Maximal expiratory flow rates such as Peak Expiratory Flow Rate (PEFR), rates

at 25%, 50% and 75% of forced vital capacity (VE 25%, VE 50% and VE 75%)

were studied in twenty untreated tropical eosinophilia (TE) patients. All

measurements were significantly lower in patients with TE compared to their mean

predicted values. These data suggest that inflammation of airways is an important

mechanism of pathophysiology of tropical eosinophilia

Kuppurao, K V

Sankaran, K

Venkatesan, P

Vijayan, V K

NIRT Institutional Repository

Biomedicine: 1992; 12(2)59 - 62.MAXIMAL EXPIRATORY FLOW RATES IN TROPICAL EOSINOPHILIAKuppu Rao KV, Vijayan VK, Venkatesan P and Sankaran KCardio-Pulmonary Medicine UnitTB Research CentreIndian Council of Medical ResearchMadras 600 031, India.AbstractMaximal expiratory flow rates such as Peak Expiratory Flow Rate (PEFR), ratesat 25%, 50% and 75% of forced vital capacity (VE 25%, VE 50% and VE 75%)were studied in twenty untreated tropical eosinophilia (TE) patients. Allmeasurements were significantly lower in patients with TE compared to their meanpredicted values. These data suggest that inflammation of airways is an importantmechanism of pathophysiology of tropical eosinophilia.IntroductionThe pulmonarymanifestations oftropical eosinophilia (TE) arecharacterized bycough, dyspnoea,nocturnal wheezing and diffusereticula-nodular infiltrates on chest X-rays(Udwadia, 1964).Pulmonary functionstudies (Vijayan et al., 1991; Nesarajiah,1972; Ray, 1974) had shown restrictive andobstructive ventilatory defects.Histopathological studies had revealed(Udwadia, 1967) dense accumulation ofeosinophils in interstitial tissue. A strikingeosinophilic alveolitis with markedelevation in both the proportion andconcentrationof eosinophils in therecovered fluid has also been described bybronchoalveolar lavage studies (Pinkstonet al., 1987). The lung functionabnormalities in TE could, therefore, bedue to the abnormally accumulatedinflammatory cells in the lung. Themaximal expiratory flow rates duringforced vital capacity manoeuvre had beenshown to reflect histopathological changesin lungs (Cosio et al., 1978). Thus, inconformity with these findings, we hadpreviously shown that there was acorrelation between lung function changesand lower respiratory tract inflammation(Vijayan et al., 1991). However, there areno reported studies of maximal expiratoryf low rates  in  untreated Tropica lEosinophilia patients.Therefore, weundertook a study to evaluate changes inmaximal expiratory flow rates and theirrel tionship with peripheral  bloodeosi ophilia.Materials and MethodsTwenty male patients with symptomsof one week to six months duration andfulfilling the diagnostic criteria (Neva etal., 1978) of residence in the endemic areaof Madras city, respiratory symptoms suchas cough, dyspnoea and nocturnal whe zing, chest X-ray infiltrates,peripheral blood eosinophilia of more than2000 cells per cubic millimeters, highserum titres of antifilarial IgG and arespo se to diethylcarbamazine therapywer  included in the study. Clinicalevaluation of each patientincludeddetailed history, physical examination,chest x-ray, blood and stool examinationsBiomedicine:1992;12(2) 60for the presence of other parasites and IgGfilarial antibody determinations.Maximal flow volume spirogram testswere carried out using Transfer TestModel C (P.K. Morgan P. Ltd. ChathamUK). This instrument is provided withData Dee Computer and X-Y recorder forelectronic memory and recording flowvolume loops.The instrument has aresolution of 0.05 litre in measuring lungvolume and 0.1 litre per second inmeasuring flow rates.The results are printed out aftercorrection to body temperature andpressure saturated with water vapour (BTPS). Best of three well attemptedefforts is utilised for analysis of ForcedVital Capacity (FVC) and ForcedExpiratory Volume in one second. Thehighest value of peak expiratory flow(PEFR) in any of the attempts, and valuesof flow rates at 25% (VE25), 50% (VE50);75% (VE75) of vital capacity obtainedfrom the attempt in which the sum of FVCand FEV1 was highest, were used forfurther statistical analysis (AmericanThoracic Society Workshop Report, 1979).The predicted values of maximalexpiratory flow rates for this study wereobtained from the regression equationsestablished in our laboratory (Vijayan etal., in press). Total and differentialleucocyte counts were utilised to obtainblood eosinophils. Data were analysed bythe students t-test.ResultsOf the twenty male patients, nine weresmokers andremaining 11 werenon-smokers: The mean age was 22.7±5(SD) years (range 18 - 40 years). Meanheight was 163.1±6.5 (SD) centimetersand mean weight was 46.7±8.0(SD)ki logrammes. Since there was no significantdifference in mean values of maximalexpiratory flow measurements betweensmokers and non- smokers, the data wereamalgamated.Spirometric lung volumesre shown in Table 1.The maximalexpiratory flow rates, viz, PEFR VE 25%,VE50% and VE75% are as given in Table2.Table 1: Spirometric Lung VolumesTable 2 Maximal Expiratory Flow Rates in TE* P<0.01 ** P<.001PEFR (5.25±1.71 L/S VS 6.74±0.68L/S P < 0.001); VE25% (4.08±1.66 L/S VS5.44±0.62 L/S P< 0.01); VE50% (2.77±1.02 L/S VS 3.72 ±0.42 L/S P < 0.001) andVE 75% (1.28±0.90 L/S VS 1.92±0.32L/S P< 0.01) were significantly lower inpatients compared to their mean predictedvalues (Fig.1). PEFR was less than 70%predicted in 6 patients, VE 25%, VE 50%and VE 75% were less than 70% predictedin 8, 8 and 12 patients respectively.On further analysis it was found thatthere was no correlation between any ofthe expiratory flow rates and peripheralblood eosinophilia.Biomedicine:1992;12(2) 6 1MAXIMAL EXPIRATORYFLOW RATES IN TEPEFR VE 25%DiscussionThe predominant pulmonary functionabnormality in untreated TE had beenshown to be a reduction in single breathtransfer factor (Vijayan et al., 1988) and aproportion of patients had obstructiveventilatory defects as well (Vijayan et al.,1991). The observation of significantlyreduced expiratory flow rates in our studysubjects suggeststhe involvement ofairways in the inflammatory process inaddition to parenchymal inflammation.The lower respiratory tract inflammationin untreated TE had been shown to be dueto an intense macrophage-eosinophilicalveolitis (Vijayan et al., 1991). We hadalso shownthat inflammatorycellsespecially macrophages recovered fromlower respiratory tract had negativecorrelation with pulmonoary function testssuch as FVC and FEV1 (Vijayan et al.,1991). Therefore, signficant reductions inexpiratory flow rates in this study maysuggest that inflammation of airway mayalso play an important role inpathophysiology of the disease.VE 50% VE 75%FLOWActivated eosinophils had been shownto be capable of injuring airways andparenchymal cells (Barnes et al., 1987;Davis et al., 1984; Frigas et al., 1980).Eventhough there was no correlation ofperipheral blood eosinophils with flowrates in this study, the abnormallyacumulated lung eosinophils may causeinjury to airway epithelium; as it had beenshown that eosinophilic cationic proteinand major basic protein released fromactivated eosinophils arecapable ofinjuring airway epithelium in subjects withbronchial asthma and Adult RespiratoryDistress Syndrome (Hallgren et al., 1987;Laitenen et al., 1985). Inflammatory cellsrecovered from lower respiratory tracthave been shown to be capable ofreleasing various inflammatory mediatorssuch as Platelet Activating Factor (PAF),leukotrines, histamine and prostaglandins(Barnes et al., 1987).We had shownpreviously that the eosinophils recoveredfrom the lower respiratory tract of patientswith untreated TE are activated (Pinkstonet al., 1987) and thus capable of releasingtoxic mediators. It had also been shownBiomedicine:1992;12(2) 6 2that there was airway hyperreactivity in TE(Chhabra et al., 1988) and the mechanismof this hyperresponsiveness in TE may bedue to the toxic mediators especially PAFproduced by these inflammatory cells(Barnes et al., 1987; Lee et al., 1984).References1.2.3.4.5.6.Udwadia FE and Joshi VV. A study of TropicalEosinophilia. Thorax 1964; 19:548-554.Vijayan VK, Kuppu Rao KV, Sankaran K,Venkatesan Pand Prabhakar R. TropicalEosinophilia; Clinical and physiological respto diethylcarbamazine. dionseRespiratory Me cine,1991, 85:17-20.Nesarajah MS, Pulmonary function in Tropicaleosinophilia Thorax, 1972, 27:185-187.Ray D, Lung function in Tropical eosinophilia.Ind J Chest Dis., 1974; 16:368-373.Udwadia FE,  Tropical  eosinophi l ia :  acorrelation of clinical, histopathologic and lungfunction studies, Dis Chest 1967, 52:531-538.Pinkston P, Vijayan VK, Nutman TB et al., Acutetropical pulmonaryCharacterisation ofle o s i n o p h i l i a  :ower respiratory tractinflammation and its response to treatment, JClin Invest 1987; 80:216-25.Cosio M, Gheezzo M, Hogg JC, Cobin R,Loveland M, Dosman J, The relation betweenstructural changesin small airwaysandpulmonary function tests, N Engl J Med, 1978;298:1277-1281.Vijayan VK, Sankaran K, Venkatesan P, KuppuRao KV, Correlation of lower respiratory tractinflammation with changes in lung function andchest roentgenogams in patients with tropicalpulmonary eosinophilia, Singapore MedicalJournal 1391; 32:122-125.Neva FA and Ottesan EA, Tropical (Filarial)Eosinophilia, N Engl J Med, 1978;298:1129-1131.10. American Thoracic Society : Snowbird workshopon standardisation of spirometry, Am Rev RespirDis 1979; 193:831-838.11. Vijayan VK, Kuppu Rao KV, Venkatesan P,Sankaran K and Prabhakar R, Reference valuesThe finding of significantly reducedexpiratory flow rates in this study,therefore suggests that inflammation ofairways is also an important mechanism inthe pathophysiology of TE, in addition toparenchymal inflammation (Vijayan et al.,1991).and prediction equations for maximal expiratoryflow rates in non-smoking normal subjects inMadras (in press)12. VijayankVK, KuppubhRao KV, Sankaran K,Ven atesan P, Praakara R, Diffusing capacityin acute untreated Tropical Eosinophilia, Ind JChest Dis and All Sci 1988; 30:71-77.13. Vijayan VK, Sankaran K, Venkatesan P andPrabhakara R, Effect of Diethylcarbamazine onlveolitis of tropical eosinophilia, Respiration1991; 58:255-259.14. Barnes NC, Costel lo JF, Airwayhyperresponsivness and inflammation, Br MedBull 1987; 43(2):445-459.15. Davis WB, Fells GA, Sun X, Gadek JE, Venet A,Crystal RG, Eosinophil mediated injury to lungparenchymal cells and interstitial matrix, J ClinInvest 1984; 74:249-278.16. Frigas E, Loegering DA, Gleich GI, Cytotoxiceffects of guinea pig eosinophil major basicprotein on tracheal epithelium, Lab Invest 1980;42:35-43.17. Hallgren R, Samulsson T, Vengc P, Modig J,Eosinophil activation in lung is relate, to lungdamage in adult respiratory distress syndrome,Am Rev Respir Dis 1987; 135:639-642.18. Laitenen LA, Heino M., Laitenen A, Kava T,Hachtcla T, Damage of airway epithelum andbronchial reactivity in patients with asthma, AmRev Respir Dis 1985; 313:599-606.19. Chhabra SK, Gaur, Airway hyperreactivity intropical pulmonary eosinophilia, Chest 1988;93:1105-1106.20. Lee TC, Lenihan DJ, Malone D, Roddy LL,Wasserman SI, Increased biosynthesis of pl  teletaactivating factor in activated human eosinophils,J Biol Chem 1984; 259:5526-5530.

Maximal respiratory flow rates in tropical eosinophilia

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