Scandinavian Journal of Infectious Diseases
ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19
Acute Phase Response in Pneumocystis carinii Pneumonia Hannu Syrjälä, Juhani Lähdevirta, Petri Ruutu, Liisa Jokipii, Anssi M. M. Jokipii & Tapani Ruutu To cite this article: Hannu Syrjälä, Juhani Lähdevirta, Petri Ruutu, Liisa Jokipii, Anssi M. M. Jokipii & Tapani Ruutu (1990) Acute Phase Response in Pneumocystis carinii Pneumonia, Scandinavian Journal of Infectious Diseases, 22:6, 713-716, DOI: 10.3109/00365549009027125 To link to this article: http://dx.doi.org/10.3109/00365549009027125
Published online: 08 Jul 2009.
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Article views: 4
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=infd19 Download by: [McMaster University]
Date: 06 April 2016, At: 17:55
Scand J Infect Dis 22: 7 13-7 16, 1990
Acute Phase Response in Pneumocystis carinii Pneumonia HANNU SYRJALA,' JUHANI LAHDEVIRTA,' PETRI RUUTU,' LIISA JOKIPII,' ANSSI M.M. JOKIPI14 and TAPANI RUUTU'
Downloaded by [McMaster University] at 17:55 06 April 2016
From the 'Second and 'Third Departments oJMedicine. Helsinki University Cenrral Hospital, the 2Department of Medicine. Aurora Hospital, the 'Department of Bacteriology and Immunology, Universily of Helsinki, Helsinki, and the 4Deparrment of Medical Microbiology. University of Turku, Turku, Finland
The acute phase response induced by 19 episodes of Pneumocystis carinii pneumonia (PCP) was analysed in a retrospective study. 'There were 9 men and 1 woman with HIV, aged 25-45 years (mean 37.2) and 4 men and 4 women with other immunodeficiencies, aged 18-35 years (mean 26.2). The outcome of these two groups with PCP did not differ: in the HIV group 4 died and in the non-HIV group 2 died. In the HIV group, peak serum C-reactive protein (S-CRP) ranged 41-228 mgtl, mean 126 (77.3), and in the non-HIV group 19-290 mg/l, mean 105 (89.1) (NS). 'The patients with a fatal outcome had higher mean peak S-CRP: 186 (73.8) mg/l versus 85.3 (63.5) mg/l in the survivors (p=0.007). The HIV infection itself did not increase the S-CRP concentration, which was normal before or after P C P in all 7 survivors of the 11 episodes. Thus, P C P induces a clear-cut S-CRP response, which may be used for monitoring the treatment and evaluating the prognosis of the patient.
H . Syrjala, MD, Nationai Public Health Institute, Box 310, SF-90101, Oulu 10, Finland
INTRODUCTION Pneumocystis carinii pneumonia (PCP) was initially identified among premature and debilitated infants. Subsequently PCP has been reported in association with the administration of cytotoxic or immunosuppressive drugs and after organ transplantation. The worldwide problem of HIV infection has greatly increased the incidence of PCP, the most common opportunistic infection of AIDS patients (1). To our knowledge, little information exists on the acute phase response in PCP. Many infectious and noninfectious stimuli causing tissue damage will induce the acute phase response. At least 3 monokines (interleukin 1, tumor necrosis factor and interleukin 6) stimulate production of acute phase proteins by poorly understood mechanisms (2). The acute phase response can be easily quantified by the determination of, for example, the serum C-reactive protein (S-CRP) concentration. Among protozoan infections at least malaria induces an acute phase response (3). In this retrospective study, we analysed the acute phase response induced by PCP among patients infected with HIV or with other immunodeficiencies. MATERIAL AND METHODS Between January 1986 and December 1988, at Helsinki University Central Hospital and at Aurora Hospital, 18 patients (Table I) with PCP were treated in whom the S-CRP concentration had been quantified with sufficient frequency during the acute phase of PCP; S-CRP had been determined at least 5 times (with the exception of 2 episodes, with 3 and 4 determinations, respectively). There were 4 more episodes with PCP; one patient had simultaneously PCP and Mycobacterium avium-intracellulare infection and another had PCP and M. tuberculosis infection. A third patient had 2 PCP episodes, but during the first episode bronchoalveolar lavage (BAL) fluid was also positive for Mycoplasma pneumoniae and varicellazoster virus, and during the second episode he had concomitant extensive candida infection. These 4 episodes of mixed infections were excluded from this series. 46-908556
7 14 H. Syrjala et al.
Scand J Infect Dis 2 2 (1990)
The diagnosis of PCP was confirmed by the identification of Pneumocystis by the Grocott-Gomori methenamine silver (4) and Giemsa staining methods. The diagnostic specimen was BAL in 16 episodes, sputum in 3 and open lung biopsy in 2 episodes. The HIV-antibody positivity was based on an enzyme-linked immunosorbent assay, confirmed by Western blot analysis. S-CRP was quantified by an immunoturbidometric method (5). The non-paired Student’s t-test and Fisher’s exact test were used for the statistical analyses.
Downloaded by [McMaster University] at 17:55 06 April 2016
RESULTS The mean age of the 10 HIV-positive patients (9 men and 1 woman) was 37.2 (SD 6.4) years. The PCP was the first sign of the HIV infection in 4/11 episodes. One patient suffered from 2 separate PCP episodes with an interval of 10 months (patient 6). Table I also shows the underlying conditions causing immunodeficiency in the 8 non-HIV PCP patients. The nonHIV patients were younger-mean age 26.2 (5.4)years-than those in the HIV-positive group (p =0.00 1). When the radiographic presentation was compared, the PCP process affected more often both lungs in the HIV-positive group than in the HIV-negative group: 10/11 episodes (90.9%) in HIV-infected versus 5 / 8 episodes (62.5%) in the non-HIV patients (p=O.18). The survival in these two groups was similar. The mean individual peak S-CRP value was 126 (77.3) mg/l for the HIV-positive group and 105 (89.1) mgll for the non-HIV group (p=0.60). The fatal PCP episodes had a higher mean peak S-CRP, 186 (73.8) mg/l, than the non-fatal, 85.3 (63.5) mg/l, p=0.007 (Fig. 1). The HIV group had a higher mean peak erythrocyte sedimentation rate (ESR) than the non-HIV group: 102 (14.4) mm/h and 63.0 (26.7) mm/h. respectively. The ESR was determined prior to the PCP episode in 5/11 HIV episodes, and was pathological in all samples: mean 73.8 (33.0) Table I. Clinical data of 18 patients with I 9 episodes of Pneumocystis carinii pneumonia HIV = human immunodeficiency virus infection, CML = chronic myeloid leukaemia, BMT = bone marrow transplantation, ALL = acute lymphoblastic leukaemia, AML = acute myeloblastic leukaemia, SLE = systemic lupus erythematosus, ST = high dose pulse steroid treatment, BL = Burkitt’s lymphoma, AP = aplastic anaemia; ESR = erythrocyte sedimentation rate; CRP = serum C-reactive protein concentration (normal value < 12 mg/l) ~
Case no.
Age (Y.)
Sex
Underlying diseases
Peak ESR (mm/h)
Peak CRP (mg/l)
I 2 3 4
43 42 36 44 34 33
M F M M M M M M M M M M F M M F F
HIV HIV HIV HIV HIV HIV HIV HIV HIV HIV HIV CML + BMT CML BMT ALL+BMT AML+BMT SLE + ST CML+BMT BL AP BMT
87 100 I20 87 107
89 55 167 43 41 70 66 197 219 228 208
~
5 6a 6b I 8 9 10 11 12 13 14 15 16 17 18
31 45 42 28 35 28 30 29 23 26 18 21
M F
+
+
101
I20 96 115 72 110 23 62 93 26 75 87 82 56
19
290 99 78 35 1 I3 168 40
~~~
Outcome ~
~~~~
Died Survived Survived Survived Survived Survived Survived Died Died Survived Died Survived Died Survived Survived Survived Died Survived Survived
PCP and S-CRP 7 15
Scand J Infect Dis 22 ( 1 990)
CRP mg/l
I
0
0.
2oo 150 .
0
100 '-
0 0 _L
.. :
Downloaded by [McMaster University] at 17:55 06 April 2016
50 .-
0
0
0
0 . A
B
,
Fig. I . The peak S-CRP concentrations of the patients who survived (A) and died (B). The difference between the groups was significant (p=0.007). Line = arithmetic mean value.
mm/h, range 32-1 12. On the other hand, all survivors in the HIV group had a normal S-CRP concentration before or after PCP (Table 11).
DISCUSSION Our results show that PCP induces a marked acute phase response. Thus, the intracellular protozoan P. carinii seems to cause a stronger acute phase response than intracellular bacterial infections such as tuberculosis and tularemia (6, 7). Another interesting finding was that the S-CRP response in PCP did not differ between the HIV-positive patients and patients with other immunosuppressed conditions. Although the HIV infection will profoundly disturb the immune system, it does not seem to influence the acute phase response. The ESR is obviously still the most widely used method to quantify the acute phase response. The ESR is usually pathological in the AIDS phase of the HIV infection due to immunocomplexes, anaemia, etc. Therefore, the determination of ESR for monitoring the acute phase response is of little value in HIV infected patients. According to our experience, Table 11. S-CRP responses in the survioors among AIDS patients with Pneumocystis carinii pneumonia PCP = Pneumocystis carinii pneumonia, ND = not determined
Case no."
2 3 4 5 6a 6b 9
'See Table I .
Before PCP
During PCP (peak value)
After PCP
< 12 16 < 12 < 10 12 < 12 ND
55 167 43
ND < 12 < 12 < 12 < 12 < 12 16
41
70 66 228
Downloaded by [McMaster University] at 17:55 06 April 2016
I I6 H. Syrjalu et a/.
Scand J Infect Dis 22 (1990)
the HIV infection itself does not increase the S-CRP concentration. Thus, S-CRP is superior to ESR for monitoring possible complications of HIV infection. The increase in S-CRP is proportional to the amount of tissue damage triggering the response. This has been demonstrated, e.g. in myocardial infarction by a good correlation between S-CRP and the CK-MB fraction of creatinine kinase (8). In falciparum malaria, another acute parasitic disease, highest serum CRP levels have been reported among patients with high Plasmodium falciparum parasitaemia (9). Our results show that the severity of PCP, as measured by fatality rate, significantly correlates with the peak concentration of S-CRP. 4/5 patients, whose highest S-CRP was > 180 mg/l died during the acute phase of the disease. Previously, it has been shown that the survival rate is similar in PCP among HIV patients and other immunosuppressed groups (10). as was the case also in our patients. AIDS patients with a first episode of PCP usually survive. However, even with mechanical ventilation AIDS patients with PCP and respiratory failure have a poor prognosis (1 1, 12), although better survival rates have recently been reported (13, 14). Estimating the clinical outcome of PCP is often difficult. AIDS patients with PCP usually have diffuse bilateral interstitial infiltrates, as was the case in our patients. Thus, the extent of infiltration in chest X-rays does not correlate well with the outcome of PCP ( 1 5). In conclusion, our results show that PCP induces a clear-cut acute phase response. Monitoring S-CRP concentration, by a simple and rapid method, may provide guidance for the treatment and prognostic considerations in PCP. REFERENCES 1. Centers for Dibease Control CDC Update. Acquired immunodeficiency syndrome United States. MMWR 35: 17-21, 1986. 2. Brown GE, Lanser ME. Control of acute-phase protein production. In: Faist E, Ninneman J, Green D, eds. Immune consequences of trauma. Shock and sepsis. Berlin: Springer-Verlag, 21 7-228, 1989. 3. Eriksson B, Hellgren U, Rombo L. Changes in erythrocyte sedimentation rate, C-reactive protein and hematological parameters in patients with acute malaria. Scand J Infect Dis 21: 435-441, 1989. 4. Grocott RG. A stain for fungi in tissue sections and smears using Gomori’s methenamine silver nitrate technique. Am J Clin Pathol 25: 975-979, 1955. 5. Harmoinen A, Perko M, Gronroos P. Rapid quantitative determination of C-reactive protein using LKB 8600 Reaction Kate Analyzer. Clin Chim Acta 111: 117-120, 1981. 6. de Beer FC, Kirsten GF, Gie RP, Beyers N, Strachan AF. Value of C-reactive protein measurement in tuberculosis, bacterial and viral meningitis. Arch Dis Child 59: 653-656, 1984. 7. Syrjala H. Peripheral blood leukocyte counts, erythrocyte sedimentation rate and C-reactive protein in tularemia caused by the type B strain of Francisella tularensis. Infection 14: 51-54, 1986. 8. de Beer FC, Hind CRK, Fox KM, Allan RM, Maseri A, Pepys MB. Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction. Br Heart J 47: 239-243, 1982. 9. Naik P, Voller A. Serum C-reactive protein levels and falciparum malaria. Trans R SOCTrop Med Hyg
78: 812-813, 1984. 10. Kovacs JA, Hiemenz JW, Macher AM, Stover D, Murray HW, Shelhamer J , Lane HC, Urmacher C, Honig C, Longo DL. Parker MM, Natanson C, Parrillo JE, Fauci AS, Pizzo PA, Masur H. Pneumocystis carinii pneumonia: A comparison between patients with acquired immunodeficiency syndrome and patients with other immunodeficiencies. Ann Intern Med 100: 663-671, 1984. 1 1 . Wachter RM. Luce JM, Turner J , Volberding P, Hopewell PC. Intensive care of patients with the acquired immunodeficiency syndrome. Outcome and changing patterns of utiiization. Am Rev Respir Dis 134: 891-896, 1986. 12. Schein RMH, Fischl MA. Pitcheriik AE, Sprung CL. ICU survival of patients with the acquired immunodeficiency syndrome. Crit Care Med 14: 1026-1027, 1986. 13. Mills J. Pneumocystis carinii and Toxoplasma gondii infections in patients with the acquired immunodeficiency syndrome. Rev Infect Dis 8: 1001-101 I , 1986. 14. Luce JM, Wachter RM, Hopewell PC. Intensive care patients with the acquired immunodeficiency syndrome: time for a reassessment? Am Rev Respir Dis 137: 1261-1263, 1988. 15. Pedersen C , Lundgren JD, Nielsen T, Andersen WH. The outcome of Pneumocystis carinii pneumonia in Danish patients with AIDS. Scand J Infect Dis 21: 375-380, 1989.
ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19
Acute Phase Response in Pneumocystis carinii Pneumonia Hannu Syrjälä, Juhani Lähdevirta, Petri Ruutu, Liisa Jokipii, Anssi M. M. Jokipii & Tapani Ruutu To cite this article: Hannu Syrjälä, Juhani Lähdevirta, Petri Ruutu, Liisa Jokipii, Anssi M. M. Jokipii & Tapani Ruutu (1990) Acute Phase Response in Pneumocystis carinii Pneumonia, Scandinavian Journal of Infectious Diseases, 22:6, 713-716, DOI: 10.3109/00365549009027125 To link to this article: http://dx.doi.org/10.3109/00365549009027125
Published online: 08 Jul 2009.
Submit your article to this journal
Article views: 4
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=infd19 Download by: [McMaster University]
Date: 06 April 2016, At: 17:55
Scand J Infect Dis 22: 7 13-7 16, 1990
Acute Phase Response in Pneumocystis carinii Pneumonia HANNU SYRJALA,' JUHANI LAHDEVIRTA,' PETRI RUUTU,' LIISA JOKIPII,' ANSSI M.M. JOKIPI14 and TAPANI RUUTU'
Downloaded by [McMaster University] at 17:55 06 April 2016
From the 'Second and 'Third Departments oJMedicine. Helsinki University Cenrral Hospital, the 2Department of Medicine. Aurora Hospital, the 'Department of Bacteriology and Immunology, Universily of Helsinki, Helsinki, and the 4Deparrment of Medical Microbiology. University of Turku, Turku, Finland
The acute phase response induced by 19 episodes of Pneumocystis carinii pneumonia (PCP) was analysed in a retrospective study. 'There were 9 men and 1 woman with HIV, aged 25-45 years (mean 37.2) and 4 men and 4 women with other immunodeficiencies, aged 18-35 years (mean 26.2). The outcome of these two groups with PCP did not differ: in the HIV group 4 died and in the non-HIV group 2 died. In the HIV group, peak serum C-reactive protein (S-CRP) ranged 41-228 mgtl, mean 126 (77.3), and in the non-HIV group 19-290 mg/l, mean 105 (89.1) (NS). 'The patients with a fatal outcome had higher mean peak S-CRP: 186 (73.8) mg/l versus 85.3 (63.5) mg/l in the survivors (p=0.007). The HIV infection itself did not increase the S-CRP concentration, which was normal before or after P C P in all 7 survivors of the 11 episodes. Thus, P C P induces a clear-cut S-CRP response, which may be used for monitoring the treatment and evaluating the prognosis of the patient.
H . Syrjala, MD, Nationai Public Health Institute, Box 310, SF-90101, Oulu 10, Finland
INTRODUCTION Pneumocystis carinii pneumonia (PCP) was initially identified among premature and debilitated infants. Subsequently PCP has been reported in association with the administration of cytotoxic or immunosuppressive drugs and after organ transplantation. The worldwide problem of HIV infection has greatly increased the incidence of PCP, the most common opportunistic infection of AIDS patients (1). To our knowledge, little information exists on the acute phase response in PCP. Many infectious and noninfectious stimuli causing tissue damage will induce the acute phase response. At least 3 monokines (interleukin 1, tumor necrosis factor and interleukin 6) stimulate production of acute phase proteins by poorly understood mechanisms (2). The acute phase response can be easily quantified by the determination of, for example, the serum C-reactive protein (S-CRP) concentration. Among protozoan infections at least malaria induces an acute phase response (3). In this retrospective study, we analysed the acute phase response induced by PCP among patients infected with HIV or with other immunodeficiencies. MATERIAL AND METHODS Between January 1986 and December 1988, at Helsinki University Central Hospital and at Aurora Hospital, 18 patients (Table I) with PCP were treated in whom the S-CRP concentration had been quantified with sufficient frequency during the acute phase of PCP; S-CRP had been determined at least 5 times (with the exception of 2 episodes, with 3 and 4 determinations, respectively). There were 4 more episodes with PCP; one patient had simultaneously PCP and Mycobacterium avium-intracellulare infection and another had PCP and M. tuberculosis infection. A third patient had 2 PCP episodes, but during the first episode bronchoalveolar lavage (BAL) fluid was also positive for Mycoplasma pneumoniae and varicellazoster virus, and during the second episode he had concomitant extensive candida infection. These 4 episodes of mixed infections were excluded from this series. 46-908556
7 14 H. Syrjala et al.
Scand J Infect Dis 2 2 (1990)
The diagnosis of PCP was confirmed by the identification of Pneumocystis by the Grocott-Gomori methenamine silver (4) and Giemsa staining methods. The diagnostic specimen was BAL in 16 episodes, sputum in 3 and open lung biopsy in 2 episodes. The HIV-antibody positivity was based on an enzyme-linked immunosorbent assay, confirmed by Western blot analysis. S-CRP was quantified by an immunoturbidometric method (5). The non-paired Student’s t-test and Fisher’s exact test were used for the statistical analyses.
Downloaded by [McMaster University] at 17:55 06 April 2016
RESULTS The mean age of the 10 HIV-positive patients (9 men and 1 woman) was 37.2 (SD 6.4) years. The PCP was the first sign of the HIV infection in 4/11 episodes. One patient suffered from 2 separate PCP episodes with an interval of 10 months (patient 6). Table I also shows the underlying conditions causing immunodeficiency in the 8 non-HIV PCP patients. The nonHIV patients were younger-mean age 26.2 (5.4)years-than those in the HIV-positive group (p =0.00 1). When the radiographic presentation was compared, the PCP process affected more often both lungs in the HIV-positive group than in the HIV-negative group: 10/11 episodes (90.9%) in HIV-infected versus 5 / 8 episodes (62.5%) in the non-HIV patients (p=O.18). The survival in these two groups was similar. The mean individual peak S-CRP value was 126 (77.3) mg/l for the HIV-positive group and 105 (89.1) mgll for the non-HIV group (p=0.60). The fatal PCP episodes had a higher mean peak S-CRP, 186 (73.8) mg/l, than the non-fatal, 85.3 (63.5) mg/l, p=0.007 (Fig. 1). The HIV group had a higher mean peak erythrocyte sedimentation rate (ESR) than the non-HIV group: 102 (14.4) mm/h and 63.0 (26.7) mm/h. respectively. The ESR was determined prior to the PCP episode in 5/11 HIV episodes, and was pathological in all samples: mean 73.8 (33.0) Table I. Clinical data of 18 patients with I 9 episodes of Pneumocystis carinii pneumonia HIV = human immunodeficiency virus infection, CML = chronic myeloid leukaemia, BMT = bone marrow transplantation, ALL = acute lymphoblastic leukaemia, AML = acute myeloblastic leukaemia, SLE = systemic lupus erythematosus, ST = high dose pulse steroid treatment, BL = Burkitt’s lymphoma, AP = aplastic anaemia; ESR = erythrocyte sedimentation rate; CRP = serum C-reactive protein concentration (normal value < 12 mg/l) ~
Case no.
Age (Y.)
Sex
Underlying diseases
Peak ESR (mm/h)
Peak CRP (mg/l)
I 2 3 4
43 42 36 44 34 33
M F M M M M M M M M M M F M M F F
HIV HIV HIV HIV HIV HIV HIV HIV HIV HIV HIV CML + BMT CML BMT ALL+BMT AML+BMT SLE + ST CML+BMT BL AP BMT
87 100 I20 87 107
89 55 167 43 41 70 66 197 219 228 208
~
5 6a 6b I 8 9 10 11 12 13 14 15 16 17 18
31 45 42 28 35 28 30 29 23 26 18 21
M F
+
+
101
I20 96 115 72 110 23 62 93 26 75 87 82 56
19
290 99 78 35 1 I3 168 40
~~~
Outcome ~
~~~~
Died Survived Survived Survived Survived Survived Survived Died Died Survived Died Survived Died Survived Survived Survived Died Survived Survived
PCP and S-CRP 7 15
Scand J Infect Dis 22 ( 1 990)
CRP mg/l
I
0
0.
2oo 150 .
0
100 '-
0 0 _L
.. :
Downloaded by [McMaster University] at 17:55 06 April 2016
50 .-
0
0
0
0 . A
B
,
Fig. I . The peak S-CRP concentrations of the patients who survived (A) and died (B). The difference between the groups was significant (p=0.007). Line = arithmetic mean value.
mm/h, range 32-1 12. On the other hand, all survivors in the HIV group had a normal S-CRP concentration before or after PCP (Table 11).
DISCUSSION Our results show that PCP induces a marked acute phase response. Thus, the intracellular protozoan P. carinii seems to cause a stronger acute phase response than intracellular bacterial infections such as tuberculosis and tularemia (6, 7). Another interesting finding was that the S-CRP response in PCP did not differ between the HIV-positive patients and patients with other immunosuppressed conditions. Although the HIV infection will profoundly disturb the immune system, it does not seem to influence the acute phase response. The ESR is obviously still the most widely used method to quantify the acute phase response. The ESR is usually pathological in the AIDS phase of the HIV infection due to immunocomplexes, anaemia, etc. Therefore, the determination of ESR for monitoring the acute phase response is of little value in HIV infected patients. According to our experience, Table 11. S-CRP responses in the survioors among AIDS patients with Pneumocystis carinii pneumonia PCP = Pneumocystis carinii pneumonia, ND = not determined
Case no."
2 3 4 5 6a 6b 9
'See Table I .
Before PCP
During PCP (peak value)
After PCP
< 12 16 < 12 < 10 12 < 12 ND
55 167 43
ND < 12 < 12 < 12 < 12 < 12 16
41
70 66 228
Downloaded by [McMaster University] at 17:55 06 April 2016
I I6 H. Syrjalu et a/.
Scand J Infect Dis 22 (1990)
the HIV infection itself does not increase the S-CRP concentration. Thus, S-CRP is superior to ESR for monitoring possible complications of HIV infection. The increase in S-CRP is proportional to the amount of tissue damage triggering the response. This has been demonstrated, e.g. in myocardial infarction by a good correlation between S-CRP and the CK-MB fraction of creatinine kinase (8). In falciparum malaria, another acute parasitic disease, highest serum CRP levels have been reported among patients with high Plasmodium falciparum parasitaemia (9). Our results show that the severity of PCP, as measured by fatality rate, significantly correlates with the peak concentration of S-CRP. 4/5 patients, whose highest S-CRP was > 180 mg/l died during the acute phase of the disease. Previously, it has been shown that the survival rate is similar in PCP among HIV patients and other immunosuppressed groups (10). as was the case also in our patients. AIDS patients with a first episode of PCP usually survive. However, even with mechanical ventilation AIDS patients with PCP and respiratory failure have a poor prognosis (1 1, 12), although better survival rates have recently been reported (13, 14). Estimating the clinical outcome of PCP is often difficult. AIDS patients with PCP usually have diffuse bilateral interstitial infiltrates, as was the case in our patients. Thus, the extent of infiltration in chest X-rays does not correlate well with the outcome of PCP ( 1 5). In conclusion, our results show that PCP induces a clear-cut acute phase response. Monitoring S-CRP concentration, by a simple and rapid method, may provide guidance for the treatment and prognostic considerations in PCP. REFERENCES 1. Centers for Dibease Control CDC Update. Acquired immunodeficiency syndrome United States. MMWR 35: 17-21, 1986. 2. Brown GE, Lanser ME. Control of acute-phase protein production. In: Faist E, Ninneman J, Green D, eds. Immune consequences of trauma. Shock and sepsis. Berlin: Springer-Verlag, 21 7-228, 1989. 3. Eriksson B, Hellgren U, Rombo L. Changes in erythrocyte sedimentation rate, C-reactive protein and hematological parameters in patients with acute malaria. Scand J Infect Dis 21: 435-441, 1989. 4. Grocott RG. A stain for fungi in tissue sections and smears using Gomori’s methenamine silver nitrate technique. Am J Clin Pathol 25: 975-979, 1955. 5. Harmoinen A, Perko M, Gronroos P. Rapid quantitative determination of C-reactive protein using LKB 8600 Reaction Kate Analyzer. Clin Chim Acta 111: 117-120, 1981. 6. de Beer FC, Kirsten GF, Gie RP, Beyers N, Strachan AF. Value of C-reactive protein measurement in tuberculosis, bacterial and viral meningitis. Arch Dis Child 59: 653-656, 1984. 7. Syrjala H. Peripheral blood leukocyte counts, erythrocyte sedimentation rate and C-reactive protein in tularemia caused by the type B strain of Francisella tularensis. Infection 14: 51-54, 1986. 8. de Beer FC, Hind CRK, Fox KM, Allan RM, Maseri A, Pepys MB. Measurement of serum C-reactive protein concentration in myocardial ischaemia and infarction. Br Heart J 47: 239-243, 1982. 9. Naik P, Voller A. Serum C-reactive protein levels and falciparum malaria. Trans R SOCTrop Med Hyg
78: 812-813, 1984. 10. Kovacs JA, Hiemenz JW, Macher AM, Stover D, Murray HW, Shelhamer J , Lane HC, Urmacher C, Honig C, Longo DL. Parker MM, Natanson C, Parrillo JE, Fauci AS, Pizzo PA, Masur H. Pneumocystis carinii pneumonia: A comparison between patients with acquired immunodeficiency syndrome and patients with other immunodeficiencies. Ann Intern Med 100: 663-671, 1984. 1 1 . Wachter RM. Luce JM, Turner J , Volberding P, Hopewell PC. Intensive care of patients with the acquired immunodeficiency syndrome. Outcome and changing patterns of utiiization. Am Rev Respir Dis 134: 891-896, 1986. 12. Schein RMH, Fischl MA. Pitcheriik AE, Sprung CL. ICU survival of patients with the acquired immunodeficiency syndrome. Crit Care Med 14: 1026-1027, 1986. 13. Mills J. Pneumocystis carinii and Toxoplasma gondii infections in patients with the acquired immunodeficiency syndrome. Rev Infect Dis 8: 1001-101 I , 1986. 14. Luce JM, Wachter RM, Hopewell PC. Intensive care patients with the acquired immunodeficiency syndrome: time for a reassessment? Am Rev Respir Dis 137: 1261-1263, 1988. 15. Pedersen C , Lundgren JD, Nielsen T, Andersen WH. The outcome of Pneumocystis carinii pneumonia in Danish patients with AIDS. Scand J Infect Dis 21: 375-380, 1989.
