An unusual cause of a mediastinal mass.

Our case report describes an unusual cause of a mediastinal mass. The patient is a current smoker with a background of neurofibromatosis (NF) type 1 who presented with a right apical mass. Initial investigations suggested a probable malignant cause. The final diagnosis was one of a haematoma from a ruptured thyrocervical aneurysm. The association between neurofibromatosis and vascular aneurysms is an often unrecognised but documented phenomenon. We would like to raise an awareness of this infrequent presentation, as it is associated with a high mortality and may be prevented by early diagnosis.

Fever of unknown origin in pregnancy: the need for a full history.

A 26-year-old woman with 29 weeks gestation presented with headache, photophobia and fever. She had deranged liver function tests and low platelets on admission. Blood film, performed to look for haemolysis, revealed she had Plasmodium vivax malaria, despite not having travelled to an endemic malaria area for over 1 year. The diagnosis was confirmed on PCR test performed in the HPA malaria reference laboratory in London and she was treated with chloroquine. She delivered a healthy baby at 33+3 weeks gestation, and once the patient and the baby had both tested negative for glucose-6-phospate dehydrogenase deficiency, she was given primaquine to clear the hypnozoite phase in the liver. This case highlights the importance of an extended travel history in a patient with fever of unknown origin and the difficulties of treating non-falciparum malaria in pregnancy.

Mycobacterium microti infection associated with spindle cell pseudotumour and hypercalcaemia: a possible link with an infected alpaca.

A 44-year-old woman who had recently been on immunosuppressive therapy presented with malaise, cough, fever, weight loss, lymphadenopathy, severe hypercalcaemia and a paratracheal mass on imaging. The initial impression was of disseminated malignancy, and lymphoma was suspected. A mediastinal biopsy showed a mycobacterial spindle cell pseudotumour containing acid and alcohol fast bacilli (AAFB). Sputum microscopy demonstrated AAFBs, confirmed as Mycobacterium tuberculosis complex by PCR. Prolonged culture grew Mycobacterium microti, an organism often associated with disease in small rodents and llamas. M microti isolates from postmortem samples of an alpaca at a nearby farm were genetically indistinguishable. Although the patient had not visited the farm, concurrent illness in her adopted stray cat suggested a possible zoonotic connection. The patient responded to antituberculous therapy, and rehydration and pamidronate for hypercalcaemia. We believe the hypercalcaemia was caused by a similar mechanism to raised calcium levels sometimes seen in tuberculosis.

Nasal epithelial cells as surrogates for bronchial epithelial cells in airway inflammation studies.

The nose is an attractive source of airway epithelial cells, particularly in populations in which bronchoscopy may not be possible. However, substituting nasal cells for bronchial epithelial cells in the study of airway inflammation depends upon comparability of responses, and evidence for this is lacking. Our objective was to determine whether nasal epithelial cell inflammatory mediator release and receptor expression reflect those of bronchial epithelial cells. Paired cultures of undifferentiated nasal and bronchial epithelial cells were obtained from brushings from 35 subjects, including 5 children. Cells were subject to morphologic and immunocytochemical assessment. Mediator release from resting and cytokine-stimulated cell monolayers was determined, as was cell surface receptor expression. Nasal and bronchial cells had identical epithelial morphology and uniform expression of cytokeratin 19. There were no differences in constitutive expression of CD44, intercellular adhesion molecule-1, alphavbeta3, and alphavbeta5. Despite significantly higher constitutive release of IL-8, IL-6, RANTES (regulated on activation, normal T cell expressed and secreted), and matrix metalloproteinase (MMP)-9 from nasal compared with bronchial cells, the increments in release of all studied mediators in response to stimulation with IL-1beta and TNF-alpha were similar, and there were significant positive correlations between nasal and bronchial cell secretion of IL-6, RANTES, vascular endothelial growth factor, monocyte chemoattractant protein-1, MMP-9, and tissue inhibitor of metalloproteinase-1. Despite differences in absolute mediator levels, the responses of nasal and bronchial epithelial cells to cytokine stimulation were similar, expression of relevant surface receptors was comparable, and there were significant correlations between nasal and bronchial cell mediator release. Therefore, nasal epithelial cultures constitute an accessible surrogate for studying lower airway inflammation.

Home warmth and health status of COPD patients.

BACKGROUND: Home Energy Efficiency guidelines recommend domestic indoor temperatures of 21 degrees C for at least 9 h per day in living areas. Is health status of patients with Chronic Obstructive Pulmonary Disease (COPD) associated with maintaining this level of warmth in their homes? METHODS: In a cross-sectional observational study of patients, living in their own homes, living room (LR) and bedroom (BR) temperatures were measured at 30 min intervals over 1 week using electronic dataloggers. Health status was measured with the St George's Respiratory Questionnaire (SGRQ) and EuroQol: EQ VAS. Outdoor temperatures were provided by Met Office. RESULTS: One hundred and forty eight patients consented to temperature monitoring. Patients' mean age was 69 (SD 8.5) years, 67 (45%) male, mean percentage of predicted Forced Expiratory Volume in one second (FEV(1)) 41.7 (SD 17.4). Fifty-eight (39%) were current smokers. Independent of age, lung function, smoking and outdoor temperatures, poorer respiratory health status was significantly associated (P = 0.01) with fewer days with 9 h of warmth at 21 degrees C in the LR. A sub analysis showed that patients who smoked experienced more health effects than non-smokers (P < 0.01). CONCLUSION: Maintaining the warmth guideline of 21 degrees C in living areas for at least 9 h per day was associated with better health status for COPD patients. Patients who were continuing smokers were more vulnerable to reduction in warmth.

Indoor air quality in homes of patients with chronic obstructive pulmonary disease.

RATIONALE: Outdoor air quality is associated with respiratory morbidity and mortality. Less is known of the relationship of indoor air quality to respiratory health of groups vulnerable to outdoor air, such as those with chronic obstructive pulmonary disease (COPD). OBJECTIVES: To investigate among patients with COPD the association of health status with indoor air quality in their homes. METHODS: Observational study of indoor environmental characteristics of homes of 148 patients with severe COPD in North East Scotland. MEASUREMENTS AND MAIN RESULTS: Airborne living room levels of particulate matter with a diameter of 2.5 microm or less (PM(2.5)) (microg/m(3)) were measured over 8 to 14 hours using DustTrak monitors. Nitrogen dioxide exposure (ppb) in living rooms was measured over 1 week. Endotoxin (EU [endotoxin units]/mg) in living room dust was measured. Health status of participants was assessed by the St. George's Respiratory Health Questionnaire (symptoms, activity limitation, and disease impact). The mean age of participants was 69 years. Approximately 45% were male, 39% were smokers, and 49% lived in smoking households. Average indoor PM(2.5) levels were 18 mug/m(3), nitrogen dioxide was 7.8 ppb, and endotoxin levels were 95.8 EU/mg of dust. PM(2.5) was significantly higher in smoking households (P < 0.001) and was associated with higher levels of endotoxin and NO(2). PM(2.5) was significantly associated with increased symptom burden (P < 0.01), with greater effect for current smokers. Endotoxin and nitrogen dioxide exposure were not related to health status. CONCLUSIONS: Higher levels of PM(2.5) are associated with worse health status of these patients with severe COPD. Indoor levels of PM(2.5) are significantly higher in homes with smokers.

Measurement of respiratory rate from the photoplethysmogram in chest clinic patients.

OBJECTIVE: We studied the application of our algorithm for the robust extraction of respiratory information from the pulse oximeter signal acquired from a selection of patients attending the chest clinic. METHODS: Photoplethysmograms were obtained from 16 individuals: 13 patients with various conditions in the respiratory ward and three healthy subjects. Wavelet transforms were generated from which respiratory information was extracted to obtain a measure of respiratory rate. This measured rate was compared with the respiratory rate determined by one of a variety of other means (a digital end tidal CO(2) signal, the output from a non-invasive ventilation device, or a switch actuated by the patient or observer.) RESULTS: Respiratory rates varied from 6.2 to 35.8 breaths per minute (bpm). The oximeter rate determined through our method matched the marker rate obtained for all patients to within 1 bpm. CONCLUSION: The technique allows the measurement of respiratory rate directly from the photoplethysmogram of a pulse oximeter, and leads the way for development of a simple non-invasive combined respiration and saturation monitor useful for patients with all forms of breathlessness.

A fully automated algorithm for the determination of respiratory rate from the photoplethysmogram.

OBJECTIVE: To determine if an automatic algorithm using wavelet analysis techniques can be used to reliably determine respiratory rate from the photoplethysmogram (PPG). METHODS: Photoplethysmograms were obtained from 12 spontaneously breathing healthy adult volunteers. Three related wavelet transforms were automatically polled to obtain a measure of respiratory rate. This was compared with a secondary timing signal obtained by asking the volunteers to actuate a small push button switch, held in their right hand, in synchronisation with their respiration. In addition, individual breaths were resolved using the wavelet-method to identify the source of any discrepancies. RESULTS: Volunteer respiratory rates varied from 6.56 to 18.89 breaths per minute. Through training of the algorithm it was possible to determine a respiratory rate for all 12 traces acquired during the study. The maximum error between the PPG derived rates and the manually determined rate was found to be 7.9%. CONCLUSION: Our technique allows the accurate measurement of respiratory rate from the photoplethysmogram, and leads the way for developing a simple non-invasive combined respiration and saturation monitor.

Wheezy bronchitis in childhood: a distinct clinical entity with lifelong significance?

BACKGROUND: Historically, clinicians have recognized the existence of the clinical syndrome of childhood wheezy bronchitis. In the late 1960s, children with this syndrome were relabeled as having asthma, and the term wheezy bronchitis was abandoned. In a 1989 study of a cohort that originally had been studied in 1964, we reported that those who had childhood wheezy bronchitis had as adults attained lung function similar to that of healthy control subjects and had less significant symptoms than did those who had experienced childhood asthma, in whom lung function was reduced. In this study, we reexamined these subjects 12 years later to determine whether the improved outcome of the wheezy bronchitis group had been maintained. METHODS: In 2001, we followed up the 283 participants of the 1989 study, who were now aged 45 to 50 years. In interviews, respiratory symptoms and smoking status were assessed. Spirometry was measured. RESULTS: One hundred seventy-seven subjects (63%) completed the study. After adjusting for age, height, gender, socioeconomic status, smoking status, and number of pack-years smoked, the current FEV(1) in the childhood asthma group (mean, 2.45 L; 95% confidence interval, 2.29 to 2.62) was significantly lower than the wheezy bronchitis group (2.78 L, 95% confidence interval, 2.64 to 2.91; p < 0.01) and the control group (2.96 L; 95% confidence interval, 2.83 to 3.1; p < 0.01). The difference between the wheezy bronchitis group and the control subjects was not significant (p = 0.06). Between 1989 and 2001, both the childhood wheezy bronchitis group (p < 0.01) and the childhood asthma group (p = 0.01) had greater declines in FEV(1) than did the control group (asthma group decline, - 0.75 L [95% confidence interval, - 0.66 to - 0.84]; wheezy bronchitis group decline, - 0.75 L [95% confidence interval, - 0.68 to - 0.83]; control group decline, - 0.59 L [95% confidence interval, - 0.52 to - 0.67]). In 2001, the asthma group had more symptoms than did the wheezy bronchitis group (p < 0.01), who were more symptomatic than the control group (p < 0.01). CONCLUSION: Those with childhood wheezy bronchitis, having achieved normal lung function in earlier adulthood, now show a more rapid decline in lung function than did control subjects. If this rate of decline persists, these subjects may develop obstructive airways disease in later life.