Autoreactive Antibodies Associated with Castleman Disease Triad.

The Castleman triad has been described in a select few patients presenting with a retroperitoneal mass, mucocutaneous pemphigus vulgaris, and bronchiolitis obliterans. Here, we describe the Castleman triad in a 19-year-old male with unicentric hyaline vascular type Castleman disease (HV-CD). This patient presented with an array of positive antibodies, including anti-cyclic citrullinated peptide, anti-double-stranded DNA, and Sjogren's IgG. Interestingly, the patient's rheumatologic symptoms resolved after tumor resection, while his antibody profile remained relatively unchanged. HV-CD, with a triad presentation, was thought to be from a paraneoplastic syndrome secondary to an underlying lymphoproliferative disorder. The findings presented here identify multiple autoantibodies potentially contributing to this patient's presentation with HV-CD.

Greater nasal nitric oxide output during inhalation: effects on air temperature and water content.

The nose conditions the temperature and humidity of nasal air, and the nasal mucosal vasculature supplies heat and water for these processes. We hypothesize that nitric oxide (NO) modulates these processes through vasoactive effects on nasal mucosal vasculature. We measured the temperature, humidity and NO concentrations of nasal air during inhalation and exhalation across the nose and calculated net heat, water and NO output before (controls, n=7) and after inhibition of NO synthase by topical l-NAME (N=5) in healthy humans. We found that calculated NO output across the nasal passages is approximately three-fold greater during inhalation (503+/-105 nL/min) compared with exhalation (162+/-56 nL/min). Moreover, topical administration of l-NAME decreased nasal air temperature and humidity conditioning and NO output, but these effects were limited to inhalation. We conclude that nasal NO output is greater during inhalation than exhalation in humans. Our findings also support a role of nasal NO in temperature and humidity conditioning of nasal air.

Exhaled nasal nitric oxide output is reduced in humans at night during the sleep period.

The physiologic function of nasal nitric oxide (NO) release is unknown. In prior experiments, topical NG-nitro-L-arginine methyl ester (L-NAME) on nasal mucosa reduced exhaled nasal NO output and caused daytime sleepiness. We hypothesized that nasal NO output is reduced at night during the sleep period. We measured exhaled nasal NO concentration and minute ventilation and calculated nasal NO output in humans over 24 h. Daytime awake NO output was greater than NO output at night during sleep or transient wakefulness. Exhaled NO concentration decreased during sleep along with minute ventilation. A daytime voluntary reduction in minute ventilation also decreased nasal NO output but exhaled NO concentration increased. Nasal NO output was not changed by body position. We conclude that exhaled nasal NO output is decreased at night due to decreased mass flow of NO into nasal air in addition to decreased minute ventilation. Our findings suggest a role of nasal NO in sleep or in the physiologic processes accompanying sleep.