Obstructive sleep apnea secondary to chronic lymphocytic leukemia
Authors: A. Chehal, J.H. Haidar, R. Jabbour, B. Yammout, A. Bazarbachi
Journal: Annals of Oncology (2002)

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.Fogel R.B. White D.P. Obstructive sleep apnea.Adv Intern Med. 2000; 45: 351-389PubMed Google Scholar]). 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. Symptomscan 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.Fogel R.B. White D.P. Obstructive sleep apnea.Adv Intern Med. 2000; 45: 351-389PubMed Google Scholar]). OSA has also been described in benign or malignant lymphoid hyperplasia [2.Carbone J.E. Barker D. Stauffer J.L. Sleep apnea in amyloidosis.Chest. 1985; 87: 401-403Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar], plasmacytoma [3.Zorick F. Roth T. Kramer M. Flessa H. Exacerbation of upper-airway sleep apnea by lymphocytic lymphoma.Chest. 1980; 77: 689-690Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar], amyloidosis [4.Byrd Jr, R.P. Roy T.M. Bentz W. Mehta J.B. Plasmacytoma as a cause of obstructive sleep apnea.Chest. 1996; 109: 1657-1659Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar], 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.Nolan P. Chronic lymphatic leukaemia presenting as severe obstructive sleep apnoea.Respirology. 1996; 1: 299-301Crossref PubMed Scopus (6) Google Scholar].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. 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.Fogel R.B. White D.P. Obstructive sleep apnea.Adv Intern Med. 2000; 45: 351-389PubMed Google Scholar]). 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. Symptomscan 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.Fogel R.B. White D.P. Obstructive sleep apnea.Adv Intern Med. 2000; 45: 351-389PubMed Google Scholar]). OSA has also been described in benign or malignant lymphoid hyperplasia [2.Carbone J.E. Barker D. Stauffer J.L. Sleep apnea in amyloidosis.Chest. 1985; 87: 401-403Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar], plasmacytoma [3.Zorick F. Roth T. Kramer M. Flessa H. Exacerbation of upper-airway sleep apnea by lymphocytic lymphoma.Chest. 1980; 77: 689-690Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar], amyloidosis [4.Byrd Jr, R.P. Roy T.M. Bentz W. Mehta J.B. Plasmacytoma as a cause of obstructive sleep apnea.Chest. 1996; 109: 1657-1659Abstract Full Text Full Text PDF PubMed Scopus (14) Google Scholar], 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.Nolan P. Chronic lymphatic leukaemia presenting as severe obstructive sleep apnoea.Respirology. 1996; 1: 299-301Crossref PubMed Scopus (6) Google Scholar]. 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.