Background: Nighttime reflux has been shown to be associated with esophageal mucosal injury, complications, and extra-esophageal manifestations. However, few studies have assessed the impact of gastroesophageal reflux on reported quality of sleep and quality of sleep on gastroesophageal reflux. Aims: The aims of this study were (1) to determine the correlation between the severity of gastroesophageal reflux disease (GERD) symptoms and esophageal acid contact time and subjects' perceived quality of sleep; (2) to investigate the correlation between reported quality of sleep of the night prior and severity of GERD symptoms and esophageal acid contact time the following day; and (3) to define in a sleep laboratory the correlation between acid reflux events and sleep architecture. Methods: Subjects with typical GERD symptoms ≥3 times a week underwent upper endoscopy and pH monitoring. These subjects subsequently completed the GERD Symptom Assessment Score (GSAS), and the Sleep Heart Health Study Sleep Habits (SHHS) Questionnaire to assess baseline sleep symptoms and GERD symptoms, including an index of GERD symptom severity (GERD symptom index). Before and after the pH test, the patients completed a different instrument, the Sleep Quality Questionnaire, utilized specifically to assess the quality of each subject's sleep before and after pH testing. Fifteen randomly selected subjects also underwent a polysomnographic study during the pH test. Results: Forty-eight (33 males/15 females, mean age 48.8 ± 17.1 y) subjects were prospectively recruited. Using data from the GSAS and SHHS questionnaires, disorders of initiating and maintaining sleep were found to be positively associated with greater severity of the GERD symptom index (r = 0.33, p <0.05). More frequent awakenings also correlated with a higher GERD symptom index (r = 0.4, p <0.01). Correlations between the Sleep Quality Questionnaire on the night before sleep testing and pH monitoring data showed that subjects with poorer sleep quality had longer acid reflux events (r=-0.34, p<0.05). More perceived awakenings also were correlated with the number of supine acid reflux events > 5 min (r=0.31, p<0.05) and the duration of the longest supine acid reflux event (r = 0.28, p = 0.05). Inverse correlations were observed between overall sleep quality on the pH testing night and a higher percentage of time spent with pH<4 supine (r=-0.432, p <0.002), and the duration of the longest acid reflux event during the entire night (r = -0.38, p <0.01) and supine (r=-0.37, p<0.02). Conclusions: Persons with worse GERD symptoms report poorer subject sleep quality. Poor sleep quality on the night prior to pH testing was associated with more acid exposure the following day. Greater acid exposure at night was related to a worse perception of sleep quality the next day. These findings suggest important interactions between GERD and sleep quality.

This study was designed to determine the effects of a single injection of a species-specific preparation of cytokines into rabbit patellar tendons and to compare the results with a known model of tendinitis, the collagenase-injection model. New Zealand White rabbits were divided into two groups and two time periods (4 and 16 weeks) and injected in the midsubstance of the right patellar tendon with either cytokines or collagenase under ultrasound guidance to confirm intratendinous needle placement. The left patellar tendon was injected with 0.025 ml of saline solution and served as a control. The rabbits were returned to cage activity after injection. At death, two rabbits in each group underwent histological analysis; the remaining eight animals in each time frame were evaluated biomechanically and then biochemically with use of the patella/whole patellar tendon/tibia complex. Histologic results at 4 weeks in the tendons injected with cytokines demonstrated increased cellularity, which was resolving by 16 weeks. The matrix appeared unchanged. The tendons injected with collagenase demonstrated increased angiogenesis of the matrix, hypercellularity, and fibrosis around the tendon at 4 weeks. At 16 weeks, myxoid changes, focal fibrosis, and collagen-bundle disarray with persistent increase in cellularity were noted. Biomechanically, a significant decrease in ultimate load at 16 weeks was seen in the tendons injected with cytokines but no change was seen in cross-sectional area. The tendons injected with collagenase demonstrated a significant increase in cross-sectional area at 4 and 16 weeks compared with those injected with cytokines. Biochemically, there was no significant difference in collagen content between the two groups at 4 or 16 weeks but the tendons injected with collagenase demonstrated a significant increase in crosslinking at 16 weeks. Our conclusion is that the tendons injected with the cytokine preparation represent a model of mild, seemingly reversible tendon injury. The cytokine preparation produces no matrix damage or evidence of collagen degradation and is species specific.

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Patients with FH demonstrate increased reports of chest pain and somatization, an alteration in autonomic function but lack a uniform increase in chemoreceptor sensitivity to acid as compared to those with NERD+. This suggests that while FH patients harbor clinical traits of a functional bowel disorder, hypersensitivity to acid is not a general phenomenon.