Amoebic liver abscess in a renal transplant recipient - A rare entity- Case report

Vishnu Dev Urs; VN Unni; Nanda Kachare; Vinod Kumar Kunjappa; Abhinav Menon; PK Bipi

doi:10.4103/ijot.ijot_61_20

CASE REPORT

Year : 2020 | Volume : 14 | Issue : 4 | Page : 366-368

Amoebic liver abscess in a renal transplant recipient - A rare entity- Case report

Vishnu Dev Urs¹, VN Unni¹, Nanda Kachare², Vinod Kumar Kunjappa¹, Abhinav Menon¹, PK Bipi¹
¹ Department of Nephrology, Aster Medcity, Kochi, Kerala, India
² Department of Pathology, Aster Medcity, Kochi, Kerala, India

Date of Submission	21-Jun-2020
Date of Acceptance	22-Nov-2020
Date of Web Publication	30-Dec-2020

Correspondence Address:
Dr. V N Unni
Department of Nephrology, Aster Medcity, Kuttisahib Road, Cheranelloor, Kochi - 682 027, Kerala
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_61_20

Abstract

Infections are the most common cause of morbidity and mortality in renal transplant recipients; respiratory, urinary, and gastrointestinal infections are the most common. Gastrointestinal manifestations are usually associated with cytomegalovirus. Although opportunistic infections are common in solid organ transplant recipients in view of the immunosuppressed state, amoebic liver abscess is uncommon in renal transplant recipients and has not been reported in literature, to the best of our knowledge. We describe a patient with an amoebic liver abscess 3 months after renal transplantation surgery.

Keywords: Alkaline phosphatase, amoebic liver abscess, case report, metronidazole, renal transplantation

How to cite this article:
Urs VD, Unni V N, Kachare N, Kunjappa VK, Menon A, Bipi P K. Amoebic liver abscess in a renal transplant recipient - A rare entity- Case report. Indian J Transplant 2020;14:366-8

How to cite this URL:
Urs VD, Unni V N, Kachare N, Kunjappa VK, Menon A, Bipi P K. Amoebic liver abscess in a renal transplant recipient - A rare entity- Case report. Indian J Transplant [serial online] 2020 [cited 2021 Jan 25];14:366-8. Available from: https://www.ijtonline.in/text.asp?2020/14/4/366/305429

Introduction

Amoebic infection of the gastrointestinal tract is caused by the protozoan parasite Entamoeba histolytica; this organism is transmitted by the ingestion of fecally contaminated food and water. Among symptomatic infections, amoebic dysentery is the most common clinical presentation, and amoebic liver abscess is the most common extraintestinal manifestation. We report a patient with an amoebic liver abscess, 3 months after live related donor renal transplantation. Amoebic liver abscess in solid organ recipients is extremely rare and has never been reported in literature. This is probably the first case to be reported, to the best of our knowledge.

Case Report

A 32-year-old female presented with severe renal failure (serum creatinine - 5.6 mg/dl), requiring hemodialysis. She was diagnosed to have systemic lupus erythematosus 1 year ago and had received immunosuppression with corticosteroids, Mycophenolate mofetil and Rituximab. Renal biopsy was suggestive of Class VI lupus nephritis. There was no family history of renal disease. She was dialysis dependent and there were no signs of lupus activity for over 8 months. She underwent live-related donor renal transplantation with mother as the kidney donor. She received Basiliximab as induction immunosuppression and Tacrolimus, Mycophenolate mofetil and Prednisolone as maintenance immunosuppression. Postoperative period was uneventful. Serum creatinine normalized by the 4^th post-operative day (0.8 mg/dl). Tacrolimus level at one and 3 months posttransplant was 6.5 and 4.8 ng/ml, respectively. She was asymptomatic for next 3 months.

Three months after surgery, she presented with fever and diarrhea of 2 days duration. There was no vomiting, jaundice, abdominal pain. Physical examination was unremarkable. There was worsening of graft function (serum creatinine - 1.8 mg/dl). Urine, stool, and blood cultures were negative. Ultrasonogram and Doppler evaluation of the graft kidney was normal. She was treated with broad-spectrum antibiotics. Two weeks later, she developed abdominal pain, and ultrasonogram abdomen showed solitary hypoechoic lesion in the right lobe of the liver [Figure 1]a. Computerized tomogram (CT) abdomen showed a well circumscribed hypodense lesion measuring 6 cm × 5.8 cm × 6.8 cm noted in the right lobe of the liver, involving segments 4b and 5 [Figure 1]b. Direct bilirubin (1.5 mg/dl) and serum alkaline phosphatase (228U/L) levels were elevated. Ultrasonogram-guided aspiration from lesion revealed anchovy sauce aspirate [Figure 2]a. Wet mount of aspirate showed multiple free-living single celled organisms of the size of 45–50 μ with large nucleus [Figure 2]b and endoplasm suggestive of trophozoites of E. histolytica. Cytology smears stained with Giemsa, Hematoxylin, and Eosin stains showed extensive necrotic debris, trophozoites of E. histolytica with large prokaryote and distinct membranes [Figure 2]c. Serum IgM anti amoeba antibodies were positive. Diagnosis of amoebic liver abscess was made, and she was treated with oral Metronidazole (400 mg thrice daily) for 2 weeks. Tacrolimus level after 1 week of treatment was 17.6 ng/ml. As metronidazole is known to increase Tacrolimus levels, the drug levels were monitored, and doses were adjusted.

Figure 1: (a) Ultrasonogram abdomen showing hypoechoic lesion in the right lobe of liver. (b) Computerized tomogram abdomen showing abscess in right lobe of liver (circle)

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Figure 2: (a) Anchovy sauce aspirate. (b) Wet mount microscopy showing trophozoite of Entamoeba histolytica (arrow). (c) Trophozoites of Entamoeba histolytica (arrow) with single large prokaryocyte and distinct membranes (Giemsa stain, ×400)

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Two weeks after treatment, she still had persisting abdominal pain. Repeat ultrasonogram showed an increase in the size of the abscess. Serum alkaline phosphatase levels were markedly elevated [Table 1]. Pigtail catheter was placed, and 400 ml of pus was drained. Metronidazole was continued for two more weeks. After 4 weeks of treatment, she was better and serum alkaline phosphatase levels normalized. Ultrasonogram showed complete resolution of the abscess.

Table 1: Liver function tests

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Discussion

Infections are an important cause of morbidity and mortality in transplant recipients. The risk of infection is determined by duration of exposure to infectious agents and cumulative immunosuppression.^[1],[2] Liver abscess is an uncommon complication following solid organ transplantation, especially after renal transplantation. Though pyogenic liver abscess has previously been reported in a hemodialysis patient, amoebic liver abscess in renal allograft recipients is not reported in literature.

Although amoebiasis is endemic in certain parts of India, it is not reported in renal transplant recipients. Even the well-known Rubin's time table of infections in renal transplant recipients and the Indian time table by John,^[3] do not mention amoebic liver abscess. Amoebic infections occur when mature cysts are ingested through fecally contaminated water or food. When the parasite reaches the small intestine, excystation occurs, releasing trophozoites which penetrate colonic mucosa. Once established in the colon, it has the propensity to invade mucosa, leading to ulceration and colitis. It may disseminate to extraintestinal sites, most commonly liver, where amoebae generate inflammatory reaction and necrosis of hepatocytes, producing an abscess.

Amoebic liver abscess is ten times common in adult males than females and males are susceptible for invasive disease. Possible factors include alcoholic hepatocellular damage and protective effect of iron-deficiency anemia and hormonal factors in women.^[2] The definitive reason remains elusive. Our patient was a female.

Amoebic liver abscess commonly presents with acute or subacute history of fever, right hypochondrial pain; although in 20%–50% cases, chronic presentation can occur with protracted history of diarrhea, weight loss and abdominal pain. The median duration of symptoms before the presentation is 14 days.^[2] History of diarrhea or dysentery is present in 38% of patients and 50% of patients were found to exhibit colonic ulceration on colonoscopy, suggesting a possible portal of entry. Jaundice or icterus is uncommon, occurring in 24% patients and when present, it may suggest severe disease, like multiple abscesses.^[2]

Our patient presented with history of fever, diarrhea and abdominal pain. There was no weight loss or jaundice. The classic triad of fever, right upper quadrant pain and jaundice is suggestive of the diagnosis.[4] These are rarely observed now, making diagnosis difficult, especially in immunosuppressed patients. Clinical signs, symptoms, and laboratory tests, including liver function test abnormalities, do not help to distinguish amoebic from pyogenic liver abscesses. Serology for antibodies to E. histolytica is useful to establish current or past infection.^[1]

Our patient had direct hyperbilirubinemia, markedly raised alkaline phosphatase levels and hypoalbuminemia. This is consistent with the findings of Wuerz et al., who demonstrated the presence of raised alkaline phosphatase levels and hypoalbuminemia in two-thirds of the patients with amoebic liver abscess, especially in those with indolent disease.

As a diagnostic tool, ultrasonography is the primary imaging modality for evaluating potential liver abscess, with sensitivity ranging from 80% to 100%.^[4] CT scanning has sensitivity similar to ultrasonogram and is usually performed to detect very small abscesses. If clinical suspicion is high and the initial ultrasound is negative, CT scan is recommended. Compared with pyogenic abscesses, amoebic liver abscesses are commonly solitary and likely to involve the right lobe of the liver. The presence of multiple abscesses in the liver does not rule out amoebic liver abscess.^[1] Ultrasonogram and CT abdomen in our patient showed a solitary right lobe liver abscess. In an appropriate clinical setting, diagnosis can be made with positive serology. The absence of antibody to E. histolytica after 1 week of symptoms argues strongly against the diagnosis of amoebic liver abscess or invasive bowel disease. Serum antibodies are detected in 85%–95% of patients after one or more weeks of symptoms.^[2] Demonstration of the motile organism on fresh mount preparation of the aspirate confirms the diagnosis, which was also seen in our patient.

Routine aspiration of amoebic liver abscess is not indicated for diagnostic or therapeutic purposes. A combination of ultrasonographic findings with positive serology in an appropriate clinical setting is adequate to start medical therapy. Aspiration is indicated if there is a lack of clinical improvement in 48–72 hours, left lobe abscess, thin rim of tissue around abscess (<10 mm), and seronegative abscesses.^[5]

Nitroimidazoles, mainly metronidazole, is the standard treatment for amoebic liver abscess, which is given for 7–10 days, although a case series have demonstrated the potential efficacy of a single dose of 2.5 g.^[2] Residual liver abscess can persist in 5%–28% cases irrespective of treatment modality (medical or drainage) and can persist up to 36 months or longer in asymptomatic individuals. Follow up with ultrasound is required.^[6],[7] The response to treatment is prompt, and the prognosis is excellent. Around 15% of patients can have failure of medical treatment, and percutaneous needle aspiration or catheter drainage may be required. Between the two modalities, studies have shown that the latter is superior, with a higher success rate and quicker resolution.^[6],[7]

Our patient required treatment with oral metronidazole for 4 weeks and percutaneous catheter drainage. She showed excellent clinical improvement. Liver function tests and graft functions improved. Ultrasonogram after 4 weeks showed resolving abscess and complete resolution of the abscess was achieved by 12 weeks. Recurrence of amoebic liver abscess after treatment is rare.^[8] Our patient is being followed up every 2 months and there is no recurrence so far. Metronidazole increases Tacrolimus levels; the probable mechanism is CYP3A4 inhibition due to specific pharmacokinetics in certain patients.^[9] We monitored Tacrolimus levels, and doses were adjusted to maintain trough levels at 6–10 ng/ml.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1.	Alalawi F, AlNour H, Julie BM, Sharma A, Halawa A. Liver abscess; uncommon complication following renal transplantation: Case report with review of literatures. J Transplant Technol Res 2016,6:159-62.
2.	Wuerz T, Kane JB, Boggild AK, Krajden S, Keystone JS, Fuksa M, et al. A review of amoebic liver abscess for clinicians in a nonendemic setting. Can J Gastroenterol 2012;26:729-34.
3.	John GT. Infections after renal transplantation in India. Indian J Nephrol 2003;13:14-9. [Full text]
4.	Sucak GT, Yagoci M, Karakan T, Haznedar R. Unusual presentation of amebic liver abscess with thrombocytopenia and splenomegaly. Int J Infect Dis 2001;5:53-5.
5.	Sharma MP, Ahuja V. Amoebic liver abscess. JIACM 2003;4:107-11.
6.	Waghmare M, Shah H, Tiwari C, Khedkar K, Gandhi S. Management of liver abscess in children: Our experience. Euroasian J Hepatogastroenterol 2017;7:23-6.
7.	Cai YL, Xiong XZ, Lu J, Cheng Y, Yang C, Lin YX, et al. Percutaneous needle aspiration versus catheter drainage in the management of liver abscess: A systematic review and meta-analysis. HPB (Oxford) 2015;17:195-201.
8.	Creemers-Schild D, Genderen PJ, Visser LG, Hellemond JJ, Wismans PJ. Recurrent amoebic liver abscesses over a 16 year period: A case report. BMC Res Notes 2016;9:472-6.
9.	Catic-Djordjevic A, Velickovic-Radovanovic R, Stefanovic N, Cvetkovic T. Interactions between tacrolimus and metronidazole in a renal transplant patient. Eur J Med 2012;7:587-90.