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Biomedical subjects

F M Baroody

Publications and source records attributed to F M Baroody.

At least 55 records · Page 3Linked to original sources

Fine-needle aspiration biopsy of cervicofacial masses in children.

OBJECTIVE: To show the usefulness of fine-needle aspiration biopsy (FNAB) in the diagnosis of cervicofacial masses in children. DESIGN: Case series. SETTING: Pediatric otolaryngology referral center, ambulatory and hospitalized patients. PATIENTS: Seventeen pediatric (age, < 18 years) patients with cervicofacial masses. INTERVENTION: Fine-needle aspiration biopsy. OUTCOME MEASURES: Cytologic diagnosis, resolution of mass, and need for further surgical diagnosis or treatment. RESULTS: Following FNAB, 10 patients underwent open surgery; in seven, the surgery was indicated based on FNAB diagnosis; in three, surgery provided diagnoses where FNAB was insufficient. Based on FNAB data, seven patients were observed without surgery. CONCLUSIONS: Fine-needle aspiration biopsy is a useful early step in diagnosing cervicofacial masses in children.

Adolescent↗

Eosinophilia in chronic childhood sinusitis.

OBJECTIVES: To quantify eosinophilia in sinus tissues obtained from children with chronic sinusitis and to correlate the degree of eosinophilia with history of asthma, allergy, cystic fibrosis, and preoperative computed tomographic (CT) scans. DESIGN: Examination of surgical specimens from children who underwent functional endoscopic sinus surgery and controls. SETTING: Tertiary care medical center. PATIENTS: Thirty-four children who underwent functional endoscopic sinus surgery for chronic sinusitis refractory to medical treatment were divided into three groups: 13 with asthma, 11 without asthma, and 10 with cystic fibrosis. Normal sphenoid sinus mucosa was also obtained from six adults undergoing transsphenoidal hypophysectomies. MAIN OUTCOME MEASURES: Number of lamina propria and intraepithelial eosinophils in surgical specimens, allergic status, presence or absence of asthma, and CT scans obtained preoperatively. RESULTS: There were significantly more lamina propria and intraepithelial eosinophils in the tissue of children with chronic sinusitis compared with normal sphenoid sinus mucosa. More eosinophils were counted in the tissues of patients with asthma and cystic fibrosis compared with patients without concomitant disease, but this did not reach statistical significance. Allergy status did not affect the degree of tissue eosinophilia. Eosinophilia did not correlate with severity of mucosal disease as assessed by CT scans. CONCLUSIONS: Tissue eosinophilia is a characteristic histologic feature of chronic sinusitis in children, especially those with asthma. The presence of allergy does not predict tissue eosinophilia. Furthermore, the degree of tissue eosinophilia does not correlate with the severity of mucosal thickening seen on CT scans.

Adolescent↗

Implicating adhesion molecules in nasal allergic inflammation.

Allergic rhinitis is now considered an inflammatory disorder where many leukocyte types, including eosinophils and T-lymphocytes, accumulate in increased numbers. Along with mast cells and other cells, they release a wide variety of mediators, cytokines, and granule constituents that can directly cause inflammation or activate the local vascular endothelium to further enhance the recruitment of leukocytes through the expression and function of adhesion molecules. While the understanding of the importance of leukocyte and endothelial adhesion molecules is still at a very early stage, recent evidence has already begun to implicate these cell surface molecules in the pathogenesis of allergic diseases such as rhinitis and asthma. Additional studies, including the use of adhesion molecule antagonists when available, will clarify the importance of these structures in the pathophysiology of these disorders.

Cell Adhesion Molecules↗

In vivo human models for the study of anticholinergic drugs.

BACKGROUND: The parasympathetic nervous system plays an important role in the nasal response to external stimuli. OBJECTIVE: To review studies showing the role of the parasympathetic nervous system in the nasal response and the effect of topical, intranasal anticholinergic agents on that response. METHOD: Literature review of in vivo human studies. RESULTS: Nasal provocation with methacholine leads to glandular stimulation. The response to methacholine provocation can be blocked by treatment with ipratropium bromide. Stimulation of one nostril with histamine, antigen, and cold, dry air leads to a bilateral secretory response that is partially inhibited by topical treatment with atropine. CONCLUSION: Topical anticholinergic agents should be useful in the reduction of glandular hypersecretion regardless of the etiology.

Administration, Intranasal↗

Nasal challenge with allergen upregulates the local expression of vascular endothelial adhesion molecules.

To understand the events involved in selective eosinophil migration into allergic inflammatory sites, we studied the expression of vascular endothelial adhesion molecules in the nasal mucosa. Ten subjects with asymptomatic seasonal allergic rhinitis and 13 nonallergic subjects underwent localized allergen challenge of one inferior turbinate. Twenty-four hours later, biopsy specimens were obtained from the inferior turbinates, bilaterally in the seasonally allergic subjects and unilaterally in the nonallergic control subjects. The specimens were divided, sectioned, and either stained for identification of eosinophils or analyzed immunohistochemically for intercellular adhesion molecule-1, E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and von Willebrand's factor. Intercellular adhesion molecule-1 expression was observed in all mucosal specimens, with no significant difference among groups. E-selectin showed minimal baseline expression, and low levels were significantly induced on the challenged mucosa of the allergic compared with nonallergic subjects (p < 0.05). VCAM-1 was expressed basally and was significantly upregulated by allergen challenge, compared with the nonchallenged side and nonallergic control subjects (p < 0.05). Submucosal eosinophils increased significantly in allergic subjects 24 hours after antigen challenge, compared with nonallergic control subjects and weakly correlated with VCAM-1 expression (rs = 0.33, p = 0.06). Our results suggest that endothelial activation accompanies allergic inflammation. Furthermore, because the counterligand for VCAM-1, very late activation antigen-4, is present on eosinophils, VCAM-1 upregulation may contribute to the selective recruitment of these cells to the nasal mucosa.

Adult↗

The human nasal response to capsaicin.

Airway sensory nerves play a role in reactions to inhaled allergens, irritants, and physical stimuli. Capsaicin, the pungent principle of hot peppers, stimulates a subcategory of sensory nerves. To study the consequences of selective activation of airway sensory nerves in the human nose, we administered capsaicin nasal challenges to eight volunteers (four normal subjects and four subjects with perennial allergic rhinitis). Capsaicin (20 mumol/L), when sprayed into the nose, induced burning, rhinorrhea, and lacrimation. Capsaicin also induced a significant increase in total protein content of nasal lavage fluid after challenge compared with vehicle (increase from before challenge to 1 minute after challenge, 172 +/- 55 vs 46 +/- 29 micrograms/ml, p < 0.001). In contrast to many animal studies, capsaicin did not increase vascular permeability in the airway, because albumin content of nasal lavage fluid was not increased (p = 0.86). On the other hand, lactoferrin, a marker of glandular secretion, was increased (p < 0.005). Repetitive capsaicin challenge every 10 minutes led to tachyphylaxis of symptoms, total protein secretion, and lactoferrin secretion. Compared with vehicle, unilateral capsaicin (6 mmol/L) disk challenge induced significant secretion both ipsilateral (21.3 +/- 4.2 vs 4.9 +/- 2.1 mg, p < 0.01) and contralateral (18.2 +/- 4.4 vs 7.4 +/- 1.9 mg, p < 0.04) to challenge. Thus we have shown that capsaicin challenge to the human nose leads to airway sensory nerve activation. Further, we have demonstrated that capsaicin stimulates a predominantly central neuronal response and that the induced secretory response is of glandular rather than vascular origin.

Adult↗

The effect of terfenadine on unilateral nasal challenge with allergen.

To investigate the role of H1 receptor-mediated effects in allergic rhinitis, we challenged 12 allergic volunteers with allergen 2 hours after administration of either placebo or 60 mg of terfenadine. Filter paper discs were used for the unilateral administration of allergen and the collection of nasal secretions. Secretion weights, levels of histamine in recovered nasal secretions, and nasal airway resistance (NAR) were measured for each nostril separately, and the number of sneezes was counted. After placebo treatment, allergen challenge led to significant increases in ipsilateral and contralateral secretion weights, ipsilateral histamine levels, ipsilateral NAR, and sneezing. Contralateral histamine levels were not elevated. H1 antagonism with terfenadine markedly reduced the number of sneezes and partially decreased ipsilateral and contralateral secretion weights, without affecting the increase in NAR. Terfenadine premedication also lowered the amount of histamine in ipsilateral secretions after allergen challenge. Performing identical nasal challenges with a 10-fold lower dose of antigen produced similar results. Previous studies showed that terfenadine had no effect on methacholine provocation and completely abolished ipsilateral and contralateral secretion weights after histamine challenge. We conclude that sneezing after allergen challenge is caused almost exclusively by a reflex initiated through H1 receptors and that H1 antagonism has no influence on allergen-induced increases in NAR. Unilateral allergen challenge leads to bilateral increases in secretion weights, which are only partially inhibited by terfenadine, suggesting the involvement of mediators other than histamine in the nasonasal reflex. As reported earlier, terfenadine also decreases allergen-induced histamine release after challenge with the highest dose of antigen.

Adult↗

Onset and duration of inhibition of ipratropium bromide nasal spray on methacholine-induced nasal secretions.

We performed a randomized, double-blind, placebo-controlled cross-over study with two different concentrations of ipratropium bromide (Atrovent) nasal spray to evaluate its onset and duration of inhibition. Twenty-four subjects with perennial rhinitis participated in the trial. Fifteen minutes to 12 hours after administration of ipratropium bromide (42 or 168 micrograms/nostril) or placebo nasal spray, methacholine challenges were performed and nasal secretion weights measured. After placebo administration the effect of methacholine remained unchanged over the 12-h-period. Both the 42 and 168 micrograms/nostril doses significantly inhibited the nasal hypersecretions induced by methacholine challenge within 15 min of treatment (P < 0.05). The 168 micrograms dose of ipratropium bromide continued to significantly reduce secretion weights through 6 hours, but the effectiveness of the 42 micrograms dose disappeared within 3 h. In addition to having a longer duration, the 168 micrograms/nostril dose produced approximately twice the inhibitory effect of the 42 micrograms dose.

Adult↗

Nasal allergen challenge generates 1-0-hexadecyl-2-lyso-sn-glycero-3-phosphocholine.

We studied antigen-induced platelet activating factor and the 1-0-hexadecyl-2-lyso-sn-glycero-3-phosphocholine (lyso-PAF) in nasal lavage fluids (NLF) by combined gas chromatography/mass spectrometric analysis (GC/MS). During the early allergic reaction, there was a dramatic increase in the levels of lyso-PAF that peaked at 15 min (2.6 +/- 5.2 ng/ml, mean +/- SEM, n = 6). Increasing doses of antigen produced a dose-dependent increase in the levels of lyso-PAF that peaked at the highest dose. Levels of lyso-PAF correlated strongly with those of N-alpha-tosyl-L-arginine methyl ester (TAME)-esterase activity (rs = 0.82, p = 0.0001) and histamine (rs = 0.57, p = 0.002). There was a no significant increase in the quantity of lyso-PAF found in NLF from allergic individuals challenged with diluent or nonallergic individuals challenged with antigen. In subjects showing a late phase reaction, as indicated by symptoms and histamine release, we detected lyso-PAF along with TAME-esterase activity and histamine during the late phase reaction. In contrast to lyso-PAF, PAF levels were near or below the detection limit of the assay in NLF and remained unchanged after antigen challenge. We also investigated the potential pathways for lyso-PAF generation from 2-acetylated phospholipids. We found that the time required for deacetylation of 50% of [3H]PAF (t1/2) to lyso-PAF was 50 min in baseline secretions and 10 and 22 min in NLF obtained 10 min and 24 h after antigen challenge, respectively. These data suggested that catabolic pathways were present in NLF.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗

Physiologic responses and histamine release after nasal antigen challenge. Effect of atropine.

We enrolled nine allergic subjects in a double blind, placebo-controlled study to examine the effect of premedication with 0.6 mg of atropine on nasal antigen challenge. The challenge consisted of unilaterally stimulating the nasal septum with diluent followed by three increasing doses of antigen and recording responses bilaterally. Sneezes, symptoms, and nasal airway resistance (NAR) were recorded. Secretions were collected using preweighed filter paper discs and histamine was measured. Antigen challenge with the subjects on placebo led to significant dose-dependent increases in sneezes, symptom scores, ipsilateral and contralateral secretion weights, ipsilateral NAR, and total amount of ipsilateral histamine (p < 0.05 versus diluent). Bilaterally applied atropine led to significant inhibition of ipsilateral and contralateral nasal secretions as well as rhinorrhea scores (p < 0.05 versus placebo) but had no significant effect on other parameters. Challenge after atropine premedication led to higher increases in histamine concentration than placebo (p < 0.01). These results suggest that parasympathetically stimulated fluids did not contain histamine and diluted the histamine released by mast cells. To support this hypothesis, we challenged the same subjects with methacholine. The concentration of histamine decreased and was significantly lower than after challenge with antigen (p < 0.01). The data suggest that: (1) histamine is released locally at the site of antigen challenge, (2) the volume of glandular secretions is primarily controlled by parasympathetic stimulation, and (3) the total amount of a mediator recovered in a fixed time interval best reflects the underlying pathophysiologic events.

Adult↗

Observations on the response of the nasal mucosa to allergens.

Allergic rhinitis is the sixth most prevalent chronic health condition in the United States. To study the pathogenesis of the allergic response, we have used a model of nasal provocation with antigen. During the initial reaction of an allergic subject to allergen provocation, increases occur in the levels of histamine, tryptase, and prostaglandin D2. This pattern of mediator release, combined with histologic evidence of mast-cell degranulation, strongly supports the role of the mast cell in the acute allergic reaction. The response to antigen, however, does not end with mast-cell degranulation. Hours after challenge we observed the spontaneous recurrence of symptoms and increased responsiveness to antigenic and nonantigenic stimuli. Our central hypothesis is that cellular infiltration and activation after antigen challenge are responsible for the observed increase in nasal reactivity. The predominant cells in nasal lavage 24 hours after challenge are eosinophils and neutrophils, whereas the predominant cell in the mucosa is the CD4+ lymphocyte. An early step in the movement of cells from the peripheral blood involves adhesion between circulating leukocytes and the endothelium. Evidence suggests that vascular endothelial adhesion molecule may be responsible in part for the selective adherence of eosinophils to the endothelium.

Allergens↗

Medical treatment of sinusitis.

Sinusitis is a very common and increasingly recognized disorder affecting patients of all ages and genders. It is most commonly due to infection of the paranasal sinuses with symptoms varying from cough and anterior nasal drainage in children to headache and post nasal drip in adults. Diagnosis relies heavily on medical history with corroboration by careful physical examination including nasal endoscopy. The most accurate imaging technique to evaluate sinusitis and to delineate the extent of involvement of individual sinuses and identify possible anatomic abnormalities is computerized tomography scanning in the coronal plane. The mainstay of medical treatment of sinusitis is antibiotics with adjuvant treatments such as saline irrigation, decongestants, mucolytics and antiinflammatory agents playing a more secondary role. The use of these agents will be discussed in detail after an introduction about the risk factors, diagnosis and bacteriology of the disease. Surgical treatment of sinusitis will be the subject of another article.

Adult↗

Intranasal steroids inhibit seasonal increases in ragweed-specific immunoglobulin E antibodies.

We performed two seasonal studies to evaluate the effect of continuous treatment with intranasal steroids, beginning approximately 1 week before the appearance of ragweed pollen, on the level of ragweed-specific IgE antibodies in serum. In both studies the control groups showed the anticipated rise in ragweed-specific IgE antibodies after the ragweed season. In the first study, employing aqueous beclomethasone dipropionate (168 micrograms twice daily), no rise occurred in serum ragweed IgE after seasonal exposure and the level actually decreased in eight of 12 treated subjects. In the second study, with triamcinolone acetonide (220 micrograms twice daily), the expected rise in ragweed IgE antibody was also reduced, although less dramatically, probably as a result of the lower potency of the dose delivered. Our studies not only support the benefits of intranasal steroids in the treatment of seasonal allergic rhinitis but also suggest that specific IgE production may be down-regulated by their continuous use, which may alter the subsequent clinical course of the disease.

Administration, Intranasal↗

Comparison of the secretory response of the nasal mucosa to methacholine and histamine.

To better understand the secretory response of the nasal mucosa, we must be able to accurately measure its physiological response. To this end, we developed a localized challenge technique using paper disks to stimulate the mucosa on one side and measure secretions from both sides to study both direct and reflex responses. Both methacholine and histamine induced a dose-dependent increase in secretion weights on the challenge side, whereas only histamine induced a contralateral reflex. Repeated stimulation with histamine, but not methacholine, resulted in tachyphylaxis. Pretreatment with atropine resulted in inhibition of the contralateral secretory response to histamine and the ipsilateral response to methacholine with only partial inhibition of the ipsilateral histamine response. Terfenadine pretreatment resulted in the complete inhibition of both the ipsilateral and contralateral responses to histamine with no effect on methacholine-induced secretions. Ipsilaterally applied lidocaine had no effect on the histamine response but, when applied contralaterally, partially inhibited that response. Topical diphenhydramine applied ipsilaterally led to significant inhibition of the ipsilateral and contralateral secretory responses to histamine but had no effect when applied contralaterally. We conclude that methacholine and histamine have different effects on the nasal mucosa. We speculate that methacholine stimulates glands directly, whereas histamine includes both direct and neurogenic stimulation.

Adult↗

Effect of terfenadine on nasal provocation.

The effect of premedication with terfenadine, an H1 antagonist, on nasal challenge with antigen, histamine and methacholine was evaluated. A single dose of terfenadine had no effect on the response to a localized challenge with methacholine but completely blocked the secretory response to histamine on both the ipsilateral and contralateral sides. These results suggest that terfenadine has no anticholinergic activity and that the direct and reflex secretory response to challenge with histamine is mediated by the H1 receptor. A single dose of terfenadine significantly reduced sneezing and nasal secretion after challenge with antigen but had no effect on nasal congestion. A double-blind placebo-controlled clinical trial was undertaken to compare the effects of pretreatment with terfenadine for 1 week on the response to sequential nasal challenge with antigen and histamine. Terfenadine significantly reduced the number of sneezes and the levels of kinins, albumin and TAME esterase activity following challenge with antigen. The levels of histamine were also significantly reduced, suggesting inhibition of the degranulation of mast cells. The number of sneezes and the levels of albumin were also significantly reduced by terfenadine following challenge with histamine.

Humans↗