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Biomedical subjects

A Grove

Publications and source records attributed to A Grove.

At least 37 records · Page 2Linked to original sources
PubMed1996

Effects of prior treatment with salmeterol and formoterol on airway and systemic beta 2 responses to fenoterol.

BACKGROUND: Previous studies have shown that both salmeterol and formoterol act as partial beta 2 receptor agonists in terms of antagonising the extrapulmonary responses to fenoterol in normal subjects. The aim of the present study was to extend previous observations in evaluating the effect of prior treatment with salmeterol and formoterol on bronchodilator responses to fenoterol, a full beta 2 receptor agonist, in patients with asthma. METHODS: Ten stable asthmatic patients of mean (SE) age 37 (3.7) years and forced expiratory volume in one second (FEV1) 59.5 (4.1)% of predicted completed the study. One hour after inhaling single doses of placebo, salmeterol 25 micrograms, or formoterol 12 micrograms, dose-response curves to repeated doses of inhaled fenoterol were constructed (cumulative doses of 100-3200 micrograms). Measurements of airway and systemic beta 2 receptor mediated responses were made at baseline, after inhalation of placebo, salmeterol, or formoterol, and after each dose of fenoterol. RESULTS: Salmeterol and formoterol produced significant bronchodilation compared with placebo (mean difference and 95% CI compared with placebo): FEV1, salmeterol 0.41 (95% CI 0.13 to 0.69) 1, formoterol 0.47 (95% CI 0.19 to 0.75) 1. Salmeterol and formoterol had no significant effect on systemic responses compared with placebo. There were no significant differences in peak airway responses to fenoterol after treatment with salmeterol or formoterol compared with placebo (mean (pooled SE)): FEV1, placebo 2.84 (0.03) 1, salmeterol 2.87 (0.03) 1, and formoterol 2.88 (0.03) 1. There were no significant differences in the area under the dose-response curve for any of the parameters during the dose-response curve following treatment with salmeterol or formoterol compared with placebo. There was no difference in the slope of the dose-response curves to fenoterol for FEV1 or forced expiratory flow (FEF25-75) after treatment with salmeterol or formoterol compared with placebo, although there was a significant (p < 0.05) attenuation of the slope in the dose-response curve for the peak expiratory flow rate (PEFR). CONCLUSIONS: Prior treatment with low doses of salmeterol or formoterol does not significantly alter bronchodilator dose-response curves to repeated doses of fenoterol in stable asthmatic patients.

Adrenergic beta-Agonists↗
PubMed1996

Effects of regular salmeterol on lung function and exercise capacity in patients with chronic obstructive airways disease.

BACKGROUND: The aim of this study was to evaluate the effects of single and chronic dosing with salmeterol on exercise capacity and lung function in patients with chronic obstructive pulmonary disease. METHODS: Twenty nine patients of mean (SE) age 64 (1.5) years, forced expiratory volume in one second (FEV1) 42(3)% of predicted, and 5-15% reversibility to salbutamol 200 micrograms were randomised to receive four weeks treatment with salmeterol 50 micrograms twice daily or placebo in a double blind crossover fashion with a one week washout period in between. Measurements of spirometric parameters, static lung volumes, and exercise capacity were made one and six hours after a single dose, and six hours after the final dose of salmeterol or placebo. RESULTS: Salmeterol produced a small increase in FEV1 at one and six hours after a single dose, and this was maintained after chronic dosing (mean difference and 95% CI versus placebo): single dosing at one hour 0.07 (95% CI 0.02 to 0.11) 1, single dosing at six hours 0.16 (95% CI 0.09 to 0.22) 1, chronic dosing at six hours 0.11 (95% CI 0.03 to 0.19) 1. The increase in forced vital capacity (FVC) was greater with salmeterol than with placebo six hours after single but not chronic dosing: single dosing at six hours 0.17 (95% CI 0.04 to 0.29) 1, chronic dosing at six hours 0.02 (95% CI -0.18 to 0.22) 1. Slow vital capacity was increased after treatment with salmeterol compared with placebo one and six hours after single but not after chronic dosing. There were no significant differences in static lung volumes or exercise capacity after single or chronic dosing with salmeterol compared with placebo. Patients reported a significantly lower Borg score for perceived exertion following the six minute walk after chronic treatment with salmeterol compared with placebo. CONCLUSIONS: Salmeterol produced a small improvement in spirometric values compared with placebo consistent with the degree of reversibility originally shown by the subjects to salbutamol 200 micrograms. This was not associated with improvements in static lung volumes or exercise capacity, but there was some symptomatic benefit in that patients were able to walk the same distance in six minutes with less perceived exertion.

Albuterol↗
PubMed1996

Effects of inhaled fluticasone propionate and oral prednisolone on lymphocyte beta 2-adrenoceptor function in asthmatic patients.

The aim of the study was to evaluate the facilitatory effects of inhaled corticosteroid on in vitro parameters of lymphocyte beta 2-adrenoceptor function in asthmatic patients. Serum cortisol level was also evaluated as a measure of systemic bioactivity. Ten (four female) asthmatic subjects were evaluated, mean (SEM) age was 28.6(2.0) years, and FEV1 was 79.9%(8.7) predicted. Single doses of inhaled placebo (PL), fluticasone propionate, 1,000 micrograms (F1000), fluticasone propionate, 2,000 micrograms(F2000), or oral prednisolone, 50 mg(PRED), were given at 10 PM the previous night and measurements were made 10 h later. Values for beta 2-receptor density (logBmax: fmol/10(6)cells) were significantly (p < 0.05) greater than PL with PRED but not with inhaled fluticasone (as means and 95% confidence interval [CI] for difference vs PL): PL, 0.27; F1000, 0.30; F2000, 0.32; and PRED, 0.48 (95% CI vs PL, 0.075 to 0.341). Maximal cyclic adenosine monophosphate (cAMP) responses to isoproterenol hydrochloride (isoprenaline (Emax; pmol/10(6)cells) mirrored those for Bmax: PL, 4.00; F1000, 4.68; F2000, 4.26; and PRED, 7.46 (95% CI vs PL, -0.01 to 6.91). Receptor affinity (Kd) was not significantly altered by any treatment. There was significant (p < 0.05) suppression of serum cortisol (nmol/L) with F2000 and PRED compared with PL: PL, 307.9; F1000, 323.2; F2000, 130.1 (95% CI vs PL, 69.76 to 285.8) and PRED, 51.8 (95% CI vs PL, 144.11 to 368.01). Thus, high-dose inhaled fluticasone propionate did not have any facilitatory effects on lymphocyte beta 2-adrenoceptor parameters as compared with oral prednisolone which upregulated beta 2-receptor density and increased cAMP response. In contrast, high-dose inhaled fluticasone (2,000 micrograms) significantly suppressed serum cortisol. In conclusion, there would appear to be a dissociation in systemic sensitivity between effects of inhaled corticosteroid on adrenal suppression and lymphocyte beta 2-adrenoceptor regulation.

Administration, Topical↗
PubMed1995

Bronchodilator subsensitivity to salbutamol after twice daily salmeterol in asthmatic patients.

In view of current concerns about use of regular beta-2 agonists, and the place of the newer long-acting drugs, we decided to evaluate whether continuous exposure to twice daily salmeterol results in a blunting of the acute bronchodilator response to repeated doses of salbutamol, as might be administered in the management of an acute asthma attack. After a 2 week run-in without beta-2 agonists, 17 asthmatic patients (mean [SE] age 34 [3] years, mean forced expiratory volume in 1 s [FEV1] 64 [2.7]% of predicted) were randomised to receive salmeterol 50 micrograms twice daily or placebo for 4 weeks in a double-blind cross-over fashion. A histamine challenge test was done 12 h after the last dose of each treatment period, and dose-response curves to inhaled salbutamol (200-3200 micrograms) were constructed 36 h after the last dose. Patients treated with salmeterol had reduced bronchodilator responses to salbutamol in terms of FEV1 and peak expiratory flow rate (PEFR) than those treated with placebo. The reduction in response equated with a 2.5-fold and a fourfold greater dose of salbutamol being required to produce a given FEV1 and PEFR, respectively. There was a significant reduction in lymphocyte beta-2 adrenoceptor density after salmeterol compared with placebo and run-in. Salmeterol remained effective in terms of disease control, with a significant improvement in morning PEFR compared with placebo that was maintained over the 4 week treatment period.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1995

A comparison of the effects of prednisolone and mianserin on ventilatory, exercise and psychometric parameters in patients with chronic obstructive pulmonary disease.

There is controversy as to whether effects on mood play a role in mediating the response to corticosteroids in chronic obstructive pulmonary disease (COPD). If alterations in mood are important, it is conceivable that psychotropic drugs such as mianserin might produce similar responses to prednisolone in patients with COPD. Twelve patients age 62.5 y, with FEV1 29% of predicted and < 15% reversibility to salbutamol completed a randomised, double-blind crossover study. After an initial three week placebo run-in period patients received three weeks of prednisolone 40 mg daily or mianserin 60-90 mg daily with an intervening three week placebo washout period. Full respiratory function tests, bicycle ergometry and 6 minute walks were performed before and after the run-in and at the end of each period. Psychological and functional assessments were also made at each visit. Prednisolone significantly increased FVC, maximum ventilation (VEmax) and maximum heart rate (HRmax) compared with placebo, with mean for the difference of 0.25 l, 2.56 l.min-1 and 12 beats.min-1 respectively. FVC, maximum oxygen uptake (VO2max) and HRmax were also significantly increased with prednisolone compared with mianserin. Anxiety scores were significantly lower with prednisolone compared with placebo. In contrast, mianserin had no significant effects on lung function, exercise or psychological parameters compared with placebo. The improvements in ventilation, exercise and anxiety scores following treatment with prednisolone were not reproduced by mianserin, suggesting that the effects of prednisolone in COPD are unlikely to be due to alterations in mood.

Aged↗
PubMed1995

Tolerance with beta 2-adrenoceptor agonists: time for reappraisal.

1. In spite of the widespread use of beta 2-adrenoceptor agonists in the treatment of asthma controversy continues regarding their possible role in increasing asthma mortality and morbidity. There is however no evidence available to suggest that tolerance to the bronchodilator or anti-bronchoconstrictor effects of these drugs is responsible for the deleterious effects reported with the regular use of bronchodilators. 2. There is no conclusive evidence to suggest that tolerance develops to the bronchodilator effects of short-acting beta 2-adrenoceptor agonists. Tolerance does however appear to develop to the anti-bronchoconstrictor effects of these drugs. 3. With regard to the long-acting beta 2-adrenoceptor agonists, there is evidence to suggest that tolerance develops both to their anti-bronchoconstrictor, and bronchodilator effects. Tolerance was however demonstrated in the presence of improved symptom control, therefore the clinical relevance of this phenomenon is uncertain. 4. Systemic corticosteroids can modulate lymphocyte beta 2-adrenoceptor function both preventing, and reversing tolerance. The situation regarding the effects of systemic or inhaled corticosteroids on modulating bronchodilator responses in asthmatics is less clear. There is some evidence to suggest that inhaled corticosteroids are unable to prevent bronchodilator or systemic tolerance to long-acting beta 2-adrenoceptor agonists. 5. On the basis of the current evidence, the British Thoracic Society guidelines for the management of asthma appear appropriate with regard to their recommendations for the use of long-acting beta 2-adrenoceptor agonists.

Adrenergic beta-2 Receptor Agonists↗
PubMed1995

Abnormal myocardial repolarisation in response to hypoxaemia and fenoterol.

BACKGROUND: Prolongation of the QTc interval has been associated with cardiac dysrhythmias and sudden death. QTc dispersion (interlead variability in QTc interval) has recently been proposed as being a more sensitive marker of repolarisation abnormalities and shown to be a more specific index of arrhythmia risk. Although hypoxaemia and fenoterol have previously been shown to prolong the QTc interval, this does not reflect regional myocardial repolarisation abnormalities. METHODS: Electrophysiological effects were measured at baseline and after 30 minutes steady state hypoxaemia at an arterial oxygen saturation (SaO2) of 75-80% (study 1) and at baseline then 30 minutes after inhaled fenoterol 2.4 mg (study 2). From the ECG, lead II corrected QT interval (QTc) and overall corrected QT dispersion were measured using a computer linked digitising tablet according to standard criteria. RESULTS: QTc dispersion was increased during hypoxia compared with baseline values (mean (SE) 69 (6) ms v 50 (5) ms) and after fenoterol compared with baseline (79 (13) v 46 (4) ms), respectively. There was also an increase in QTc interval and heart rate after fenoterol (493 (23) v 420 (6) ms and 98 (3) v 71 (6) bpm, respectively). The heart rate was increased during hypoxaemia compared with baseline (78 (3) v 64 (2) bpm), but no change occurred in the QTc interval. CONCLUSIONS: Both hypoxaemia and fenoterol cause myocardial repolarisation abnormalities in man in terms of increased QTc dispersion, but only fenoterol increased the QTc interval. This may be relevant in the aetiology of arrhythmias in patients with acute severe asthma where beta agonist therapy and hypoxaemia coexist.

Adrenergic beta-Agonists↗
PubMed1995

Expression of the beta 2 adrenoceptor partial agonist/antagonist activity of salbutamol in states of low and high adrenergic tone.

BACKGROUND: Salbutamol exhibits partial agonist/antagonist activity at airway beta 2 receptors in vitro in that it attenuates the bronchorelaxant effect of the full agonist isoprenaline. The aim of the present study was to characterise the partial beta 2 agonist/antagonist activity of salbutamol in vivo during supine rest and exercise, in states of low and high adrenergic tone. METHODS: Eight normal subjects were randomised to receive single oral doses of salbutamol 2 mg, 4 mg, 8 mg (S2, S4, S8), placebo (PL), or propranolol 80 mg (PR). The beta 2 adrenoceptor responses were evaluated after supine rest and subsequently in response to maximal exercise. RESULTS: Salbutamol demonstrated a dose-related increase in resting heart rate and tremor and a fall in serum potassium level consistent with beta 2 agonism. On exercise, the hyperkalaemic response was augmented by propranolol compared with placebo consistent with beta 2 blockade: mean difference for delta response (95% CI) PR v PL was 0.60 (0.02 to 1.27) mmol/l. This effect also occurred with salbutamol in a dose-related fashion: S8 v PL 0.33 (0.01 to 0.71) mmol/l, S8 v S2 0.31 (-0.02 to 0.61) mmol/l. Whilst propranolol blunted exercise heart rate in keeping with beta 1 blockade, salbutamol had no effect. Exercise produced an increase in lymphocyte beta 2 receptor binding density (Bmax) which was not affected by salbutamol. Plasma levels of adrenaline and noradrenaline at peak exercise were also unaltered by salbutamol in comparison with placebo. CONCLUSIONS: In a state of low adrenergic tone at rest salbutamol produces effects consistent with beta 2 agonism. In contrast, in a state of increased adrenergic tone during exercise salbutamol produced beta 2 selective antagonism as evidenced by its effects on exercise-induced hyperkalaemia (beta 2) but not on exercise-induced tachycardia (beta 1). The effects of salbutamol on beta 2 receptor density do not explain its effects on exercise-induced hyperkalaemia since upregulation rather than downregulation was observed. This in vivo phenomenon of partial beta 2 agonist/antagonist activity of salbutamol may be of relevance in the setting of acute asthma if adrenergic tone is increased.

Adrenergic beta-Agonists↗
PubMed1995

Subsensitivity of bronchodilator and systemic beta 2 adrenoceptor responses after regular twice daily treatment with eformoterol dry powder in asthmatic patients.

BACKGROUND: There is controversy as to the role of long acting beta 2 agonists such as eformoterol and, in particular, whether bronchodilator tolerance occurs during continuous therapy. The purpose of this study was to extend previous observations of bronchodilator subsensitivity with metered dose eformoterol aerosol in order to assess whether tolerance also occurs with a dry powder formulation of the same drug. METHODS: Sixteen asthmatic patients of mean age 33 (range 18-53) years and FEV1 (% predicted) of 64 (3)%, of whom 13 were receiving inhaled corticosteroids, received regular treatment with eformoterol 24 micrograms twice daily or placebo twice daily (without beta 2 agonists) given concurrently for four weeks in a randomised double blind cross-over design. An initial two week run-in was used when beta 2 agonists were withdrawn and substituted with ipratropium bromide. Dose-response curves to eformoterol (cumulative dose 6-102 micrograms) for airways and systemic beta 2 responses were constructed at the end of each treatment period. RESULTS: Baseline values for airways and systemic responses were similar. The peak delta FEV1 response from the dose-response curve (as change from baseline) and the delta response for FEV1 and FEF25-75 at six hours after the last dose were attenuated after eformoterol compared with placebo: peak delta FEV1 response 1.001 with placebo v 0.841 with eformoterol (95% CI 0.04 to 0.28); at six hours 0.931 with placebo v 0.581 with eformoterol (95% CI 0.20 to 0.50); and for delta FEF25-75 at six hours 1.29 1/s with placebo v 0.87 1/s with eformoterol (95% CI 0.15 to 0.69). Morning peak expiratory flow rate was significantly improved during treatment with eformoterol (451 1/min) compared with placebo (399 1/min) (95% CI 21 to 82). Systemic beta 2 responses were blunted after eformoterol, together with a reduction in lymphocyte beta 2 receptor binding density. CONCLUSIONS: Regular twice daily eformoterol dry powder may produce bronchodilator subsensitivity in terms of both peak and duration of response to cumulative repeated doses of eformoterol. Systemic beta 2-mediated adverse effects also showed tolerance, which was mirrored by downregulation of lymphocyte beta 2 adrenoceptors.

Adolescent↗
PubMed1994

Asthma control.

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Albuterol↗
PubMed1994

The magical and medicinal usage of Stangeria eriopus in South Africa.

The underground caudex of the cycad Stangeria eriopus is used extensively by several ethnic groups in South Africa, mainly as an ingredient in magical potions but also as an emetic. An assessment of two main outlets showed that 3410 plants were sold in the month of July 1992; continued usage of this material now threatens the remaining plant populations. A proximate analysis of the caudex material gives high carbohydrate content with only small percentages of fat, protein, fibre and ash. An unusually high content of sodium sulphate may explain the efficacy of Stangeria-containing preparations as an emetic. The phytosterols sitosterol and stigmasterol are present in a 4:1 ratio while the fatty acid component comprises palmitic, oleic, stearic and arachidic acids. Twelve amino acids were identified in the material, including the non-protein amino acids beta-alanine, gamma-aminobutyric acid and pyroglutamic acid. The candidate neurotoxin beta-N-methylamino-L-alanine could not be detected but cycasin is present at the levels of 0.17% and 0.21% in fresh and dry caudex material, respectively and appears to be accompanied by the related toxin, macrozamin.

Attitude to Health↗
PubMed1994

The value of immunohistochemistry of pleural biopsy specimens in the differential diagnosis between malignant mesothelioma and metastatic carcinoma.

The aim of the present study was to evaluate the aid of immunohistochemistry in the differential diagnosis between pleural malignant mesothelioma (MM) and secondary pleural carcinoma in pleural biopsy specimens. A series of MM (epithelial or biphasic type) (n = 39), and a series of secondary pleural carcinomas (n = 25) were studied with a panel of monoclonal antibodies against Ber-EP4, CEA, and Leu-MI (CD-15). Considering the markers one, two or three at a time, computer analysis was conducted to identify the immunophenotype with the highest sensitivity and specificity for both MM (n = 39) and adenocarcinoma (n = 19). The CEA/CD-15 marker combination had the highest specificity (MM = 100%; adenocarcinoma = 82.1%), and sensitivity (MM = 82.1%; adenocarcinoma = 100%) considering both categories of tumours. Positive reaction for CEA and/or CD-15 was the best indicator of metastatic adenocarcinoma. Negative reaction for CEA/CD-15 and Ber-EP4/CD-15 showed up to be 100% specific for MM. Positive reaction for one, two or even all these antigens, however, occurred in nine tumours predetermined as MM according to their gross appearance, and absence of other primary malignancies at autopsy. Ultrastructural examination (n = 7) of these tumours strongly supported the diagnosis in one case, and did by no means exclude the diagnosis MM in the other six cases. Neither did any of the tumours reveal ultrastructural signs of adenomatous differentiation, and they did not express PAS/diastase resistant globules, amylase or surfactant. Anti -Ber-EP4 was the antibody most frequently expressed in MM (n = 8). Until antibodies specific for MM are available, the limitation of immunohistochemistry to solve the diagnosis in all cases of pleural malignant tumours has to be considered.

Carcinoma↗
PubMed1994

A comparison of the systemic bioactivity of inhaled budesonide and fluticasone propionate in normal subjects.

1. The aim of this study was to compare the systemic bioactivity of low and high doses of inhaled budesonide and fluticasone propionate given by respective dry powder inhaler devices. 2. A randomised, single blind cross-over design was used in nine healthy subjects who were given 800 micrograms day-1 of budesonide Turbohaler (B800) for 1 week, followed by 1 week of 1600 micrograms day-1 (B1600), or fluticasone Diskhaler 750 micrograms day-1 (F750) for 1 week followed by 1 week of 1500 micrograms day-1 (F1500). There was a 1 week washout between treatments with fluticasone or budesonide. A twice daily dosing regime was used and mouth-rinsing was employed to reduce gut bioavailability as well as to obviate local adverse effects. 3. Parameters of hypothalmic-pituitary adrenal (HPA) axis activity and bone metabolism were measured at baseline (B0/F0), at the end of each week of treatment and after the 1 week washout (F0 or B0). 4. Both fluticasone and budesonide significantly (P < 0.05) attenuated the post tetracosactrin serum cortisol at low and high doses whilst early morning cortisol was unchanged. No dose-response effect was observed with either drug, and there was no significant difference between treatment with fluticasone or budesonide. 5. Neither budesonide nor fluticasone produced significant suppression of plasma osteocalcin, although the higher doses of both drugs significantly reduced fasting urinary calcium levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1994

Chemical synthesis and characterization of peptides and oligomeric proteins designed to form transmembrane ion channels.

A strategy for the synthesis of peptides and oligomeric proteins designed to form transmembrane ion channels is described. A folding motif that exhibits a functional ionic pore encompasses amphipathic alpha-helices organized as a four-helix bundle around a central hydrophilic pore. The channel-forming activity of monomeric amphipathic peptides may be examined after reconstitution in lipid bilayers in which peptides self-assemble into conductive oligomers. The covalent attachment of channel-forming peptides to the lysine epsilon-amino groups of a template molecule (KKKPGKEKG) specifies oligomeric number and facilitates the study of ionic permeation and channel blockade. Here we describe detailed protocols for the total synthesis of peptides and template-assembled four-helix bundle proteins, exemplified with the sequence of M2 delta (EKM-STAISVLLAQAVFLLLTSQR), considered involved in lining the pore of the nicotinic acetylcholine receptor channel. For comparison, the synthesis of a second four-helix bundle, T4CaIVS3 with the sequence of predicted transmembrane segment S3 (DPWNVFDFLIVIGSIIDVILSE) of the fourth repeat of the L-type voltage-gated calcium channel, is included. Peptides and proteins are synthesized step-wise by solid-phase methods, purified by reversed-phase HPLC, and homogeneity ascertained by analytical HPLC, capillary zone electrophoresis, SDS/PAGE, amino acid analysis and sequencing. Optimization of synthetic procedures for hydrophobic molecules include reducing resin substitution to avoid steric hindrance and aggregation of the final product. Protocols for the preparation of the samples prior to HPLC purification as well as the conditions and columns required for successful purification are presented. The methods developed are generally applicable for the chemical synthesis, purification and characterization of amphipathic peptides and template directed helical bundle proteins.

Amino Acid Sequence↗
PubMed1994

Amylase in lung carcinomas. An ultrastructural and immunohistochemical study of two adenocarcinomas, and a review of the literature.

The ultrastructure of two lung adenocarcinomas with immunohistochemical and biochemical expression of amylase is reported. Isoenzyme determination performed on tumour tissue showed a salivary-type amylase. None of the carcinomas was associated with hyperamylasaemia. Ultrastructurally, the adenocarcinomas contained a varying number of heterogeneous granules resembling lysosomes. None of the tumours contained mature zymogen granules. The findings are discussed in relation to previous cases of amylase-containing lung carcinomas subjected to electron microscopy. The vast majority of these carcinomas were associated with a significant elevation of serum amylase. Various theories which might explain the absence of hyperamylasaemia in the presented cases are proposed. The biological and diagnostic significance of amylase production is discussed.

Adenocarcinoma↗
PubMed1994

alpha-Amylase in resectable lung cancer.

Biochemical analysis and immunohistochemical techniques support the theory that hyperamylasaemia in lung cancer is due to amylase production in carcinoma cells. The vast majority of amylase-producing carcinomas are adenocarcinomas with amylase isoenzyme similar to the salivary type. This prospective study assesses alpha-amylase expression in resectable lung cancer. Seventy four patients with resectable lung cancer were studied. Amylase activity in tumour tissue was analysed and isoamylase identification performed. Immunohistochemical analysis was performed using a polyclonal rabbit antibody against human salivary amylase. Hyperamylasaemia occurred in 13 out of 70 patients. Increased amylase activity in tumour tissue was found in 10 out of 52 cases, of which only two were associated with hyperamylasaemia. With the exception of one large cell carcinoma and one squamous cell carcinoma, the tumours were adenocarcinomas. Immunohistochemical analysis revealed amylase expression in seven adenocarcinomas and two adenosquamous carcinomas. In conclusion, immunohistochemical amylase expression was restricted to carcinomas with adenomatous differentiation. Biochemical analysis confirmed amylase production in 5 of 7 cases examined, the tissue amylase isoenzymes being of salivary type. However, hyperamylasaemia and a slightly increased amylase activity in tumour tissue may be caused by factors other than amylase-producing carcinoma cells.

Adenocarcinoma, Papillary↗