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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2017  |  Volume : 28  |  Issue : 2  |  Page : 401-404
Eosinophilic peritonitis in a continuous ambulatory peritoneal dialysis patient: Inflammation and irritation without infection


Department of Medicine, Nephrology Section, Hamad General Hospital, Doha, Qatar

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Date of Web Publication23-Mar-2017
 

   Abstract 

A 52-year-old patient developed idiopathic eosinophilic peritonitis (EP) four weeks after starting continuous ambulatory peritoneal dialysis that resolved spontaneously without any clinical sequelae. This case is reported to emphasize the fact that EP can mimic infectious peritonitis in its mode of clinical presentation and that distinction between these two entities is important given their prognostic and therapeutic differences.

How to cite this article:
Asim M. Eosinophilic peritonitis in a continuous ambulatory peritoneal dialysis patient: Inflammation and irritation without infection. Saudi J Kidney Dis Transpl 2017;28:401-4

How to cite this URL:
Asim M. Eosinophilic peritonitis in a continuous ambulatory peritoneal dialysis patient: Inflammation and irritation without infection. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2019 Jun 24];28:401-4. Available from: http://www.sjkdt.org/text.asp?2017/28/2/401/202771

   Introduction Top


Peritonitis is one of the serious complications of continuous ambulatory peritoneal dialysis (CAPD) and contributes to approximately 16% of deaths on peritoneal dialysis (PD).[1] Most episodes of CAPD peritonitis are bacterial in origin, resulting from touch contamination with pathogenic skin bacteria or from catheter-related infections. These episodes are characterized by peritoneal leukocytosis with high percentage (>50% of total leukocytes) of neutrophils in the peritoneal fluid. A much infrequently encountered subcategory of peritonitis is eosinophilic peritonitis (EP) which is typified by the presence of >100 leukocytes/μL of PD fluid, with with eosinophils constituting >10% of the total leukocyte count in a patient with clinical signs of peritonitis.[2] This usually develops as an “allergic” response of the peritoneum to an array of mechanical or chemical deleterious stimuli during the first few weeks of initiation of CAPD.


   Case Report Top


A 52-year-old Asian male developed end-stage renal disease secondary to hypertensive nephrosclerosis. A silicone double-cuff curled PD catheter (Argyle™ PD catheter - Covidien™ USA) was inserted, and CAPD was commenced following a break-in period of two weeks using four daily exchanges of 2 L of 1.36% dextrose-containing dialysate. One month later, he presented with two days’ history of dull abdominal pain. On the day of presentation, he had noted that the effluent dialysate was hazy. There was no history of fever, vomiting, or change in bowel habits. He denied any breaks in the aseptic exchange technique, contamination, or disconnection. He did not experience catheter inflow/outflow problems or any change in ultrafiltration.

On examination, he appeared well. The body temperature was 37.2°C and blood pressure was 110/70 mm Hg. There was no skin rash. The abdomen was soft but mildly tender on deep palpation. Hernial sites were intact, and bowel sounds were normal. The exit site looked clean and healthy. Inspection of a bag of spent dialysate showed cloudy effluent but no fibrin strands. After sending the peritoneal fluid for laboratory analysis, he was started on cefazolin and ceftazidime, 1 g each intraperitoneally once daily. Abdominal X-ray demonstrated satisfactory position of the peritoneal catheter; there was no pneumoperitoneum.

Microscopic analysis of peritoneal effluent showed 1558 white cells/μL with eosinophils 80%, neutrophils 6%, lymphocytes 8%, and monocytes 6%. Peripheral blood counts revealed white blood cells (WBCs) of 10.3×103/μL, neutrophils of 55.5%, eosinophils of 27.5%, lymphocytes of 10.5%, monocytes of 4%, and basophils of 2%. Hemoglobin was 12.6 g/dL and platelets were 330×103/μL. In essence, there was a striking peripheral and peritoneal eosinophilic response. Gram’s stain as well as microscopy for fungal elements and acid-fast bacilli were negative. PD fluid and blood cultures did not reveal any bacterial growth.

The patient did not have any history of asthma, hay fever or allergies, or history of atopic disease in the family. Serum level of immunoglobulins (Ig) A, G, E, and M and PD fluid IgE levels were within the normal range. A search for secondary causes of eosinophilia was made. Fecal direct smear was negative for ova, cysts, and parasites. Cytopathologic examination of PD fluid showed a mixture of eosinophils and neutrophils in a background of scattered mesothelial cells and red blood cells, but no malignant cells. Flow cytometric analysis of peripheral blood did not demonstrate any myeloproliferative or lymphoproliferative features. Chest X-ray and ultrasound examination of abdomen were unrevealing.

CAPD was continued with no changes in its prescription. Repeated microbiological cultures of effluent dialysate did not show growth of aerobic or anaerobic bacteria. Tuberculosis polymerase chain reaction (TB PCR; Gene Xpert) carried out on PD fluid was also negative. Antibiotics were discontinued on the 4th day after confirmation of negative bacteriological cultures.

The peritoneal and systemic WBC as well as eosinophil counts continued to increase during the 1st week, but then plateaued and started to decrease during the 2nd week [Figure 1] and [Figure 2]. Peritoneal effluent dialysate cleared on day 16. Interestingly, the abdominal pain completely resolved on day 6, i.e., well before the peak eosinophilic response was observed. The patient never required analgesia and remained apyrexial throughout. Fungal and TB cultures came back negative. Scratch test and intradermal test using 1.36% dextrose-containing peritoneal dialysate were negative. During the subsequent six-month follow-up period, the patient did not have any further episodes of EP or infectious peritonitis. Furthermore, we did not notice any changes in peritoneal ultrafiltration or dialysis adequacy.
Figure 1: Cell counts in the peritoneal dialysis fluid.

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Figure 2: Cell counts in the peripheral blood.

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   Discussion Top


Our patient presented with abdominal pain associated with cloudy PD fluid and was promptly treated for presumed bacterial peritonitis as delay in the initiation of antibiotic treatment can potentially result in serious consequences of peritonitis including relapse, catheter removal, and permanent transfer to hemodialysis.[1] Although the peritoneal dialysate total WBC count suggested severe peritoneal inflammation, bacterial peritonitis was ruled out by the absence of a significant neutrophilic response and negative bacterial cultures. The constellation of clinical presentation and intense peritoneal eosinophilic reaction with eosinophils accounting for 80% of the total leukocytes in the dialysate established the diagnosis of EP. Screen for secondary causes of EP was negative; hence, a diagnosis of idiopathic EP was made.

Peritoneal cavity can mount an eosinophilic reaction to a variety of mechanical or chemical insults; a phenomenon quite similar to the production of an eosinophilic pleural effusion that develops in response to noxious stimuli.[3] Accordingly, EP is typically observed during the initial weeks of commencement of CAPD when the anatomical integrity of normal peritoneum is breached by the dialysis catheter, thereby exposing the peritoneum to a diverse array of “foreign” agents. The list of these inciting agents includes blood or air in peritoneum, dialysis apparatus (plastics or plasticizers from PD catheter or dialysate bags), dialysate (icodextrin based), or pharmacological additives (vancomycin, heparin). Our patient did not have any evidence of hemo-peritoneum or pneumoperitoneum and had not been exposed to icodextrin-based dialysate, intraperitoneal vancomycin or heparin. It must be borne in mind that peritoneal eosinophilia can also be seen during genuine infections including fungal[4] and tuberculous peritonitis.[5] Hence, these conditions were carefully ruled out by repeated microbiological cultures and other appropriate diagnostic tools. Lymphomas and parasitic infections have rarely been implicated in the development of EP but were excluded by stool evaluation, cytopathological analysis of PD fluid, and flow cytometric studies of peripheral blood.

Serum IgE concentrations have previously been reported to be high in some patients with EP.[6] However, EP appeared to be a non-IgE-mediated phenomenon in our patient as evidenced by normal levels of IgE in blood and PD fluid, lack of skin-scratch test reactivity, and absence of history of atopy. It is plausible that a foreign substance provoked a cellular immune response quite similar to that seen in non-allergic rhinitis. This offending substance could have induced eosinophil chemotaxis either directly or indirectly through desensitization of the mast cells with consequent release of eosinophilic chemotactic factors.[7] Spontaneous resolution of EP and peripheral blood eosinophilia despite continuation of PD indicated that either the exposure to the foreign substance was transitory or that the body developed a state of tolerance to persistent antigenic exposure with subsequent abrogation of the inflammatory process.

EP in our patient was a mild and self-limiting illness that resolved without any specific therapeutic intervention. Systemic steroids,[8],[9] ketotifen[10] and Montelukast,[11] have been described as successful treatments for unremitting or severely symptomatic disease.


   Conclusion Top


Advances in the development of biocompatible PD solutions, catheters, and dialysis sets as well as implementation of innovative and minimally traumatic techniques of CAPD catheter insertion have led to a decreased incidence of EP.[12] Nevertheless, one should remain cognizant of the fact that EP can mimic infectious peritonitis in its mode of clinical presentation (cloudy peritoneal effluent and/or abdominal pain) and distinction between these two entities is essential given their prognostic and therapeutic dissimilarities.

Conflict of interest:

None declared.

 
   References Top

1.
Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections recommendations: 2010 update. Perit Dial Int 2010;30:393-423.  Back to cited text no. 1
    
2.
Oh SY, Kim H, Kang JM, et al. Eosinophilic peritonitis in a patient with continuous ambulatory peritoneal dialysis (CAPD). Korean J Intern Med 2004;19:121-3.  Back to cited text no. 2
    
3.
Adelman M, Albelda SM, Gottlieb J, Haponik EF. Diagnostic utility of pleural fluid eosinophilia. Am J Med 1984;77:915-20.  Back to cited text no. 3
    
4.
Sridhar R, Thornley-Brown D, Kant KS. Peritonitis due to Aspergillus niger: Diagnostic importance of peritoneal eosinophilia. Perit Dial Int 1990;10:100-1.  Back to cited text no. 4
    
5.
Wang HH, Yang LY, Chang JW, Hung YT, Lee TY, Tang RB. Eosinophilic peritonitis: An unusual manifestation of tuberculous peritonitis in peritoneal dialysis patient. J Chin Med Assoc 2011;74:322-4.  Back to cited text no. 5
    
6.
Chan MK, Chow L, Lam SS, Jones B. Peritoneal eosinophilia in patients on continuous ambulatory peritoneal dialysis: A prospective study. Am J Kidney Dis 1988;11:180-3.  Back to cited text no. 6
    
7.
Boswell RN, Austen KF, Goetzl EJ. Intermediate molecular weight eosinophil chemotactic factors in rat peritoneal mast cells: Immunologic release, granule association, and demonstration of structural heterogeneity. J Immunol 1978;120:15-20.  Back to cited text no. 7
    
8.
Asghar R, Woodrow G, Turney JH. A case of eosinophilic peritonitis treated with oral corticosteroids. Perit Dial Int 2000;20:579-80.  Back to cited text no. 8
    
9.
Albilali AS, Rahim KA, Edrees BM, Alshaya HO. Resolution of eosinophilic peritonitis with oral prednisolone in a child receiving peritoneal dialysis. Perit Dial Int 2011;31:359-60.  Back to cited text no. 9
    
10.
Tang S, Lo CY, Lo WK, Chan TM. Resolution of eosinophilic peritonitis with ketotifen. Am J Kidney Dis 1997;30:433-6.  Back to cited text no. 10
    
11.
Forbes TA, Lunn AJ. Montelukast: A novel therapeutic option in eosinophilic peritonitis. Pediatr Nephrol 2014;29:1279-82.  Back to cited text no. 11
    
12.
Jo YI, Song JO, Park JH, Lee JH, Shin SK. Idiopathic eosinophilic peritonitis in continuous ambulatory peritoneal dialysis: Experience with percutaneous catheter placement. Nephrology (Carlton) 2007;12:437-40.  Back to cited text no. 12
    

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Correspondence Address:
Muhammad Asim
Department of Medicine, Nephrology Section, Hamad General Hospital, P. O. Box 3050, Doha
Qatar
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DOI: 10.4103/1319-2442.202771

PMID: 28352028

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    Abstract
   Introduction
   Case Report
   Discussion
   Conclusion
    References
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