Pyogenic vertebral osteomyelitis presenting as exudative pleural effusion: a series of five cases.

Five patients are reported who have pleural effusion and pyogenic vertebral osteomyelitis. In four of the five patients, the presenting problem was a large pleural effusion, and three of these four patients had an exudative effusion. Initial evaluation and investigations in these patients were directed toward the pleuropulmonary disease, delaying the diagnosis of osteomyelitis, and in two patients, this delay resulted in neurologic complications. In the fifth patient, the pleural effusion was initially small; however, during the course of a workup for osteomyelitis, the effusion increased rapidly. Two out of the five patients had empyema, and the other three patients had a large pleural effusion associated with and apparently caused by vertebral osteomyelitis. Vertebral osteomyelitis should be considered in the differential diagnosis of pleural effusion of uncertain cause especially if there is associated back pain.

Upper airway obstruction due to inhalation of a tracheal T-tube resulting in pulmonary edema.

Acute upper airway obstruction may present with pulmonary edema. Following is a report of pulmonary edema secondary to acute upper airway obstruction due to inhalation of a Montgomery tracheal T-tube. The principal factor causing pulmonary edema is the generation of large negative transpulmonary pressures. This may be enhanced by changes in the cardiovascular function due to the Müller maneuver.

Dynamic T-cell changes in peripheral blood and bronchoalveolar lavage after antigen bronchoprovocation in asthmatics.

We previously demonstrated decrease of peripheral blood CD4+ cells 48 to 72 h after antigen-induced bronchoprovocation in asthmatic subjects. To determine if this was accompanied by reciprocal changes in bronchoalveolar lavage (BAL) fluid, we sampled BAL before and 48 h after antigen administration. Peripheral blood lymphocytes (PBL) and BAL T-cell subset composition were examined in eight extrinsic asthmatics during three different weeks. During control week (CW) BAL was preformed at baseline, and PBL subsets were followed for 3 days. During placebo week (PW) a placebo inhalation was followed by a BAL at 48 h and daily PBL for 3 days. Asthmatic attacks were induced by inhalation of a relevant antigen at the start of antigen week (AW) and followed by examining the BAL at 48 h and PBL daily for 72 h. We found that BAL as a stimulus had no effect on T-cell composition of the PBL after the procedure. After induction of an asthmatic attack there was a reduction of PBL CD4+ cells from a baseline mean of 52.6% to 38.8% at 48 h (p less than 0.05). At the same time BAL CD4+ cells increased from 35.6% at PW to 47.3% in AW (p less than 0.05). These data are compatible with specific recruitment of PBL CD4+ cells into the respiratory system in atopic subjects undergoing antigenic bronchoprovocation.

Antigen-induced T-cell changes: modulation by pharmacologic agents.

To determine the effect of pharmacologic modulation of alterations of peripheral blood T-cell subsets caused by antigen-induced bronchoconstriction, we administered albuterol immediately after antigen-induced bronchoconstriction in a double-blind to protocol to 12 atopic asthmatic subjects. We also administered cromolyn sodium before antigen to 7 of the same subjects. Peripheral blood T-cell subset composition (CD4, CD8, Ia) of a highly purified T-cell preparation was determined before, 24, 48, 72, and 168 h after bronchoconstriction. We found that placebo inhalation immediately after antigen-induced bronchoconstriction did not affect subsequent peripheral blood T-cell subset changes (decrease in CD4+ and increase in Ia+ T lymphocytes). In contrast, inhaled albuterol abolished these T-cell subset changes. Although cromolyn sodium significantly decreased the severity of antigen-induced bronchoconstriction, it did not affect T-cell subset composition changes at the dosage used. We conclude that albuterol can ablate T-cell subset changes associated with antigen-induced bronchoconstriction. Cromolyn sodium ameliorates bronchoconstriction, but has no affect on T-cell subset composition changes. This implies that T-cell changes and bronchoconstriction caused by antigen inhalation are mediated through different pathways.

Focus of bronchial carcinoma in situ eradicated by endobronchial biopsy.

Bronchial carcinoma in situ is not frequently diagnosed in a clinical setting. A bronchoscopic biopsy of a small mucosal abnormality in a patient with hemoptysis yielded a diagnosis of carcinoma in situ. The involved lobe was resected. On thorough histologic examination of the surgical specimen, no residual carcinoma could be found. To our knowledge, this is unprecedented in the literature. This case emphasizes the importance of biopsying subtle abnormalities and raises questions about the optimal management of in situ bronchial carcinoma.

Seasonal variation of airway function in allergic rhinitis.

We set out to examine seasonal variation in airway bronchoconstriction in patients with seasonal allergic rhinitis. Airway conductance and response to methacholine challenge were measured during pollen season, as well as in winter when pollen exposure was not present. Airway conductance and spirometry were performed on 17 subjects during allergy season and in winter. In eight of these subjects the measurements were repeated in the successive allergy season. Methacholine bronchoprovocation was performed on 17 of the subjects in winter and in eight subjects in allergy season. We found airway constriction in both allergy seasons as evidenced by specific airway conductance (SGaw) of 0.188 +/- 0.06 and 0.203 +/- 0.03. In contrast, SGaw during winter was 0.27 +/- 0.11. When winter and summer seasons were compared, both summer SGaw values were significantly lower than winter SGaw, p less than 0.01 and p less than 0.05, respectively. Mean airway sensitivity to methacholine during allergy season was 16.1 breath units and not different than out of season 11.7 breath units; p = NS. The reactivity to methacholine (slope of the dose-response curve) and spirometry (FVC, FEV1, FEV1/FVC) in and out of allergy season were likewise not different. The data indicate that patients with allergic rhinitis have unique physiologic behavior separating them from patients with asthma or normal subjects. They develop seasonal bronchoconstriction unassociated with clinical bronchospasm, but this seasonal bronchoconstriction does not potentiate their sensitivity to methacholine. However, they have increased airway sensitivity to methacholine, and this feature distinguishes them from normal subjects.

Atopic asthma: T lymphocyte subpopulations.

Atopy is associated with diminished cell-mediated immunity and increased amounts of IgE, both of which may be caused by imbalances of T lymphocyte subsets. We compared the composition of highly purified peripheral-blood T cells of fifteen atopic asthmatics with ten non-atopic control subjects. Each subject was examined on five separate occasions. Indirect immunofluorescence using monoclonal antibodies was used to define T cell subsets. We examined the proportion of T cells with T3 (most T cells), T4 (helper/inducer), T8 (suppressor/cytotoxic), M1 (natural killer), and Ia (activated T cells) surface antigens. Blood was obtained at the same time of day to eliminate the effects of circadian rhythm. Subjects were taking no medications. We found no difference between the groups of the percentage of T cells with T4, T8, M1, and Ia antigens, nor the ratio of T4+ (helper) to T8+ (suppressor) cells. T3 percent was slightly (94.3 vs 92.5%) higher in the atopic group. We conclude that atopic asthma is not associated with imbalances of peripheral-blood T cell subsets.

Atopic asthma: T-cell response to corticosteroids.

Atopic asthma is associated with diminished cell-mediated immunity and elevated levels of IgE, both of which may be caused by imbalances of T-lymphocyte subsets. We analyzed the response of peripheral blood T-cell subsets to two commonly used corticosteroid preparations as a probe of T-cell subset regulation. We administered prednisone (P) 60 mg or 20 mg, beclomethasone dipropionate (BDP) aerosol, 336 micrograms, placebo, or BDP vehicle in a double-blind protocol to 15 atopic asthmatic patients and ten nonatopic subjects. No difference was found between the groups of the baseline number of T-cells with T4, T8, M1, and Ia antigens, nor the ratio of T4+ (helper) to T8+ (suppressor) cells. Five hours after administration of BDP aerosol, BDP vehicle, and oral placebo, there was no change of these values in either the atopic or in the nonatopic group. In contrast, P, 20 and 60 mg, caused a fall of T4/T8 ratio in the atopic, but not in the nonatopic population. Atopic asthma is not associated with baseline imbalances of peripheral blood T-cell subsets, but is associated with an abnormal response to systemic, but not inhaled corticosteroid.

Prednisone and T-cell subpopulations.

Alteration of T-cell subset relationships may cause many of the anti-inflammatory and immunoregulatory effects of glucocorticosteroids. The effect of oral administration of lactose or 60 mg of prednisone on peripheral blood T-lymphocyte subset profile and total eosinophil count (TEC) was examined. A purified T-cell peripheral blood population was obtained and the proportion of T cells with T3, T4, T8, M1, and la surface antigens was determined before and five hours after ingestion of lactose or prednisone. Lactose caused no change of any of the measured values. Prednisone caused a large (72%) decrease of the total lymphocyte number and the TEC (97%) but no change of the proportion of T cells with the previously mentioned antigens. Administration of 60 mg of prednisone does not acutely selectively deplete subclasses of T lymphocytes from peripheral blood.

Changes in T-lymphocyte subpopulations after antigenic bronchial provocation in asthmatics.

To determine whether inhaled agents can alter T-cell subsets in the peripheral blood of patients with bronchial asthma, we tested six asymptomatic asthmatics who were sensitive to mixed grass (positive skin test) with mixed grass extract, methacholine, and an antigen to which they were not sensitized (negative skin test). Levels of OKT4 cells (helper T lymphocytes) were reduced in the peripheral blood immediately after the challenge with mixed grass extract, and remained low for at least 72 hours. Levels of Ia-positive (activated) T cells were increased 48 hours after the challenge. No changes were observed in any of these T-cell subpopulations after challenge with methacholine or after the inhalation of an equal amount of an antigen to which the subjects were not sensitized. These results suggest that the selective loss of circulating helper T cells and an increase in activated T cells after an asthmatic attack induced by antigenic inhalation may serve as an indicator of immune-mediated bronchoconstriction.

Elastolysis of insoluble elastin.

We developed an assay for measurement of elastolytic activity using insoluble 3H-labelled particulate elastin adherent to plastic that is capable of detecting 150 picograms of pancreatic elastase. This equals or exceeds the sensitivity of the most sensitive previously reported systems, without requiring sodium dodecyl sulfate treatment of the elastin. Elastin digestion is dependent upon substrate and elastase concentration, but is not linearly related to time. This is partially attributable to elastase denaturation or autolysis under the assay conditions. The assay could easily detect elastase secreted by either peritoneal or alveolar macrophages. Compared to previously described assays using substrates that closely resemble the physiologic substrate, this represents a considerable increase of sensitivity of detection of elastolytic activity of enzymes.

A calibrated delivery system for inhalation challenge of toluene di-isocyanate vapor.

The vapor of TDI, a chemical commonly used in the plastics industry, may be associated with pulmonary symptoms at various concentrations. Because of the high volatility and adsorptivity of TDI, it has been difficult to deliver known, dilute concentrations of TDI to test subjects in inhalation challenge studies. A delivery system has been developed which can be calibrated to deliver an air-TDI mixture having a given flow rate and TDI concentration. The delivered gas stream is produced by diluting a gas stream having a low flow rate and a fixed concentration of TDI with a high-flow-rate stream of TDI-free air. A TDI detector continuously monitors the concentration of the resultant mixture, which is delivered to the subject by means of a face mask. For dilute mixtures, the output concentration is proportional to the ratio of the input flow rates; the proportionality factor depends on temperature and the geometry of the system. The flows for the described system could be regulated to produce concentrations in the range 0.0 to 0.08 ppm which remain stable to within +/- 10%.

Pi-Z phenotypes in a pulmonary clinic. Their prevalence and physiologic state.

A series of 1,458 consecutive patients referred to the Cleveland Veterans Administration Pulmonary Clinic for pulmonary function studies was evaluated for alpha 1-antitrypsin deficiency by determination of serum trypsin inhibitory capacity (STIC). Protease inhibitor (Pi) phenotyping was performed on all sera with STIC values less than 1.6 mg/ml. The following non-MM phenotypes were found: 1FZ, 32MZ, 2ZZ, 3SZ, 5SS, 33MS, 21M. The prevalence of Pi Z heterozygosity is 2.74%. This figure is not significantly greater than that observed in a healthy population. A group ( n = 12) with heterozygous Z phenotype (MZ + SZ) was compared with a control (MM) group (n = 13) matched for age, race and smoking history from this same population. Our findings indicate similar deviations from predicted normal values in both control (MM) and Z-heterozygotic groups for physiologic tests of airway resistance, lung volumes, diffusing capacity, and static and dynamic compliance. There was no significant difference between MM controls and MZ heterozygotes in the physiologic variables measured.

A case of idiopathic hypoparathyroidism and dietary vitamin D deficiency: the requirement for calcium and vitamin D for bone, but not renal responsiveness to PTH.

A patient with concurrent idiopathic hypoparathyroidism and dietary vitamin D deficiency was studied. Acute renal responsiveness to PTH was demonstrated by immediate increases in urinary cyclic AMP and phosphorus excretion. An impaired bone response to sustained PTH administration was demonstrated by absence of significant increases in serum calcium or urine hydroxyproline during 3 days of PTH administration. Skeletal responsiveness was restored either by raising the initial serum calcium with constant calcium infusion or by raising serum 25-OH-D levels to normal by administration of 1,000 units vitamin D daily. These results extend to the human, animal observations which suggest that vitamin D is required for the skeletal but not for the renal actions of parathyroid hormone.