- Email: [email protected]
EXERCISE OXIMETRY FOR EARLY DIAGNOSIS OF PNEUMOCYSTIS CARINII PNEUMONIA
222 and respirgard II with the one-way baffle valve between nebuliser and mouthpiece removed). The system 22 mizer used by O’Docherty et al differs from the Acorn nebuliser we used in the present study by having a storage chamber to improve efficiency. Droplet size is similar with both versions. Patients received 5 mg nebulised terbutaline pre-treatment and the nebulisers were driven by a CR-60 compressor (Medic-Aid). Alveolar deposition of pentamidine was 73 (SD 12)% with respirgard II and 47 (8)% with the Acorn system 22 (p < 0-01); deposition with the respirgard II device without the baffle was 53 (13)%. Cough and breathlessness were significantly more common with the Acorn system 22 and peak expiratory flow rate (PEFR) fell with this system, but not with the other devices, the mean (SD) being 577 (75) 1/min post-terbutaline and 549 (78) 1/min
respirgard II,
post-pentamidine. Droplet size, as measured by a Malvern 2600 laser droplet analyser, was inversely related to alveolar deposition and directly related to the incidence of large-airway-related side-effects. The respirgard II nebuliser produced a mass median diameter (MMD) of 10 1ill1; the maximum droplet size was 69 Iill1 and 79% of droplets were below 2-0 1ill1. With the Acorn system 22 these figures were 3-4 1ill1, 25-3 m, and 40%, and for the respirgard device without baffle they were 17 um, 193 1ill1, and 51 %, indicating the critical role of the baffle valve in determining droplet size. We suggest that selection of a nebuliser with appropriate droplet size profile will facilitate alveolar deposition of pentamidine whilst reducing large-airway-related side-effects. The full respirgard II system has such a profile, but work in progress indicates that a similar droplet size range may be produced by incorporating an inspiratory baffle valve into some conventional British nebulisers. A. K. SIMONDS S. P. NEWMAN Department of Thoracic Medicine and Haemophilia Centre, Royal Free Hospital, London NW3 2QG 1 Miller
M. A. JOHNSON N. TALAEE C. A. LEE S. W. CLARKE
RF, Millar AB, Godfrey-Faussett P, Semple SJG. Nebulised pentamidine is effective therapy for Pneumocystis carinii pneumonia. Thorax 1988; 43: 848P
not an
EXERCISE OXIMETRY FOR EARLY DIAGNOSIS OF PNEUMOCYSTIS CARINII PNEUMONIA
SIR,-Dr Smith and colleagues (Nov 5, p 1049) report that a fall in oxygen saturation to 90% or less on exercise is a very sensitive indicator for Pneumocystis carinii pneumonia (PCP) in HIVinfected patients with pulmonary symptoms. We agree that exercise hypoxaemia is the most important sign of early PCP, but our experience suggests that it is better to measure oxygen pressure rather than oxygen saturation. Between June, 1987, and November, 1988, we did 48 exercise tests in 44 HIV-positive patients presenting with cough, dyspnoea, and fever. Patients exercised on a bicycle at 1 W/kg body weight for 3 min. Arterial capillary blood gas analysis was done at rest and immediately after exercise. An exercise-induced decrease in oxygen pressure (5 mm Hg or more) was defined as abnormal. All 15 patients with abnormal oxygen pressure after exercise underwent immediate bronchoscopy (including bronchoalveolar lavage and transbroncheal biopsy). Bronchoscopy was done in 3 patients with a normal test because of persisting symptoms or interstitial shadowing on chest X-ray: Norrnal exercise test I n 33) 28: no PCP within 2 months 2: PCP after 11 and 27 days* 3: immediate bronchoscopy (bacterial bronchitis 2, PCP Almormal exercise test I n = 151 r 11: PCP 3: interstitial pneumonia without identified pathogen 1: no abnormal finding at bronchoscopy, but treatment because of suspected PCP =
1).
at diagnosis; other not retested of PCP 11 patients had abnormal exercise At the time of diagnosis oxygen pressure and 1 had normal pressure (sensitivity 92%). If we
* had abnormal
exerase
oxunetry
all patients with interstitial pneumonia (including the 3 without identified pathogen), sensitivity becomes 93%. In contrast to Smith et al we found no decline in oxygen saturation in 8 out of 12 patients with PCP (sensitivity 33%). All patients with decline of oxygen saturation had already abnormal oxygen pressure (P02 75 mm Hg or less) at rest, and no patient with normal oxygen pressure at rest (n 5) showed saturation of 90% or below after exercise. The different findings may be explained by the more strenuous exercise protocol used by Smith et al (100 W for 10 min vs 70 W for3 min). Oxygen saturation is easier to measure than oxygen pressure, our shorter exercise test is less demanding for patients with exertional dyspnoea, and there is no loss in sensitivity.
count
=
G. FAETKENHEUER University Medical Clinic II, Polyclinic, and University Medical Clinic III, 5000 Cologne 41, West Germany
B. SALZBERGER B. ALLOLIO G. POTHOFF M. SCHRAPPE-BAECHER
CHEST PAIN AFTER INTRAVENOUS CORTICOTROPIN-RELEASING HORMONE
SiR,—Hypothalamic corticotropin-releasing hormone (CRH) has become widely accepted as a diagnostic aid in both endocrine and non-endocrine disease, either alone or sequentially with other hypothalamic releasing hormones.1,2 The test is thought to be safe when CRH doses are 100 ltg or less (1 fJg/kg) but hypotensive effects of higher doses of ovine or human CRH have been described in non-human primates and in man.3.4 Hermus and colleagues reported a sharp decrease in systolic blood pressure from 114 to 64 mm Hg with a junctional rhythm and asystole, necessitating resuscitation, 3 min after the intravenous injection of 200 gg CRH.5 In patients with adrenocortical insufficiency, in whom replacement therapy is inadequate or delayed, symptomatic hypotension can occur even with low doses of ovine CRH.6 A 55-year-old woman with rheumatoid arthritis who was on long-term glucocorticoid treatment had her adrenal function evaluated by an intravenous bolus injection of ovine CRH 100 /lg (Bachem) in 2 ml saline. Within 10 min the patient complained of oppressive chest pain accompanied by nausea and sweating. Her blood pressure fell from 140 to 95 mm Hg and ECG revealed a negative T-wave in D-1, aVL, and V4-V6. The patient was treated with glyceryl trinitrate and the T-wave returned to normal in 24 h. She mentioned two previous episodes of chest pain which had not been investigated. Coronary arteriography 2 days later was normal. This patient probably had haemodynamic angina (secondary to hypotension) or a coronary vasospasm. In non-human primates blood pressure changes after CRH have been attributed to a fall in peripheral vascular resistance due to selective dilatation of the superior mesenteric vessels.’ Serious reactions may occur with CRH, even at low doses, especially in patients with adrenal insufficiency, and this agent should be used with caution when there is a history of coronary heart disease. Rheumatology Service, Endocrinology Service, and Hormone Laboratory, Hospital D’Alacant-SVS, 03010 Alicante, Spam 1.
VELA CASASEMPERE PALOMA MAURI DOT MONTSE PASCUAL GÓMEZ ELISEO PICÓ ALFONSO ANTONIO MIGUEL
Taylor AL, Fishman LM Corticotropin-releasing hormone. N Engl J Med 1988, 319: 213-22
2. Sheldon WR
Jr, DeBold CR, Evans WS, et al. Rapid sequential intravenous administration of four hypothalamic releasing hormones as a combined anterior pituitary function test in normal subjects. J Clin Endocrinol Metab 1985; 60: 623-30. 3. Kaling NH, Shelton SE, Kraemer GW, McKinney WT Jr. Corticotropin-releasing factor causes hypotension in rhesus monkeys Lancet 1982; ii: 1042. 4. Hermus A, Pieters G, Pesman GJ, Benraad ThJ, Smals AGH, Kloppenborg PWC Safety of human and ovine corticotropin-releasing hormone. Lancet 1986; ii: 1032-33. A, Raemaekers JMM, Pieters J, Bartelink AKM, Smals AGH, Kloppenborg PWC. Serious reaction to corticotropin-releasing factor. Lancet 1983; i: 776 6 Gillies G, Grossman A. The CRFs and their control: chemistry, physiology and clinical implications. Clin Endocrinol 1985; 14: 821-43. 7. MacCannell KL, Ledens K, Hamilton PL, Rivier J. Amunine (ovine CRF), urotensin 5. Hermus
I and sauvagme, three structurally-related peptides, produce selective dilation of the mesenteric circulation. Pharmacology 1982; 25: 116-20.
respirgard II,
post-pentamidine. Droplet size, as measured by a Malvern 2600 laser droplet analyser, was inversely related to alveolar deposition and directly related to the incidence of large-airway-related side-effects. The respirgard II nebuliser produced a mass median diameter (MMD) of 10 1ill1; the maximum droplet size was 69 Iill1 and 79% of droplets were below 2-0 1ill1. With the Acorn system 22 these figures were 3-4 1ill1, 25-3 m, and 40%, and for the respirgard device without baffle they were 17 um, 193 1ill1, and 51 %, indicating the critical role of the baffle valve in determining droplet size. We suggest that selection of a nebuliser with appropriate droplet size profile will facilitate alveolar deposition of pentamidine whilst reducing large-airway-related side-effects. The full respirgard II system has such a profile, but work in progress indicates that a similar droplet size range may be produced by incorporating an inspiratory baffle valve into some conventional British nebulisers. A. K. SIMONDS S. P. NEWMAN Department of Thoracic Medicine and Haemophilia Centre, Royal Free Hospital, London NW3 2QG 1 Miller
M. A. JOHNSON N. TALAEE C. A. LEE S. W. CLARKE
RF, Millar AB, Godfrey-Faussett P, Semple SJG. Nebulised pentamidine is effective therapy for Pneumocystis carinii pneumonia. Thorax 1988; 43: 848P
not an
EXERCISE OXIMETRY FOR EARLY DIAGNOSIS OF PNEUMOCYSTIS CARINII PNEUMONIA
SIR,-Dr Smith and colleagues (Nov 5, p 1049) report that a fall in oxygen saturation to 90% or less on exercise is a very sensitive indicator for Pneumocystis carinii pneumonia (PCP) in HIVinfected patients with pulmonary symptoms. We agree that exercise hypoxaemia is the most important sign of early PCP, but our experience suggests that it is better to measure oxygen pressure rather than oxygen saturation. Between June, 1987, and November, 1988, we did 48 exercise tests in 44 HIV-positive patients presenting with cough, dyspnoea, and fever. Patients exercised on a bicycle at 1 W/kg body weight for 3 min. Arterial capillary blood gas analysis was done at rest and immediately after exercise. An exercise-induced decrease in oxygen pressure (5 mm Hg or more) was defined as abnormal. All 15 patients with abnormal oxygen pressure after exercise underwent immediate bronchoscopy (including bronchoalveolar lavage and transbroncheal biopsy). Bronchoscopy was done in 3 patients with a normal test because of persisting symptoms or interstitial shadowing on chest X-ray: Norrnal exercise test I n 33) 28: no PCP within 2 months 2: PCP after 11 and 27 days* 3: immediate bronchoscopy (bacterial bronchitis 2, PCP Almormal exercise test I n = 151 r 11: PCP 3: interstitial pneumonia without identified pathogen 1: no abnormal finding at bronchoscopy, but treatment because of suspected PCP =
1).
at diagnosis; other not retested of PCP 11 patients had abnormal exercise At the time of diagnosis oxygen pressure and 1 had normal pressure (sensitivity 92%). If we
* had abnormal
exerase
oxunetry
all patients with interstitial pneumonia (including the 3 without identified pathogen), sensitivity becomes 93%. In contrast to Smith et al we found no decline in oxygen saturation in 8 out of 12 patients with PCP (sensitivity 33%). All patients with decline of oxygen saturation had already abnormal oxygen pressure (P02 75 mm Hg or less) at rest, and no patient with normal oxygen pressure at rest (n 5) showed saturation of 90% or below after exercise. The different findings may be explained by the more strenuous exercise protocol used by Smith et al (100 W for 10 min vs 70 W for3 min). Oxygen saturation is easier to measure than oxygen pressure, our shorter exercise test is less demanding for patients with exertional dyspnoea, and there is no loss in sensitivity.
count
=
G. FAETKENHEUER University Medical Clinic II, Polyclinic, and University Medical Clinic III, 5000 Cologne 41, West Germany
B. SALZBERGER B. ALLOLIO G. POTHOFF M. SCHRAPPE-BAECHER
CHEST PAIN AFTER INTRAVENOUS CORTICOTROPIN-RELEASING HORMONE
SiR,—Hypothalamic corticotropin-releasing hormone (CRH) has become widely accepted as a diagnostic aid in both endocrine and non-endocrine disease, either alone or sequentially with other hypothalamic releasing hormones.1,2 The test is thought to be safe when CRH doses are 100 ltg or less (1 fJg/kg) but hypotensive effects of higher doses of ovine or human CRH have been described in non-human primates and in man.3.4 Hermus and colleagues reported a sharp decrease in systolic blood pressure from 114 to 64 mm Hg with a junctional rhythm and asystole, necessitating resuscitation, 3 min after the intravenous injection of 200 gg CRH.5 In patients with adrenocortical insufficiency, in whom replacement therapy is inadequate or delayed, symptomatic hypotension can occur even with low doses of ovine CRH.6 A 55-year-old woman with rheumatoid arthritis who was on long-term glucocorticoid treatment had her adrenal function evaluated by an intravenous bolus injection of ovine CRH 100 /lg (Bachem) in 2 ml saline. Within 10 min the patient complained of oppressive chest pain accompanied by nausea and sweating. Her blood pressure fell from 140 to 95 mm Hg and ECG revealed a negative T-wave in D-1, aVL, and V4-V6. The patient was treated with glyceryl trinitrate and the T-wave returned to normal in 24 h. She mentioned two previous episodes of chest pain which had not been investigated. Coronary arteriography 2 days later was normal. This patient probably had haemodynamic angina (secondary to hypotension) or a coronary vasospasm. In non-human primates blood pressure changes after CRH have been attributed to a fall in peripheral vascular resistance due to selective dilatation of the superior mesenteric vessels.’ Serious reactions may occur with CRH, even at low doses, especially in patients with adrenal insufficiency, and this agent should be used with caution when there is a history of coronary heart disease. Rheumatology Service, Endocrinology Service, and Hormone Laboratory, Hospital D’Alacant-SVS, 03010 Alicante, Spam 1.
VELA CASASEMPERE PALOMA MAURI DOT MONTSE PASCUAL GÓMEZ ELISEO PICÓ ALFONSO ANTONIO MIGUEL
Taylor AL, Fishman LM Corticotropin-releasing hormone. N Engl J Med 1988, 319: 213-22
2. Sheldon WR
Jr, DeBold CR, Evans WS, et al. Rapid sequential intravenous administration of four hypothalamic releasing hormones as a combined anterior pituitary function test in normal subjects. J Clin Endocrinol Metab 1985; 60: 623-30. 3. Kaling NH, Shelton SE, Kraemer GW, McKinney WT Jr. Corticotropin-releasing factor causes hypotension in rhesus monkeys Lancet 1982; ii: 1042. 4. Hermus A, Pieters G, Pesman GJ, Benraad ThJ, Smals AGH, Kloppenborg PWC Safety of human and ovine corticotropin-releasing hormone. Lancet 1986; ii: 1032-33. A, Raemaekers JMM, Pieters J, Bartelink AKM, Smals AGH, Kloppenborg PWC. Serious reaction to corticotropin-releasing factor. Lancet 1983; i: 776 6 Gillies G, Grossman A. The CRFs and their control: chemistry, physiology and clinical implications. Clin Endocrinol 1985; 14: 821-43. 7. MacCannell KL, Ledens K, Hamilton PL, Rivier J. Amunine (ovine CRF), urotensin 5. Hermus
I and sauvagme, three structurally-related peptides, produce selective dilation of the mesenteric circulation. Pharmacology 1982; 25: 116-20.