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The clinical, radiological, physiological and pathological features were studied in 6 cases of idiopathic bronchiolitis obliterans organized pneumonia (BOOP). Patients characteristically had a history of exertional dyspnea, cough, fever, weight loss, bilateral radiographic shadowing, elevated ESR and hypoxemia. Corticosteroids were effective; however, one patient died of cytomegalovirus pneumonia. The pathological features, distinguished by the presence of granulation tissue plugs extending from bronchioles into alveolar ducts and alveoli, are described in detail. The place of BOOP within the broad spectrum of bronchiolitis obliterans between small airways disease and usual interstitial pneumonia is discussed.

The aim of this study was to test the efficacy of nocturnal oximetry as a means of continuous recording of SaO2 in the identification of apnoeic events in the recognition of non-apnoeic desaturation. The oscillations of SaO2 in relation to successive periods of apnoea during the course of the sleep apnoea syndrome (SAS) or with apnoeic episodes in patients with chronic airflow obstruction (BPCO) or restricted disease, were identified using a new delta index quantifying the variations of SaO2 during the night. 26 successive patients in whom there was an indication for nocturnal oximetry were included in a prospective study comparing nocturnal oximetry and polysomnography during 34 nights. In the apnoeic patients we found a strong correlation (r = .85. p. less than .01) between the apnoeic period and the delta index. In BPCO the number of apnoea was correlated with the delta index (r = .96. p. less than .01). A minimal threshold of the delta index fixed at 1.5 was satisfactory for detecting apnoea if the initial SaO2 was less than 93%. The value of the adequate for affected detection ought to be fixed at .8 (95% sensitivity) when the initial SaO2 was greater than 93%. A detection of apnoeic events thus seems possible by this method.

Twenty-six asthmatic patients who were hospitalised following an acute asthmatic attack and who had a peak expiratory flow of less than 50% predicted, without hypercapnia, received 5 mg. of salbutamol delivered by a micronebulizer LSA on admission (HO). At H1, 10 mg of additional salbutamol were nebulised in cases where there had been an increase of less than 20% of the PEF. At H2, all the subjects received steroid therapy. Group 1 in which success was defined by an increase of 20% of peak flow judged at H1 and H2, and group II where the increase in peak flow was less than 20%. Group II benefited at H2 by treatment with theophylline or salbutamol intravenously given in a randomised fashion. At H8 the 2 treatments were associated in group II in cases of failures. 15 men, and 11 women aged 40 +/- 17 suffering from severe asthma (65% of Charpin Stage IV) were included. The mean peak flow at HO was 32 +/- 9% of the predicted PEF. 21 subjects, or 81% improved their peak flow by more than 20% at H2. The toleration for salbutamol was very good from the cardiovascular point of view. At HO there was no clinical criteria nor peak flow assessment which would enable one to predict the failures from nebulized salbutamol for a given subject. Nevertheless a level of dyspnoea of greater than 5 on Borg's scale and a peak flow of less than 150 l/min made failure likely.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty-seven patients who had been discharged from hospital six to eleven years after an acute episode of hemolytic uremic syndrome were studied. Glomerular filtration rates were measured by plasma slope clearance using 99mTc DTPA. Eleven patients had GFRs below 60 ml/min/1.73 m2. Hemolytic uremic syndrome may result in an appreciable deterioration in GFR undectable by routine laboratory tests and without clinical signs.

Cough and wheezing are common findings in left heart failure. However, it is still questionable whether nonallergic bronchial hyperresponsiveness, the hallmark of asthma, is also associated with this condition. In 12 subjects with acute decompensation of chronic postischemic LV failure, we assessed the PC20 methacholine during an episode of acute LV failure and after five to 15 days of intensive diuretic therapy. Weight, arterial blood gases, plethysmographic lung volumes, and expiratory flows were also measured on both visits. Extravascular lung water was estimated indirectly with a radiologic score. During acute decompensation, six subjects had significant airway obstruction and eight had a PC20 less than or equal to 16 mg/ml (significant bronchial hyperresponsiveness). After diuretic therapy, subjects improved significantly, losing an average of 2.2 kg, but they still had chronic LV failure and evidence of an obstructive breathing defect. Although mean PC20 was unchanged, three subjects had significantly improved PC20 after treatment. We conclude that: (1) left ventricular failure is often associated with mild bronchial hyperresponsiveness, although it is not excluded that smoking and the resulting possibility of bronchial obstruction can also play some role; and (2) acute treatment does not generally alter bronchial responsiveness to methacholine, suggesting that chronic LV failure can cause chronic changes to the airways.

Two cases of primary renal artery dissection in caucasian males, aged 40 and 37 years, respectively, are presented. In both subjects, the clinical picture disclosed renal infarction with transient deterioration of renal function, microhematuria and proteinuria. In 1 patient, a slight, temporary increase in blood pressure was also observed. Both men experienced contralateral relapse 12 days and 7 years, respectively, after the first episode. The diagnosis was based on characteristic (case 1) or suggestive (case 2) arteriographic findings. In 1 subject, control arteriography suggested some progression of the lesion. Both patients were treated conservatively. A comparison with 143 cases previously reported worldwide emphasizes some aspects of this 'not-so-rare' entity.

A case of severe, recurrent, macroscopic hematuria in which the diagnosis of renal vein varices was suggested by Tc-99m red blood cell blood pool imaging is described. Current diagnostic modalities are discussed and an integrated use of this test is proposed.

We have compared [Tc-99m] sodium pertechnetate with Tc-99m glucoheptonate in 52 patients studied for various brain lesions. Flow studies as well as delayed scans were performed in all. Especially in primary and metastatic lesions of the posterior fossa, the diagnostic yield was improved by the delayed glucoheptonate (GH) scans. In contrast, no advantage of GH over pertechnetate could be detected in the study of infarcts or other ischemic lesions. Various hypotheses are discussed to explain the observed differences in behavior between the two tracers.

Our study was designed to confirm the potential effects of three aminoglycosides on the disposition of thyroid hormones. Twenty-seven patients diagnosed with either cellulitis (n = 19), chronic osteitis (n = 4), or an abscess (n = 4) were selected. Thirteen patients received tobramycin, 60 to 100 mg iv q. 8 h., plus cloxacillin, 1 gm iv q. 4 h.; seven patients received netilmicin, 40 to 120 mg iv q. 8 h., plus cloxacillin, 1 gm iv q. 4 h.; and seven patients received either cloxacillin, 1.5 gm iv q. 4 h., or cefoperazone, 2 to 4 gm iv q. 12 h. for at least 7 days. Another group of six normal subjects received neomycin, 0.5 gm po q. 6 h. for 7 days. All these subjects had normal thyroid function before antibiotic dosing and none had thyroid function abnormalities. Tobramycin and cloxacillin/cefoperazone did not influence thyroid function. Netilmicin decreased the total serum concentrations of triiodothyronine (T3) from 114 +/- 9 to 75 +/- 7 ng/dl (P less than 0.01), probably because of increased clearance, as the T3 free fraction increased from 0.43% +/- 0.02% to 0.49% +/- 0.02% (P less than 0.05). Thyroxine (T4) and reverse T3 (rT3) levels were not affected. Neomycin decreased T3 levels from 104 +/- 8 to 92 +/- 7 ng/dl (P less than 0.05) and the serum concentrations of thyroglobulin from 17.3 +/- 2.0 to 11.7 +/- 2.0 ng/ml (P less than 0.001). Because T4 and rT3 levels did not change, our results suggest that neomycin may have directly affected the gland. We conclude that some aminoglycosides can alter the disposition of thyroid hormones.

Three cases of severe slow-release theophylline toxicity (plasma theophylline levels above 30 mg/l) in patients with severe chronic pulmonary disease are reported. Seizures were noted in all patients, and one had tachyarrhythmia. Two of the patients died. Several factors were present which may have impaired theophylline clearance, leading to toxic plasma levels. The mortality rate of theophylline intoxication being high, the initial doses should be sufficiently low to minimize the risk of adverse affects, and the best way to prevent theophylline toxicity is to monitor plasma concentrations. A management of patients with theophylline overdosage is suggested: oral administration of activated charcoal is the primary therapeutic measure; haemoperfusion or haemodialysis should be considered only in patients in whom conservative measures have failed.

Primary alveolar hypoventilation is a rare syndrome of unknown origin, characterized by a dysfunction of the automatic respiratory pattern in spite of normal lungs and in the absence of mechanical ventilatory defects. A reduction of the ventilatory response to CO2 is regularly found, and cardiac failure is common. The differential diagnosis mainly concerns the sleep apnoea syndrome. The usual treatments have little effectiveness.

Six women aged 31 to 70 years had folate deficiency and neuropsychiatric disorders. The three with acquired folate deficiency were depressed and had permanent muscular and intellectual fatigue, mild symptoms of restless legs, depressed ankle jerks, diminution of vibration sensation in the legs, stocking-type hypoesthesia and long-lasting constipation; D-xylos absorption was abnormal. The bone marrow was megaloblastic in only one patient, and she and one other had atrophy of the jejunal mucosa. The third was a vegan. All three recovered after folic acid therapy. The other three were members of a family with the restless legs syndrome, fatigability and diffuse muscular pain. One also had subacute combined degeneration of the spinal cord and kidney disease but no megaloblastosis; she improved spectacularly after receiving large daily doses of folic acid. The other two also had minor neurologic signs, controlled with 5 to 10 mg of folic acid daily. Unrecognized and treatable folate deficiency (with low serum folic acid values but normal erythrocyte folate values) may be the basis of a well defined syndrome of neurologic, psychiatric and gastroenterologic disorders, and the restless legs syndrome may represent the main clinical expression of acquired and familial (or inborn) folate deficiency in adults.