DOI 10.1378/chest.98.5.1159 1990;98;1159-1164Chest

 M Klockars, T Pettersson, B Fröseth, O Selroos and U H Stenman inhibitor (TATI) in pleural effusions.Concentration of tumor-associated trypsin

  http://chestjournal.chestpubs.org/content/98/5/1159

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CHEST I 98 I 5 I NOVEMBER, 1990 1159

Concentration of Tumor-AssociatedTrypsin Inhibitor (TATI) in PleuralEffusions*Matti Kiockars, M. D.; Tom Pettersson, M. D. ; Bertil Fr#{246}seth, M. Sc.;

Olof Seiroos, M. D.; and Ulf-Hdkan Stenman, M.D.

We measured the concentration oftumor-associated trypsininhibitor (TATI) in plasma and pleural fluid of 84 patients

with pleural effusions of various causes. We observedelevated (>30 p�g/L) TATI levels in pleural fluid in 45

percent of patients with pleural effusion associated with

malignant disease and in 15 percent of patients with benign

disease. Similar results were obtained for TATI in plasma.The concentration of TATI in pleural fluid closely paral-lelled that in plasma. In patients with renal insufficiency

and in patients with biliary obstruction, the TAT! levels

were elevated both in plasma and pleural fluid. A positive

correlation was seen between the concentration of TATIand the activity of alkaline phosphatase in plasma. The

results show that simultaneous determination of TATI in

plasma and pleural fluid improves the diagnosis of cancer

only marginally. Our results also support the hypothesisthat elevated TAT! levels may reflect an acute phase

reaction caused by inflammatory disease or tissue destruc-tion associated with cancer not only in inflammatory con-

ditions, but also in malignant disease where the tumor itself

is not producing TAT!. (Chest 1990; 98:1159-64)

TAll = tumor-associated trypsin inhibitor; CRP C-reactiveprotein; CHF congestive heart failure; ThC tuberculosis;CEA = carcinoembryonic antigen; PSTI pancreatic secretorytrypsin inhibitor

A number of tumor markers and biochemical assays

of pleural fluid have been evaluated as diagnostic

indicators of pleural effusions caused by or associated

with either benign or malignant diseases.’ Among the

tumor-associated proteins, the concentration of card-

noembryonic antigen (CEA) has been elevated in 45

to 88 percent,2� and cancer antigens 125, 15-3, and

19-9 have been elevated in 38 to 64 percent of pleural

effusions associated with cancer.57 Neuron-specific

enolase in pleural fluid is elevated in about 70 percent

of patients with small cell lung cancer, and determi-

nation of pleural fluid hyaluronic acid helps to differ-

entiate between effusions caused by malignant meso-

thelioma and other forms of cancer.8’#{176} The diagnostic

specificity of these observations, however, is low

because many of the tunior markers are also elevated

in pleural fluid of patients with various nonmalignant

conditions.

Tumor-associated trypsin inhibitor (FATI) is a 6-kd

peptide that is identical to the pancreatic secretory

trypsin inhibitor (PSTI), as indicated by amino acid

and DNA sequence homology.”’3 The concentrations

of TATI are elevated in serum and urine of 30 to 60

percent ofpatients with various malignant gynecologic

14 Tumor-associated trypsin inhibitor is a fairly

specific marker of mucinous ovarian cancer in which

elevated levels occur in most patients with advanced

disease and in about half of those with local disease.

Elevated levels also occur in patients with hepatocel-

lular, gastric, pancreatic, and lung cancer,’�7 in pa-

tients with severe inflammatory conditions such as

pneumonia and pancreatitis,’�’8 and in patients with

hepatobiliary � The elevation ofthe serum

concentrations of TAT! in association with severe

inflammation and after surgery has suggested that

TATI may behave like an acute phase reactant such as

C-reactive protein (CRP) and a, -antiprotease . 19,20

However, in patients with pelvic inflammatory disease,

an elevation of TATI level is observed only when the

CRP levels are strongly elevated, ie, above 80 mg/L.

The present study was undertaken to determine

the following: (1) whether TATI determinations of

pleural fluid, ie, close to the tumor or local metastases,

improve the diagnostic sensitivity and specificity for

cancer, (2) whether there is a concentration gradient

ofTATI between blood and pleural fluid, and (3) how

TATI behaves in pleural effusions associated with

benign inflammatory diseases.

PATIENTS AND METHODS*Fmm the Institute ofOccupational Health, Helsinki (Dr. Klockars);

the Fourth Department of Medicine, Helsinki University CentralHospital (Dr. Pettersson); Mj#{246}lbolsta Hospital (Drs. Fr#{246}seth andSelroos); and Departments I and II of Obstetrics and Gynecology(Dr. Stenman), Helsinki University Central Hospital, Helsinki,Finland.

Manuscript received February 20; revision accepted May 2.Reprint requests: DE Klockars institute of Occupational Health,Topeliuksenkatu 4laA, 00250 Helsinki, Finland

The series consisted of 84 patients with pleural effusion. Based

on the final diagnosis, the patients were divided into the following

groups: (1) 25 patients with cancer, including eight patients with

primary cancer of the lung, two with mesothelioma, ten with

metastatic cancer, two with undefined cancer, two with non-

Hodgkin’s lymphoma, and one with a carcinoid tumor; (2) seven

patients with pneumonia; (3) four patients with pleural empyema;

 © 1990 American College of Chest Physicians by guest on July 10, 2011chestjournal.chestpubs.orgDownloaded from

a

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(9ECl)(9

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120

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Sa

Sa.

-ra’..

;, I #{149}I I�I WV.I � : L1�I I #{149}#{149}I �‘:tit] I I i #{149}] FIGURE 1. Concentrations ofTATI in plasma of66 patients with pleural effusion of various

Pneumonia

(5)

causes (patients with normal serum creatinineEmpyema Tbc Non-specific Cancer C H F and alkaline phosphatase levels). Horizontal

(3) (14) (20) (20) (4) hars=meanvaluesineachgroup.

1160 Tumor-associated Trypsin Inhibitor in Pleural Effusions (K!ockars et a!)

Table 1-Concentration ofPlasma and Pleural Fluid TAT1(p�g/L) in Different Thtient Groups� Mean ± SD and

Individual Values�

Plasma Pleural Fluid

Benign disease (46)t 26.3 ± 23.6 18. 1 ± 8.7j

Pneumonia (5) 38.0 ± 14.9 28.8 ± 7.2

Empyema(3) 99.0±39.8 18.6±16.5

Tuberculosis (14) 18.9± 10.9 14.4 ±8.8

Nonspecific(20) 19.3±6.7 18.9±6.2�

Congestive heart failure (4) 18.0 ± 5.4 13.7 ± 4.8

Malignant disease (20) 35.2 ± 28.8 31.4 ± 30.2�

Primary cancer ofthe lung (8) 37.8 ± 22.5 31.5 ± 19.9

Adenocarcinoma (2) 6.5, 38.0 6.5, 40.0

Microcellular cancer (1) 16.0 15.0

Epidermoid cancer (1) 69.0 68.0

Anaplastic cancer (1) 23.0 24.0

Carcinosarcoma (1) 66.0 47.0

Nondefined cancer (2) 36.0, 48.0 18.0, 34.0

Metastatic cancer (7) 40.8 ± 43.6 43.5±48.8

Breast cancer (3) 10.0, 16.0, 46.0 16.0, 16.0, 59.0

Ovariancancer(1) 10.0 13.0

Thyroid cancer (1) 60.0 45.0

Stomach cancer (1) 128.0 146.0

Urogenitalcancer(1) 16.0 10.0

Mesothelioma(2) 16.0,28.0 9.9, 25.0

Carcinoid tumor (1) 19.0 10.0

Lymphoma(2) 12.0,32.0 11.0, 24.0

*patieflts with normal creatinine and alkaline phosphatase levels in

serum.

tNumber in parentheses indicate number of patients.

tStatistical significances: pleural effusion associated with malignant

disease (n = 20) vs benign disease (n = 46) (p<O.Ol) and vs nonspe-

cific pleural effusion (n = 20) (p<0.05).

(4) 16 patients with tuberculous pleurisy; and (5) 21 patients with

exudative pleural effusion of unknown etiology; this diagnosis was

accepted when all other types of pleurisy had been ruled out on

the basis of extensive investigations and clinical follow-up; and (6)

1 1 patients had transudative pleural effusion due to congestive heart

failure (CHF); this group included hvo patients with pulmonary

emboism.

Tumor-associated trypsin inhibitor in plasma and pleural fluid

was measured by radioimmunoassay. � � The mean concentration of

TATI in plasma of healthy men and women is 11 �.tgfL and the

reference interval of healthy subjects is 3 to 21 p.g/L. Serum

concentrations of creatinine, aspartate and alanine aminotransfer-

ases, and alkaline phosphatase were determined by routine labora-

� tory methods.

Differences were tested for significance by Student’s t test.

RESULTS

Table 1 and Figures 1 and 2 show the concentrations

ofTATI in plasma and pleural fluid from patients with

normal serum creatinine and normal serum alkaline

phosphatase values. There were no significant differ-

ences in plasma TATI levels between patients with

benign or malignant disease. Elevated plasma concen-

trations (>21 p.gfL) were observed in 11 (55 percent)

of 20 patients with malignant disease and in 17 (37

percent) of 46 patients with nonmalignant disease.

Using a cut-off level of 30 pigfL, nine (45 percent) of

20 patients with malignant disease and seven (15

percent) of 46 patients with benign disease had

elevated levels. All patients with pneumonia and

empyema had plasma levels of TAT! above 21 p�g/L.

The highest levels of TAll in plasma were seen in

patients with empyema and cancer. For the differential

diagnosis of cancer, elevated plasma concentrations

(>30 p.g/L) ofTATI had a sensitivity of45 percent and

specificity of85 percent.

In pleural fluid, the highest TATI levels were

detected in patients with cancer, but moderately

elevated levels of TATI were seen in a few patients

with pneumonia, empyema, and tuberculosis. As a

group, patients with malignant diseases had signifi-

cantly higher pleural fluid TAT! levels than patients

with benign diseases. Using a cut-offlevel of 30 p�g(L,

seven of 20 patients with malignant disease and six of

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100

80

60

40#{149}a.

20

a

aa

aa

aa

a.aa

a..

alp.

Pneumonia Empyema Tbc Non-specific Cancer

(5) (3) (14) (20) (20)

a � FIGURE 2. Concentrations of TAT! in pleural

fluid of 66 patients with pleural effusion of

C H F various causes (patients with normal serum

creatinine and alkaline phosphatase levels). Hor-

( 4) izontal bars = mean values in each group.

Plasma

Pleural fluid

0)

�.- 50

�40

�30

20

Oct.30 Nov.6 Dec.20 Jan.22

FIGURE 3. Variation in the concentration of TAT! in plasma and

pleural fluid in a patient with persistent pleural effusion associated

with pneumonia.

140a

CHEST I 98 I 5 I NOVEMBER, 1990 1161

46 patients with benign disease had elevated TAT!

values in pleural fluid. For the diagnosis ofcancer, the

specificity and sensitivity of elevated pleural fluid

TAT! (>30 p�g/L) were about the same as for plasma,

ie, 35 and 87 percent, respectively. There were no

differences in the concentration of TAT! between

patients with various types of cancer. By raising the

cut-off level to 40 p�WL for pleural fluid TAll, the

specificity for cancer increased to 100 percent but the

sensitivity decreased to 30 percent.

No significant difference between TAT! levels in

plasma and pleural fluid was observed. There was a

positive correlation (r = 0.87) between the concentra-

tion of TAT! in pleural fluid and plasma. In only two

patients, both of whom had pleural empyema, was

there a marked difference between TAT! levels in

plasma and pleural fluid. Pleural fluid levels of TAT!

were 5 and 14 �i.g/L, whereas those in plasma were

130 and 113 p�g/L, respectively. In 18 patients, two to

80

70

60

five repeated samples ofpleural fluid and plasma were

analyzed. Figure 3 shows the changes in TAT! levels

in plasma and pleural fluid of a patient with long-

standing pleuropneumonia over a three-month period.

The pleural fluid TAT! levels were slightly lower and

with a short delay followed those in plasma during the

resolution of the infection.

Because renal insufficiency and biliary obstruction

result in raised serum concentrations of TAT!,’4’6 we

studied nine patients with renal insufficiency and nine

patients with elevated serum levels of alkaline phos-

phatase (Tables 2 and 3). A significant positive corre-

lation was observed between the plasma levels of TAT!

and serum alkaline phosphatase (r = 0.48) (Fig 4). The

levels of TAT! in plasma and pleural fluid were

markedly elevated in patients with renal insufficiency;

the highest levels, 1,300 and 1,490 p�gfL, were seen

in a patient receiving hemodialysis.

DISCUSSION

The present study shows that determination of TAT!

levels in plasma and pleural fluid does not significantly

improve the diagnostic sensitivity and specificity for

cancer associated with pleural effusions. For the dif-

ferential diagnosis between benign and malignant

disease, a good specificity is obtained by using a cut-

offlevel of4O jigfL for TAT! in pleural fluid. However,

from a diagnostic point ofview, many pleural effusions

such as those associated with pneumonia and tuber-

culosis can usually be characterized using biochemical

and microbiologic analyses.21� For one of the most

difficult differential diagnoses, ie, that between pleural

effusions associated with cancer and nonspecific pleu-

ral effusions (still representing about 20 percent of all

pleural effusions), assay of TAT! either in plasma or

pleural fluid provides useful diagnostic information.

No patient with nonspecific pleural effusion had

 © 1990 American College of Chest Physicians by guest on July 10, 2011chestjournal.chestpubs.orgDownloaded from

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Table 2-Plasma (P) and Pleural Fluid (PF) TATI in Nine Patients with Renal insufficiency

1162 Tumor-associated Trypsin Inhibitor in Pleural Effusions (K!ockars et a!)

P-TAT!, PF-TATI, S�Creatinine,* S-alkaline

PatientlAge, yr �gfL �.tg/L �amoI/L phosphatase,* U/L Diagnosis

1163 40 27 168 259 CHFt

2184 52 36 126 224 CHF

�1(77 55 55 280 318 CHF

4/75 79 60 150 163 Pulmonary carcinoma

5/84 86 68 203 287 CHF6f84 123 11 1 205 150 Nonspecific pleural effusion

7/73 180 111 188 327 CHF

8/56 292 202 141 189 Empyema

9/56 1,492 1,300 925 NDt CHF

*Reference values: serum creatinine < 125 p.mol/L; serum alkaline phosphatase, 60 to 280 U/L.

tCHF = congestive heart failure; ND not done.

Table 3-Plasma (F) and Pleural Fluid (PF) TAT1 in Nine Patients with

Elevated Serum Alkaline Phosphatase Level (>400 UIL)

P-TATI, PF-TATI, Alkaline

Patient/Age, yr p.g/L p.g/L phosphatase,* U/L Diagnosis

1171 18 12 486 CHFt

2161 23 17 1,046 Mammary carcinoma

3/72 54 36 1,618 Pulmonary tuberculosis

4/68 59 50 414 Pneumonia

5/82 76 62 461 Pneumonia

6/71 122 85 1 ,030 Pulmonary carcinoma

7/63 170 1 14 522 Pancreatic carcinoma

8/80 183 177 1,049 Pulmonary tuberculosis

9/74 205 173 770 Thyroid carcinoma

5Reference values, as in Table 2.

tCHF = congestive heart failure.

plasma or pleural fluid TAT! levels above 40 �igfL,

whereas 30 percent of the patients with cancer had

such elevated levels. Thus, the sensitivity was rather

low, as has been observed for a number ofother tumor

markers measured in pleural fluid. However, by

combining TAT! with CEA and other tumor marker

assays, the diagnostic accuracy may be increased.

The source ofTATI in healthy subjects is not exactly

known. Part of it is apparently pancreatic, but this is

not the only source, as pancreatectomized patients

have normal serum levels)z� At least three different

mechanisms may lead to elevation of TATI in cancer

and inflammatory conditions, ie, (1) production by the

tumor, (2) an acute phase reaction, and (3) leakage

from a diseased 17

The elevation of serum TAT! levels in patients with

renal insufficiency has been related to decreased

urinary excretion of this small molecular weight pep-

12 The elevated TAT! levels in patients with signs

of biliary obstruction probably relate to a disturbed

FIGURE 4. Correlation between plasma TAT!

and alkaline phosphatase in 75 patients with

pleural effusion.

0 250 500 750 1000 1250 1500 1750

Alkaline phosphatase (U/I)

 © 1990 American College of Chest Physicians by guest on July 10, 2011chestjournal.chestpubs.orgDownloaded from

CHEST I 98 I 5 1 NOVEMBER, 1990 1113

flow of TAT! secreted by the 16

Some tumors produce large quantities of TAT! that

will be reflected in elevated plasma levels,”’7 but

elevated serum levels are also found in patients with

immunohistochemically TAT!-negative 16

Therefore, production ofTATI by the tumor probably

does not explain the elevation of TAT! in all patients

with cancer-associated pleural effusion. This interpre-

tation is supported by the observation that the levels

in pleural fluid were similar to those in plasma. The

lack of a concentration gradient between pleural fluid

and plasma may result from the fact that the small

molecular weight of TAT! permits it to freely diffuse

in and out oflocal effusion fluids.

Increased serum levels of protease inhibitors have

been observed in cancer patients,� and proteases and

their inhibitors usually occur together.� Tumor-asso-

ciated trypsin inhibitor is a very specific inhibitor of

trypsin.27 Mucinous ovarian tumors contain a serine

protease� that is immunologically identical with tryp-

sin. This protease, called tumor-associated trypsin,

activates prourokinase.� Therefore, it may participate

in the protease cascade associated with invasive tu-

mors. This cascade, which comprises at least uroki-

nase, plasmin, and collagenase, is thought to mediate

invasion by degrading interstitial tissues.� Thus, ex-

pression ofTAT! may reflect activation ofthis protease

cascade and a defense reaction ofnormal tissue against

proteolytic activity of the 17 The tissue reaction

in inflammation is in many respects similar to that in

cancer.� Therefore, the elevation of TAT! in inflam-

matory diseases and some cancer patients may be

mediated by the same mechanism.

We found highly elevated levels of TAT! in plasma

and pleural fluid of a few patients with pneumonia,

empyema, and tuberculosis. In two patients with

empyema, pleural fluid levels of TAT! were much

lower than in serum suggesting that high local prote-

olytic activity may cause consumption ofTAT!. Inter-

estingly, several lymphokines known to mediate acute

phase reactions, such as interferon beta, tumor necro-

sis factor, and interleukin 1 , stimulate the synthesis of

TATIJPST! in a human hepatoma cell line in vitro.� A

similar mechanism could explain the elevation of TAT!

both in inflammatory conditions and in malignant

tumors not producing TAT! themselves.

ACKNOWLEDGMENTS: This work was supported by grants fromthe Academy of Finland, Sigrid Juselius Foundation, the FinnishCancer Institute, the Finnish Social Insurance Institution, and theFinska Lakaresallskapet.

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DOI 10.1378/chest.98.5.1159 1990;98; 1159-1164Chest

M Klockars, T Pettersson, B Fröseth, O Selroos and U H Stenmaneffusions.

Concentration of tumor-associated trypsin inhibitor (TATI) in pleural

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