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Year : 2020  |  Volume : 14  |  Issue : 3  |  Page : 240-242

Elevated procalcitonin level in early postoperative period after liver transplantation is not an indicator for systemic infection - a case report

Department of Liver Transplantation, Medica Superspeciality Hospital, Kolkata, West Bengal, India

Date of Submission30-Apr-2020
Date of Acceptance15-Jul-2020
Date of Web Publication30-Sep-2020

Correspondence Address:
Dr. Hirak Pahari
5 Hindustan Park, Kolkata - 700 029, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_38_20

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Elevated procalcitonin (Pct) in the early postoperative phase after liver transplantation often may present a diagnostic dilemma. We report a 40-year-old patient after deceased donor liver transplant who had elevated Pct on postoperative day (POD) 2 which gradually declined by POD 6. This was not accompanied by any signs of clinical infection and did not coincide with mild rejection in the recipient. We conclude that raised Pct in early posttransplant phase is not an independent marker for systemic infection, whereas persistently elevated Pct level or a second peak may be more contributory to the diagnosis of infection. The level of Pct must be correlated with clinical symptoms, signs, and other infective markers for better diagnostic accuracy.

Keywords: Liver, procalcitonin, transplant

How to cite this article:
Pahari H, Shellagi N, Nath B. Elevated procalcitonin level in early postoperative period after liver transplantation is not an indicator for systemic infection - a case report. Indian J Transplant 2020;14:240-2

How to cite this URL:
Pahari H, Shellagi N, Nath B. Elevated procalcitonin level in early postoperative period after liver transplantation is not an indicator for systemic infection - a case report. Indian J Transplant [serial online] 2020 [cited 2021 Jul 30];14:240-2. Available from: https://www.ijtonline.in/text.asp?2020/14/3/240/296892

  Introduction Top

Procalcitonin (Pct) is a very common biomarker used to guide antimicrobial treatment in the setting of bacterial infection. However, there are several reports of raised Pct reports in the early postoperative period after solid organ transplantation.[1],[2],[3] It may be difficult to determine the significance given the already increased risk of infection due to immunosuppression in these patients. It has also been proposed that Pct may be used to differentiate between early posttransplant infection and rejection. Here, we present a case report of a patient who underwent deceased donor liver transplantation (DDLT) with raised Pct level in the early posttransplant period.

This is a retrospective case report of a patient who underwent DDLT at our institute on January 13, 2020. His preoperative demographics and results, surgical details, and postoperative course were collected and have been presented here.

  Case Report Top

This is the report of a 40-year-old male patient who was suffering from alcohol-related chronic liver disease. He was unable to work and was bedridden due to his condition. His liver disease was complicated by severe jaundice, ascites, hepatic encephalopathy, coagulopathy, and esophageal and bleeding rectal varices. His Na-MELD score at presentation was 31 points. After a thorough evaluation and surgical work-up and obtaining the necessary medical, psychosocial, and financial clearances, he was placed on the waitlist for DDLT.

On January 13, 2020, he underwent a liver transplantation from a 44-year-old male brain-dead donor with intracerebral hemorrhage with hypertension but no other known comorbidities without any known infection. The surgery lasted 5 h and 32 min. Cold ischemia time was 5 h 3 min and warm ischemia time was 46 min. Liver weight was 1.2 kg. Steroid induction was used. He was extubated on postoperative day (POD) 1 [Table 1].
Table 1: Patient details

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His bilirubin and liver enzymes continued to trend down over the next week. On POD 2, he was diagnosed with mild-to-moderate pulmonary edema which responded well to albumin infusion and diuresis. On the same day, a serum Pct level was sent which was reported to be 7.7 ng/ml. White blood cell (WBC) count on POD 2 was 8770/mm,3 and there was no fever. On POD 3, repeat Pct was 5.6 ng/ml and WBC count was 6900/mm3. On PODs 4 and 5, Pct level decreased to 2.6 ng/ml and 1.31 ng/ml, respectively. C-reactive protein (CRP) was <5 on POD 6 and continued to be negative throughout the remaining duration of the hospital stay [Figure 1].
Figure 1: Trend of procalcitonin and C-reactive protein along with liver enzymes (SGOT and SGPT). *AST (SGOT): Aspartate aminotransferase (serum glutamic-oxaloacetic transaminase); ALT (SGPT): Alanine aminotransferase (serum glutamic-pyruvic transaminase)

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On POD 6, the liver enzymes increased, without any clinical symptoms. Ultrasound Doppler of the liver and computed tomography triphasic scan of the liver were done to rule out any anatomic causes and were negative. A presumptive diagnosis of mild acute cellular rejection was done, and he was treated with 3 doses of 500 mg IV solumedrol. He responded favorably and liver function normalized. He was eventually discharged on POD 13 in stable condition. Now, he is 3 months out from transplant with normal liver function without any evidence of complication.

  Discussion Top

Historically, Pct is a known biomarker for bacterial infection, and in theory, this can be extrapolated to use in differentiating bacterial infection from acute rejection in postoperative patients of solid organ transplantation.[1],[2],[3] However, the diagnostic accuracy of Pct level in the early posttransplant period is uncertain. Reports have varied from reporting a higher rate of complication when the peak Pct is >5 ng/ml, to a higher risk if only there is a second peak of Pct elevation.[4],[5] Anecdotal reports have corroborated the possibility of differentiation of acute infection from rejection by the use of Pct level.[6],[7],[8]

In our patient, the serum Pct peak was observed on POD 2 and showed a rapidly declining trend. This was not associated with any evidence of infection or rejection. Van den Broek et al. in their study concluded that although peak Pct differed significantly between recipients with and without clinically significant infections, it was not an independent risk factor and added little prognostic accuracy.[1] The level of CRP as measured correlated with the trend of Pct in the first week after liver transplantation in our patient. Sandkovsky et al. observed that even without the presence of infection, Pct may increase as a result of surgical procedures during transplantation, implantation of devices, and use of induction immunosuppressive therapy.[2]

In the setting of both liver and heart transplantation, the elevation of Pct following antithymocyte globulin induction, as well as elevation, followed by normalization without any long term prognostic implication after cardiac transplantation, is documented.[9],[10],[11] Eberhard et al. observed that Pct values rose postoperatively to peak levels on the 1st and 2nd days and mostly declined to normal within 1 week from renal transplantation.[3] The data from lung transplant recipients are still unclear, and the level of Pct should be correlated with other clinical markers.[12],[13]

  Conclusion Top

Postoperative complications after liver transplantation may result from multifactorial causes. The correlation between Pct trend, clinical course, other markers such as CRP, and other diagnostic tools must be evaluated to ensure the detection of early signs of a postoperative complication. Pct level should be used cautiously, and false elevations due to induction therapy must be considered in the differential diagnosis. The finding of persistently elevated Pct or a second peak after initial decline should be taken seriously and the possibility of systemic infection ruled out.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

van den Broek MA, Olde Damink SW, Winkens B, Broelsch CE, Malagó M, Paul A, et al. Procalcitonin as a prognostic marker for infectious complications in liver transplant recipients in an intensive care unit. Liver Transpl 2010;16:402-10.  Back to cited text no. 1
Sandkovsky U, Kalil AC, Florescu DF. The use and value of procalcitonin in solid organ transplantation. Clin Transplant 2015;29:689-96.  Back to cited text no. 2
Eberhard OK, Langefeld I, Kuse ER, Brunkhorst FM, Kliem V, Schlitt HJ, et al. Procalcitonin in the early phase after renal transplantation–will it add to diagnostic accuracy? Clin Transplant 1998;12:206-11.  Back to cited text no. 3
Perrakis A, Stirkat F, Croner RS, Vassos N, Raptis D, Yedibela S, et al. Prognostic and diagnostic value of procalcitonin in the post-transplant setting after liver transplantation. Arch Med Sci 2016;12:372-9.  Back to cited text no. 4
Perrakis A, Yedibela S, Schellerer V, Hohenberger W, Müller V. Procalcitonin in the setting of complicated postoperative course after liver transplantation. Transplant Proc 2010;42:4187-90.  Back to cited text no. 5
Kaido T, Ogawa K, Fujimoto Y, Mori A, Hatano E, Okajima H, et al. Perioperative changes of procalcitonin levels in patients undergoing liver transplantation. Transpl Infect Dis 2014;16:790-6.  Back to cited text no. 6
Hara T, Soyama A, Hidaka M, Natsuda K, Adachi T, Ono S, et al. Pretransplant serum procalcitonin level for prediction of early post-transplant sepsis in living donor liver transplantation. Hepatol Res 2018;48:383-90.  Back to cited text no. 7
Coelho MC, Tannuri U, Tannuri AC, Reingenheim C, Troster EJ. Is procalcitonin useful to differentiate rejection from bacterial infection in the early post-operative period of liver transplantation in children? Pediatr Transplant 2009;13:1004-6.  Back to cited text no. 8
Madershahian N, Wittwer T, Franke UF, Wippermann J, Strauch J, Groetzner J, et al. Effect of induction therapy on kinetic of procalcitonin following uncomplicated heart transplantation. J Card Surg 2007;22:199-202.  Back to cited text no. 9
Zazula R, Prucha M, Tyll T, Kieslichova E. Induction of procalcitonin in liver transplant patients treated with anti-thymocyte globulin. Crit Care 2007;11:R131.  Back to cited text no. 10
Madershahian N, Wittwer T, Strauch J, Wippermann J, Rahmanian P, Franke UF, et al. Kinetic of procalcitonin in the early postoperative course following heart transplantation. J Card Surg 2008;23:468-73.  Back to cited text no. 11
Hammer S, Meisner F, Dirschedl P, Fraunberger P, Meiser B, Reichart B, et al. Procalcitonin for differential diagnosis of graft rejection and infection in patients with heart and/or lung grafts. Intensive Care Med 2000;26 Suppl 2:S182-6.  Back to cited text no. 12
Sammons C, Doligalski CT. Utility of procalcitonin as a biomarker for rejection and differentiation of infectious complications in lung transplant recipients. Ann Pharmacother 2014;48:116-22.  Back to cited text no. 13


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