False positive skin tests with Parke-Davis Aplisol.
Explore the source record for details and available documents.
False Positive Reactions↗
Biomedical subjects
C Iber
Publications and source records attributed to C Iber.
Ventilatory adaptations to resistive loading during wakefulness and non-REM sleep.
Ventilatory and timing responses to repetitive and sustained inspiratory resistive loading were assessed in six naive male subjects during wakefulness (AW) and non-REM sleep (NREM). In five of six subjects, tidal volume (VT) was maintained or increased with repetitive five-breath loading periods during wakefulness. In these five subjects, mouth occlusion pressure (P100) increased with loading during AW (1.8 +/- 0.5 control vs. 2.2 +/- 0.4 cmH2O loaded, P less than 0.05), but not during NREM (2.1 +/- 1.5 control vs. 2.1 + 1.5 cmH2O loaded). For each state, VT and frequency (f) responses to sustained loads were similar to responses to five-breath loads. During sustained loading; a) VT increased 35% during AW, decreased 28% during NREM, b) f decreased 35% during AW, increased 6% during NREM, c) minute ventilation (VE) decreased 12% during AW, decreased 23% during NREM. Ventilatory responses persisted until arousal (0.4--1.7 min) in NREM. With repetitive loading: a) inspiratory duration (TI) increased during AW but did not change during NREM, b) "duty cycle" (TI/TT) increased with loading in both states. These findings suggest that a) NREM abolishes between-breath augmentations in P100, b) within-breath load compensation is operant during both AW (preserved VT) and NREM (failure of predicted TI prolongation) by differing mechanisms, c) arousal may be a ventilatory compensation to inspiratory resistive loading in NREM.
Adult↗
Paragonimiasis in the United States. A report of nine cases in Hmong immigrants.
Nine cases of paragonimiasis have been encountered in Laotian Hmong immigrants from Camp Ban Vinai in Thailand. Symptoms included cough, hemoptysis, and fever. Chest x-ray films showed segmental infiltrates and pleural effusions, often bilateral. The clinical presentation mimics tuberculosis. All Hmong patients with chronic infiltrates and pleural disease in whom tuberculosis has not been proven should have parasitologic and serologic evaluation to exclude paragonimiasis.
Adolescent↗
Correction of CO2 retention during sleep in patients with chronic obstructive pulmonary diseases.
Three normal subjects and 5 patients with chronic obstructive pulmonary disease and chronic CO2 retention were studied to determine the effect of chronic ventilatory stimulation with medroxyprogesterone acetate (MPA) on ventilatory control and pulmonary gas exchange during sleep. All patients had lowered PaCO2 after treatment with MPA while awake. Using a randomized application of treatment and placebo conditions, 4 wk of MPA therapy in the normal subjects caused a reduction in PaCO2 while awake (delta PaCO2 -4 to -7 mmHg) and during non-REM sleep (delta PaCO2 -5 to -7 mmHg). The response consisted of an increased minute ventilation (VE), tidal volume (VT), and mean inspiratory flow (VT/TI) awake and during non-REM sleep. In the patient group, 4 wk of MPA therapy caused significant reductions in PaCO2 while awake (from 54 +/- 2 to 47 +/- 2 mmHg) and during non-REM sleep (from 57 +/- 2 to 49 +/- 2 mmHg). Minute ventilation tidal volume, and mean inspiratory flow increased to a similar extent while awake and during all sleep stages. Improvement in SaO2 during sleep induced by treatment was attributable to an increase in alveolar ventilation rather than a decrease in alveolar-arterial oxygen partial pressure difference. Medroxyprogesterone acetate elicited chronic increases in inspiratory effect, tidal volume, and alveolar ventilation while awake and during all sleep stages in selected patients with chronic CO2 retention despite severe mechanical impairment and maldistribution ventilation:perfusion. The drug drives ventilation by a mechanism of action that is independent of many other peripheral and "central" ventilatory stimuli and/or inhibitors, including higher central nervous system influenced on ventilatory control that are dependent on the state of wakefulness.
Clinical Trials as Topic↗
Disordered breathing during sleep in hypothyroidism.
A 58-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 microIU/ml (normal, less than 12 microIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (VE/VCO2), and the ventilatory response to exercise (delta VE/delta VCO2) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38 to 33 mm Hg), and an increase in VE/VCO2 (17%), mouth occlusion pressure (50%), and AVE/VCO2 (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and VE/VCO2 despite a 23% increase in VE. Mouth occlusion pressure increased 37% but delta VE/delta VCO2 was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted completed relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.
Carbon Dioxide↗
Determinants of hypoventilation during wakefulness and sleep in diaphragmatic paralysis.
A 45-yr-old man with limb girdle muscular dystrophy, bilateral diaphragmatic paralysis, chronic carbon dioxide retention, and hypersomnolence was studied to determine the causes of hypoventilation during wakefulness and during sleep. Awake hypoventilation was associated with an insufficient inspiratory effort in the presence of inefficient respiratory muscles and a shortened inspiratory time. During sleep, severe hypoventilation and oxygen desaturation occurred only during REM-induced intercostal and accessory muscle inhibition.
Diaphragm↗