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Postviral Bronchial Hyperreactivity Syndrome: Recognizing Asthma's

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Postviral Bronchial Hyperreactivity Syndrome: Recognizing Asthma's • Postviral bronchial hyperreactivity syndrome: Recognizing asthmas great mimic DAVID OSTRANSKY, DO FRANCIS X. BLAIS, DO Although there are no prospec- (Key words: Viral infections, asthma, tive studies regarding the frequency of respiratory tract infections, postviral postviral bronchial hyperreactivity syn- bronchial hyperreactivity syndrome) drome, it is a common complication of upper and lower respiratory tract viral Viral respiratory tract infections frequently infections. The respiratory symptoms cause wheezing and other asthmalike symp- closely resemble those of asthma, but they toms. Several investigators have demonstrated are present for only 3 weeks to 3 months pertinent features of this abbreviated form of following the acute infection phase. Defin- asthma, including early response phase, late ing the mechanisms of this syndrome may response phase, and bronchial hyperreac- provide insight into the pathogenesis of tivity. 1-5 Understanding the mechanisms by asthma. Postviral bronchial hyperreac- which viral respiratory tract infections precipi- tivity syndrome is frequently misdiag- tate the airway abnormalities of asthma may nosed and inappropriately managed be- be a potential key to the pathogenesis of cause many physicians are unfamiliar asthma, although whether viral respiratory with this illness. Because of its character- tract infections truly cause asthma is un- istic history, diagnosis is straightforward proved.6 when the physician knows what to look The symptom complex following viral up- for, and response to therapy is excellent. per or lower respiratory tract infections (or This report presents a case history fol- both) has not been formally identified. It is fre- lowed by a review of the proposed mecha- quently misdiagnosed by physicians who then nisms of bronchial hyperreactivity follow- institute inappropriate diagnostic studies and ing viral respiratory infections. The clini- ineffective antibiotic therapy. This article dis- cal features and criteria for diagnosing cusses the proposed mechanisms of "viral postviral bronchial hyperreactivity syn- asthma" as well as its clinical description and drome are also discussed. criteria for the diagnosis of this disorder, re- ferred to as the postviral bronchial hyperreac- tivity syndrome (PVBHS). From the Texas College of Osteopathic Medicine, Fort Worth, where, at the time this article was written, Dr Ostransky was associate professor of medicine, Division Report of case of Pulmonary and Critical Care Medicine; Dr Blais is A 38-year-old woman had a persistent cough. One associate professor of medicine, Division of Infectious Dis- month previously, she had had a viral upper respi- eases. Dr Ostransky is a physician specialist in private ratory tract infection with accompanying symptoms practice in the Dallas–Forth Worth area. Reprint requests to David Ostransky, DO, 1236 S of sore throat, cough, malaise, myalgias, and low- Ridge Ct, Suite 200, Hurst, TX 76053. grade fever. After resolution of the acute symptoms, Clinical practice • Ostransky and Blais JAOA • Vol 91 • No 5 • May 1991 • 465 the cough had persisted with occasional scant Proposed mechanisms of hyperreactivity expectoration of clear mucus. The coughing oc- The proposed mechanisms of virus-induced curred frequently, it was often paroxysmal, and it asthma discussed in several reviews include continued at night. After nighttime coughing, the epithelial inflammation or damage with en- patient was short of breath and often wheezed. Dur- ing the daytime, coughing and shortness of breath hanced airway cholinergic sensitivity,3 stimu- were precipitated by exposure to household clean- lation of peptidergic nerve fibers 11 or loss of ing materials, perfume, gasoline fumes, and ciga- "epithelial relaxant factor," 12,13 diminished rette smoke. 13-adrenergic function, enhanced mediator The patient was not able to participate in aero- release,4 and stimulation of virus-specific IgE bics because of dyspnea and coughing. Use of an antibody production.4,14-18 over-the-counter cold formula and prescribed eryth- Ramphal and coworkers, 19 using scanning romycin had not alleviated the symptoms. She also and transmission electron microscopy in a mur- complained of anterior chest wall discomfort. The ine model of influenza virus infection, have patient was a nonsmoker. Her medical history was shown that viruses damage airway epithelium. significant for a benign breast biopsy several years The series of scanning electron micrographs earlier. She had no history of asthma, sinusitis, (Figs 1 through 4) show tracheal epithelium allergies, or symptoms of gastroesophageal reflux. Her family history was positive only for breast car- before infection and at 36 hours, 5 days, and cinoma. 10 days after infection. Desquamative changes On physical examination, the patients vital begin approximately 12 hours following inocu- signs were as follows: pulse, 92 beats per minute; lation and are virtually complete in 48 to 72 respiratory rate, 24 per minute; blood pressure, 120/ hours. 19 The serous and ciliated cells of the 65 mm Hg, and temperature, 37.4°C. Physical ex- pseudostratified columnar epithelium are af- amination was significant for mild erythema of the fected with sparing of the regenerative layer.9 posterior pharynx and prolonged expiration on aus- Regeneration begins 5 days after infection and cultation of the chest. Results of spirometry were recovery is complete in 2 weeks.19 normal. A chest roentgenogram was also normal. Such dysfunctional or absent respiratory After evaluation, albuterol therapy administered tract epithelium may cause or potentiate bron- by metered-dose inhaler (two puffs four times daily) chial hyperreactivity by multiple mechanisms, was started, with instructions on the proper use of the medication. Symptoms were improved mark- including sensitization of rapidly adapting va- edly within 2 days, and the patient was asympto- gal sensory afferent nerve endings, 3 preven- matic in 1 week. tion of the protective release of large concen- trations of prostaglandin E2,2021 generation of Discussion 15-lipoxygenase pathway products,22 and the Many clinical and epidemiologic observations deficiency or absence of epithelium-derived "re- suggest that viral infections cause asthma for laxant factor."23 In humans, the duration of reasons outlined by Busse": bronchial hyperreactivity closely parallels the • Patients with recurrent wheezing or asthma time needed for epithelial repair. 24 This pa- can date the onset of their symptoms to an thogenetic schema is similar to that described acute febrile illness with catarrhal features by McIntosh,25 who surmised that there was of viral infection. a clinical continuum of infant bronchiolitis to • Viral infections cause 11% to 42% of exacer- childhood asthma. bations of asthma.? Clinical expression is thought to be deter- • Small airway abnormalities and exaggerated mined by the virulence of the particular vi- bronchial hyperreactivity occur in normal in- rus, its affinity for a specific part of the respi- dividuals during and after viral respiratory ratory tract epithelium, and host response— tract infections.3,5,8 immunologic and other—to the infection.26 • Individuals with allergic diatheses suffer However, bronchial epithelial damage is not more severe symptoms following viral respi- necessary for enhanced cholinergic sensitivity ratory tract infections.9 because bronchial hyperreactivity and wheez- • Viruses are intensely inflammatory.1° ing occur following upper respiratory tract in- 466 • JAOA • Vol 91 • No 5 • May 1991 Clinical practice • Ostransky and Blais fection, that is, parainfluenza virus infec- pable of in iating production of virus-specific tions. 1'3'15 Thus, cholinergic reflex bronchocon- IgE ant ody was advanced by Welliver and striction can arise from upper respiratory tract colleagues and supported by others. 4,14-18 In stimulation. Also, cholinergic hypersensi- studies of respiratory syncytial virus (RSV)4,18 tivity following viral respiratory tract infec- and parainfluenza virus infections, 15,17 many tion is suggested by bronchial hyperreactivity subjects demonstrated cell-bound IgE during to carbachol,2 histamine, citric acid, and cold acute and convalescent phases of viral ill- air, each of which is blocked by inhaled atro- ness.4,18 Significantly greater titers of IgE were pine sulfate.3 found in those individuals with subsequent Viral infections may cause asthma by al- wheezing or bronchiolitis. 4 Additionally, there tering the response of the peptidergic nerve was a direct relationship between the degree fibers, which are located beneath the respira- of arterial hypoxemia and histamine concen- tory tract epithelium. 1,11 Peptidergic nerve trations in nasal secretions to the level of virus- fibers release tachykinins in response to numer- specific IgE.4 ous stimuli—such as viruses, ozone, and al- Viral-induced airway inflammation may in- lergens—with resultant bronchial hyperreac- crease epithelial permeability and permit tivity.11 Usually, the tachykinins are modu- greater influx of the virus and its products lated by membrane-bound enzymes, enkephal- with subsequent IgE sensitization. The logi- inases, which inactivate the tachykinins.23 cal progression of reasoning is that virus-spe- Studies12,13 show that respiratory tract viruses cific IgE is capable of attaching to the mast cause tachykinin release with bronchial cell and precipitating the release of its numer- smooth-muscle contraction. In the presence of ous mediators. These mast
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