Biomedical subjects

A J Hance

Publications and source records attributed to A J Hance.

At least 73 records · Page 4Linked to original sources

PubMed1990

1,25(OH)2D2 production by T lymphocytes and alveolar macrophages recovered by lavage from normocalcemic patients with tuberculosis.

To compare extra-renal 1,25(OH)2D3 production in different types of granulomatous disease, and to identify the cell types responsible, we have evaluated the conversion of 25(OH)D3 in 1,25(OH)2D3 by uncultured cells recovered by bronchoalveolar lavage and blood mononuclear cells from normocalcemic patients with sarcoidosis and tuberculosis. 1,25(OH)2D3 was produced both by lavage cells (12/12 tuberculosis patients, 2/6 sarcoidosis patients) and blood mononuclear cells (3/5 tuberculosis patients, 0/3 sarcoidosis patients) from patients but not controls, but significantly greater amounts were produced by lavage cells from tuberculosis patients than those of sarcoidosis patients (P less than 0.001). 1,25(OH)2D3 production by lavage cells from tuberculosis patients correlated with the number of CD8+ T lymphocytes present but not other cell types. T lymphocytes appeared to be an important source of 1,25(OH)2D3 production, since purified T lymphocytes from all patients with tuberculosis produced 1,25(OH)2D3, and 1,25(OH)2D3 production by these cells correlated closely with that produced by unseparated lavage cells. Because 1,25(OH)2D3 can improve the capacity of macrophages to kill mycobacteria, our results support the conclusion that macrophage-lymphocyte interactions, mediated at least in part by 1,25(OH)2D3, may be an important component of a successful antituberculous immune response.

Adult↗

PubMed1989

Rapid diagnosis of tuberculosis by amplification of mycobacterial DNA in clinical samples.

A method based on DNA amplification and hybridisation for the rapid detection of Mycobacterium tuberculosis was used to test 35 clinical specimens (sputum, gastric aspirate, abscess aspirate, biopsy sample) from 34 patients in whom tuberculosis was suspected. M tuberculosis was detected in 15 specimens, 2 of which were negative by standard microbiological criteria (microscopy and/or culture). 20 specimens, negative by standard methods, were also negative by the amplification method. M tuberculosis was also detected in peripheral blood samples of 2 of 4 patients with AIDS from whom the organism had been isolated.

Acquired Immunodeficiency Syndrome↗

PubMed1989

Catalepsy induced by combinations of ketamine and morphine: potentiation, antagonism, tolerance and cross-tolerance in the rat.

Previous studies demonstrated that both ketamine and morphine induced analgesia and catalepsy in the rat. Pre-treatment with ketamine produced cross-tolerance to morphine, whereas pretreatment with morphine did not induce cross-tolerance to ketamine but rather augmented the cataleptic response; this augmentation was attributed to residual morphine in the brain. The present studies explored the duration of the loss of righting reflex induced by sub-effective doses of ketamine and morphine, administered simultaneously. There was mutual potentiation between sub-effective doses of ketamine and morphine, but sub-effective doses of ketamine partly antagonized fully-effective doses of morphine. Latency to the loss of righting reflex, rigidity and behavior on recovery, reflected the relative predominance of ketamine or morphine in each combination. Naloxone inhibited the induced cataleptic effects. The degree and time course of development of tolerance to daily administration of sub-effective dose combinations of ketamine and morphine were similar. Rats, tolerant to ketamine-dominant combinations, were cross-tolerant to both drugs, while those tolerant to morphine-dominant combinations were cross-tolerant to morphine but showed either no cross-tolerance or an augmented response to ketamine. While the mutual potentiation, antagonism and tolerance suggest common mechanisms for the induced catalepsy, differences in latency, rigidity and behavior, asymmetry of cross-tolerance and a widely-different ID50 for naloxone would argue against an action at a single opioid site.

Animals↗

PubMed1989

Comparison of isomers of ketamine on catalepsy in the rat and electrical activity of the brain and behavior in the cat.

The present study compared the relative potency and efficacy of the two isomers of ketamine on the duration of catalepsy (loss of righting reflex) in female rats and on the behavior and electroencephalogram of cats. In the rat, at small doses, the S(+) isomer was more potent than the R(-) isomer or racemic ketamine, while at larger doses, the S(+) isomer and the racemate were equipotent and the R(-) isomer was significantly less potent. Tolerance developed rapidly to the effects of either isomer and both were equally cross-tolerant to racemic ketamine. Sub-effective doses of morphine significantly increased the potency of S(+), R(-) and racemic ketamine on the duration of catalepsy. Sub-effective doses of either isomer augmented the duration of catalepsy, induced by small doses of morphine, but reduced that of large doses. In cats, there was a parallel time course and progression of behavioral and electroencephalographic states in response to equal total doses of either racemic ketamine, an artificial 50:50 mixture of S(+) and R(-) isomers, or the S(+) isomer alone; approximately equivalent effects required twice the dose of the R(-) isomer. It is concluded that there is a common site of action for the two isomers, but there is also a stereospecific difference in potency, as regards the induction of catalepsy in the rat and behavioral and electroencephalographic effects in the cat. Stereospecificity was not apparent in the development of tolerance, cross-tolerance or the augmentation of the response to morphine.

Animals↗

PubMed1989

Synthetic opioids compared with morphine and ketamine: catalepsy, cross-tolerance and interactions in the rat.

Previously it has been shown in rats that both ketamine and morphine induced analgesia and, at larger doses, catalepsy and loss of the righting reflex, all of which were reversed by naloxone at widely different doses. Tolerance developed rapidly to either ketamine or morphine and there was cross-tolerance from ketamine to morphine. However, morphine potentiated the cataleptic effect of ketamine, whether fully-effective doses of morphine were given before ketamine or subeffective doses of both were given concurrently. The present study extends these observations to three specific mu-receptor agonists (sufentanil, fentanyl and alfentanil) and two mu- and kappa-agonist, mu-antagonist opioids (nalbuphine and butorphanol). All five of these opioids potentiated the cataleptic effect of ketamine. Each of the three specific mu agonists showed rapid development of tolerance. Fentanyl and alfentanil showed mutual cross-tolerance with ketamine, but sufentanil did not. This lack of sufentanil-ketamine cross-tolerance may reflect separation of the sites of agonist action and the sites of development of tolerance for the opioids and for ketamine. The potentiating effects of nalbuphine and butorphanol suggest that they potentiate ketamine-induced catalepsy, either by kappa-receptor interactions or by a mu agonist effect. It is suggested that the cataleptic effect of a combination of individually-subeffective doses of ketamine and morphine, rather than ketamine and one of the synthetic opioids, might be of more potential clinical usefulness.

Animals↗

PubMed1989

Detection and identification of mycobacteria by amplification of mycobacterial DNA.

A 383bp segment of the gene coding for the 65kD mycobacterial antigens from Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium avium, Mycobacterium paratuberculosis, and Mycobacterium fortuitum was amplified using Taq polymerase and synthetic oligonucleotide primers and the amplified DNAs from four of these species were compared by nucleotide sequencing. Although the gene segments from these species showed considerable similarity, oligonucleotide probes which could distinguish M. tuberculosis/M. bovis, M. avium/M. paratuberculosis and M. fortuitum could be identified. Samples containing 10(6) human cells and serial dilutions of a suspension of intact mycobacteria were prepared, DNA was extracted, the segment of the mycobacterial DNA sequence amplified, and the amplified DNA hybridized with oligonucleotide probes. In two independent experiments, this procedure permitted the detection and identification of less than 100 mycobacteria in the original sample. These results suggest that this approach may prove useful in the early diagnosis of mycobacterial infection.

Amino Acid Sequence↗

PubMed1989

Beta-receptor properties in soleus muscles from spontaneously hypertensive rats.

We have compared the properties of beta-adrenergic receptors in slow-twitch, oxidative skeletal muscles (soleus) from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats at three different ages. The investigation was based on the hypothesis that the increase in Na+ content and decrease in fatigue resistance observed previously in the soleus of SHR might be the result of a down regulation of muscle beta-receptors. Activation of beta-adrenergic receptors in skeletal muscle stimulates sarcolemmal sodium-potassium adenosine triphosphatase, which produces an efflux of Na+ and an influx of K+. Receptor down-regulation would be expected to reduce hormonal stimulation of Na+ pump activity, particularly during exercise. The results of receptor binding studies, however, and an investigation of cyclic adenosine monophosphate (cAMP) production in response to applied epinephrine indicated that there were no significant differences in receptor properties in the soleus muscles of SHR and WKY rats. Receptor number and affinity were the same in the two strains, and the rate, magnitude, and duration of the increase in cAMP in response to 10(-6) M epinephrine were also similar. beta-Adrenergic receptor down-regulation does not appear to be a generalized phenomenon in tissues of SHR, despite the appearance of other physiological changes in the tissue.

Animals↗

PubMed1989

Cigarette smoking-induced changes in the number and differentiated state of pulmonary dendritic cells/Langerhans cells.

To evaluate the effect of cigarette smoking on the number, distribution, and differentiated state of dendritic cells (DC) and Langerhans cells (LC) in the human lung, we have quantitated the number of these cells present in the bronchioles and alveolar parenchyma of lung tissue from nonsmokers and cigarette smokers using anti-CD1 monoclonal antibodies which react preferentially with DC (M241) and LC (T6). M241+ DC were found in the bronchiolar submucosa and alveolar parenchyma of nonsmokers; T6+ LC were present within the bronchiolar epithelium. Cigarette smoking was associated with a twofold increase in the total number of cells of DC/LC lineage and a 30-fold increase in the number of T6+ cells, many of which contained Birbeck granules (LC), present in the alveolar parenchyma. Most LC found in the parenchyma of smokers were observed in close association with areas of alveolar type II pneumocyte hyperplasia. Cigarette smoking did not change the number of differentiated state of cells of DC/LC lineage within the bronchioles. Both DC and LC are present in the human lung. Cigarette smoking has an important effect on the number, distribution, and differentiated state of these cells, which may explain why most adult patients who develop Langerhans cell granulomatosis are smokers.

Adult↗

PubMed1988

Production of granulocyte colony-stimulating factor (G-CSF) by human cells: T lymphocyte-dependent and T lymphocyte-independent release of G-CSF by blood monocytes.

To evaluate the production of granulocyte colony-stimulating factor (G-CSF) by human immune and inflammatory cells, an assay specifically measuring G-CSF activity in the presence of other cytokines was developed which was based on the proliferation of 32Dcl cells induced by G-CSF. Successful use of the 32Dcl cells to specifically measure G-CSF activity required the selection of cells highly responsive to G-CSF and with reduced responsiveness to interleukin 2 (IL 2) by intermittent culture in medium containing G-CSF. Furthermore, the addition of exogenous IL 2 to standards and experimental samples was necessary to ensure that the concentration of IL 2 was similar in all samples, since IL 2 directly stimulated the proliferation of 32Dcl cells and increased their responsiveness to G-CSF. A variety of stimuli were found to induce G-CSF release by blood monocytes. Lipopolysaccharide and monocyte adherence appeared to directly stimulate G-CSF release, whereas stimulation of G-CSF release from monocytes by mitogenic lectins required the presence of T lymphocytes. In all cases, release of G-CSF was detectable as soon as 4 h after stimulation and was essentially complete after 48 h. These findings indicate that G-CSF release can be initiated by a variety of pathways, and therefore suggest that the production of this mediator may occur in the course of many immune and inflammatory reactions.

Biological Assay↗

PubMed1988

Diagnosis of nosocomial bacterial pneumonia in intubated patients undergoing ventilation: comparison of the usefulness of bronchoalveolar lavage and the protected specimen brush.

PURPOSE: To compare the usefulness of specimens recovered using a protected specimen brush and those recovered by bronchoalveolar lavage in the diagnosis of nosocomial pneumonia occurring in intubated patients undergoing ventilation, we performed both procedures in patients suspected of having pneumonia because of the presence of a new pulmonary infiltrate and purulent tracheal secretions. PATIENTS AND METHODS: Twenty-one patients (16 men and five women) with an average age of 57 +/- 12 years were studied. They had been receiving mechanical ventilation for 8 +/- 6 days before inclusion in the trial. The clinical suspicion for nosocomial bacterial pneumonia was high in these patients. Fiberoptic bronchoscopy was performed in each patient. Bronchoscopy specimens were obtained by a protected specimen brush and by bronchoalveolar lavage, and were then processed for quantitative bacterial and fungal culture using standard methods. Total cell counts were performed on an aliquot of resuspended original lavage fluid. Differential cell counts were made on at least 500 cells. In addition, 300 cells were examined at high-power magnification and the percentage of cells containing intracellular microorganisms and the average number of extracellular organisms per oil-immersion field were determined. RESULTS: Quantitative culture of specimens recovered using the protected specimen brush were positive (more than 10(3) colony-forming units [cfu]/ml) in five of five patients with subsequently confirmed pneumonia, and negative (less than 10(3) cfu/ml) in 13 of 13 patients without bacterial pneumonia, but results were not available until 24 to 48 hours after the procedure. Quantification of intracellular organisms in cells recovered by lavage was also useful in distinguishing patients with pneumonia (more than 25 percent of cells with intracellular organisms in five of five patients) from those without pneumonia (less than 15 percent of cells with intracellular organisms in all cases), and results were available immediately. In contrast, quantitative culture of lavage fluid and differential cell counts were of little value in identifying infected patients. CONCLUSION: The protected specimen brush and microscopic identification of intracellular organisms in cells recovered by lavage yield useful and complementary information, and together permit rapid and specific treatment of most patients with nosocomial pneumonia.

Bacteria↗

PubMed1988

Smoking and pulmonary sarcoidosis: effect of cigarette smoking on prevalence, clinical manifestations, alveolitis, and evolution of the disease.

Patients with pulmonary sarcoidosis are less likely to smoke than persons of a similar age in the general population. This could be because smoking reduces the likelihood of developing sarcoidosis, or alternatively smoking could reduce the severity of the disease process so that smoking patients are underrepresented among patients with clinically overt disease. To evaluate these possibilities 64 patients with sarcoidosis of recent onset were studied at presentation and after a one year follow up period, clinical, functional, radiographic, and bronchoalveolar lavage fluid criteria being used to identify factors that might account for the lower incidence of sarcoidosis in smokers and to determine whether the disease is less severe in smoking patients. Smoking was less common in the patients with sarcoidosis (30%) than in the control subjects (46%). The study did not support the conclusion that sarcoidosis is less severe in smokers, as clinical, radiographic, and functional abnormalities were similar in smokers and non-smokers at initial evaluation and after a one year follow up period. Nevertheless, smoking did influence various indices used to assess disease "activity." Cigarette smoking was associated with a significant increase in the serum angiotensin converting enzyme activity (SACE), and patients with very high SACE and pulmonary gallium-67 uptake were smokers. Furthermore, more CD8+ (but not CD4+) lymphocytes were recovered by lavage from smoking than from non-smoking patients, giving a lower CD4: CD8 ratio in smokers. Fewer alveolar macrophages were recovered by lavage from smokers with sarcoidosis than from normal subjects with a similar smoking history. These finding support the possibility that smokers, particularly those with a prominent accumulation of alveolar macrophages in the lower respiratory tract, may be less likely to develop sarcoidosis.

Adult↗

PubMed1988

Does de novo immunoglobulin synthesis occur on the epithelial surface of the human lower respiratory tract?

Although synthesis of immunoglobulins by cells in the human lower respiratory tract has never been directly demonstrated, local production of immunoglobulins by cells within lung parenchyma is thought to play an important role in protecting the normal human lung against a variety of pathogenic organisms, and may contribute to the development of some interstitial lung diseases. To determine whether or not the epithelial surface of the human lower respiratory tract is a site of immunoglobulin synthesis, immunoglobulin production by cells recovered by bronchoalveolar lavage and lung parenchymal tissue from normal subjects and patients with idiopathic pulmonary fibrosis (IPF) or sarcoidosis was evaluated using a reverse hemolytic plaque assay and by measuring incorporation of [35S]methionine into immunoglobulins. Although the reverse hemolytic plaque assay demonstrated immunoglobin-releasing cells to be present on the surface of the lower respiratory tract of normal subjects, and present in increased numbers in patients with IPF or sarcoidosis, these plaque-forming cells were not actively synthesizing immunoglobulins, since preincubation of lavage cells in order to remove immunoglobulin bound to the surface of the cells reduced the number of plaque-forming cells, and inhibition of protein synthesis by cycloheximide did not further reduce the number of plaque-forming cells. Furthermore, direct evaluation of immunoglobulin synthesis using radiolabeling, immunoprecipitation and SDS-polyacrylamide gel electrophoresis failed to detect de novo IgG production by cells recovered from the alveolar surface of 15 of 17 subjects, IgM by 17 of 17, and IgA by 16 of 17.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

T-lymphocytes recovered by bronchoalveolar lavage from normal subjects and patients with sarcoidosis are refractory to proliferative signals.

Granuloma formation in the lung of patients with sarcoidosis is preceded by the accumulation of large numbers of activated T-lymphocytes, which results, at least in part, from the proliferation of T-lymphocytes within the lung. To determine whether the increased proliferation of lung T-lymphocytes in sarcoidosis results from a failure of mechanisms responsible for limiting their proliferation, we have compared the ability of purified T-lymphocytes present in bronchoalveolar lavage fluid and peripheral blood from normal subjects and patients with sarcoidosis to respond to proliferative signals. The mitogen-induced proliferative response of lavage T-lymphocytes from normal subjects and patients with sarcoidosis was similar, but the response of lavage T-lymphocytes was much less than that observed using normal or sarcoid blood T-lymphocytes. The reduced proliferative response of sarcoid lavage T-lymphocytes could not be overcome by addition of accessory cells or exogenous interleukin-2, and it did not result from the presence of suppressor cells. Furthermore, sarcoid lavage lymphocytes are capable of being activated by "mitogenic" signals, as indicated by the ability of phytohemagglutinin to induce expression of the 4F2 surface antigen and stimulate interleukin-2 production. However, the expression of interleukin-2 receptors was reduced on stimulated sarcoid lavage T-lymphocytes compared with that observed on normal blood T-lymphocytes, which may account in part for their reduced proliferative capacity. Because mechanisms that render lavage T-lymphocytes from normal subjects refractory to proliferative signals appear to operate in sarcoidosis as well, these findings suggest that a defect in the inhibition of T-lymphocyte proliferation is unlikely to be an important cause of lymphocyte accumulation in this disorder.

Adult↗

PubMed1988

Detection of nosocomial lung infection in ventilated patients. Use of a protected specimen brush and quantitative culture techniques in 147 patients.

To determine the usefulness of samples obtained by bronchoscopy using a protected specimen brush and evaluated by quantitative culture techniques in establishing the diagnosis of nosocomial pneumonia in patients requiring mechanical ventilation, we prospectively studied 147 ventilated patients suspected of having nosocomial pneumonia because of the presence of a new pulmonary infiltrate and purulent tracheal secretions. Positive cultures of protected brush specimens (greater than 10(3) cfu/ml) were found in only 45 patients (31%). Subsequent follow-up confirmed the diagnosis of pneumonia in 34 of 45 patients, and in only 4 of 45 patients was a positive culture firmly established to be a false positive result. No patient with less than 10(3) cfu/ml was subsequently shown to have had pneumonia, and the diagnosis was definitely excluded in 72 of 102 patients by the absence of pneumonia at autopsy or recovery without antibiotic therapy. In contrast, when 16 clinical variables were evaluated by stepwise logistic regression analysis, no combination could be identified that was useful in distinguishing patients with bacterial pneumonia. Furthermore, when the actual costs of evaluation and therapy of our patients were compared with the projected costs entailed in treating all patients suspected of having pneumonia with antibiotics, evaluation using the protected specimen brush and quantitative cultures was less expensive after only 6 days of treatment. These results suggest that the appearance of pulmonary infiltrates and purulent tracheal secretions does not result from bacterial pneumonia in a majority of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

Vitamin D metabolism in tuberculosis. Production of 1,25(OH)2D3 by cells recovered by bronchoalveolar lavage and the role of this metabolite in calcium homeostasis.

To investigate the extrarenal production of 1,25(OH)2D3 in tuberculosis, we extensively evaluated a patient with tuberculosis, hypercalcemia, and an elevated plasma concentration of 1,25(OH)2D3. Fresh total cells and cultured alveolar macrophages obtained by bronchoalveolar lavage were demonstrated to synthesize 1,25(OH)2D3 prior to and after nine months of successful antituberculous therapy. The continued capacity to produce 1,25(OH)2D3 was associated with a persistent lymphocytic alveolitis in this patient. This extrarenal production of 1,25(OH)2D3 probably contributed to the increased levels of plasma 1,25(OH)2D observed in our patient. Nevertheless, a close correlation between plasma 1,25(OH)2D and serum calcium was not observed. These findings suggest that although extrarenal production of 1,25(OH)2D3 occurs in tuberculosis, it need not be a predominant factor producing the abnormalities in calcium homeostasis observed in such patients.

Adult↗

PubMed1988

Ketamine- and morphine-induced analgesia and catalepsy. I. Tolerance, cross-tolerance, potentiation, residual morphine levels and naloxone action in the rat.

The effects of ketamine and morphine on pain perception and catalepsy were compared in rats. Analgesia, as measured by the latency to withdrawal of the tail from a 55 degrees C water bath (tail-flick latency difference, TFLD), was produced by both ketamine and morphine, but at widely different doses, and in each case the effect was reversed by naloxone. Catalepsy, measured by the duration of loss of righting reflex (DLRR) in catatonic animals, was induced by larger doses of both ketamine and morphine and in each case was reduced by a larger dose of naloxone. DLRR and TFLD tolerance developed rapidly and with a similar time course after daily doses of ketamine or morphine. Rats tolerant to the DLRR effect of ketamine showed cross-tolerance to morphine. Rats tolerant to the DLRR effect of morphine did not show cross-tolerance to ketamine when administered the following day; instead, these rats showed potentiation of the ketamine-induced DLRR. The degree of potentiation noted 24 hr after a single or multiple daily doses of 45 mg/kg of morphine is the same as that seen when 2 mg/kg of morphine is given simultaneously with ketamine. The residual brain level of morphine 24 hr after 45 mg/kg is similar to the level 1 hr after a 2-mg/kg dose. The augmented ketamine response in morphine-tolerant rats is postulated to be a result of residual morphine still present in the brain 24 hr after the last DLRR-inducing dose of morphine.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMed1987

Role of mast cells in the pathogenesis of hypersensitivity pneumonitis.

To examine the possibility that mast cells have a central role in the pathogenesis of hypersensitivity pneumonitis, 20 patients with this disease were studied with the aim of seeking evidence for mast cell degranulation. The number of mast cells recovered by bronchoalveolar lavage from patients with hypersensitivity pneumonitis was more than 1,000 times greater than those recovered from normal individuals. Furthermore, discontinuation of antigen exposure resulted in an increase in the number of mast cells observed, consistent with the possibility that antigen exposure had induced mast cell degranulation. Cessation of antigen exposure also resulted in a rapid decrease in the number of neutrophils and eosinophils recovered by lavage, followed by an increase in the number of T8+ T lymphocytes present. In each case the time course of the changes was consistent with the possibility that mast cell degranulation had been important in regulating the number of the immune and inflammatory cells present in the lung. Histamine was present in lavage fluid supernatant from patients with hypersensitivity pneumonitis. The amount of histamine present was, however, closely correlated with the number of mast cells present and not with the interval since last antigen exposure. Delay in separating cells from lavage fluid supernatant resulted in an increase in histamine content. These results suggest that the free histamine in lavage fluid resulted from the degranulation of mast cells induced by the lavage procedure as histamine released in vivo has a short half life. We suggest that hypersensitivity pneumonitis results from a "late phase reaction" initiated by antigen induced mast cell degranulation.

Alveolitis, Extrinsic Allergic↗

PubMed1987

Acute and latent pneumonitis after subcutaneous injections of silicone in transsexual men.

We evaluated 13 transsexual men who were hospitalized for symptoms resulting from illicit subcutaneous injections of silicone. Patients with acute silicone pneumonitis were admitted because of fever, bilateral pulmonary infiltrates, and hypoxemia (mean PaO2, 58 +/- 14 mm Hg). Most patients in this group had received new silicone injections within hours of admission, but one presented with the same clinical syndrome a few hours after a brawl. The alveolitis of acute silicone pneumonitis was characterized by increased numbers of alveolar macrophages, neutrophils, and eosinophils (p less than 0.05 compared with those in normal persons with a similar smoking history). Evidence of alveolar hemorrhage was also present in some cases. Alveolar macrophages contained large, pleomorphic, cytoplasmic inclusions, which were identified as silicone by atomic absorption and infrared spectrometry. Patients with latent silicone pneumonitis underwent clinical study at much longer times after the silicone fluid injections because they developed local inflammatory phenomena at the sites of previous injections. Pulmonary function studies usually showed slight restrictive changes, and bronchoalveolar lavage disclosed abnormalities similar to those found in patients with acute silicone pneumonitis, although to a lesser degree. Thus, illicit silicone fluid injection carries a serious respiratory risk since it can induce pneumonitis, followed in some patients by respiratory failure.

Acute Disease↗