick F, Roth T, Kramer M, Flessa H. Exacerbation of upper-airway sleep apnea by lymphocytic lymphoma. Chest 1980; 77: 689690.[Abstract]
4. Byrd RP Jr, Roy TM, Bentz W, Mehta JB. Plasmacytoma as a cause of obstructive sleep apnea. Chest 1996; 109: 16571659.
5. Nolan P. Chronic lymphatic leukaemia presenting as severe obstructive sleep apnoea. Respirology 1996; 1: 299301.[Medline]