Ultrafiltration Management in Peritoneal Dialysis

Peritoneal Dialysis International, Vol. 20, Suppl. 4

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Copyright © 2000 International Society for Peritoneal Dialysis

Encapsulating Peritoneal Sclerosis: Definition,

Etiology, Diagnosis, and Treatment

Yoshindo Kawaguchi, Hideki Kawanishi, Salim Mujais,

Nicholas Topley, and Dimitrios G. Oreopoulos

For the International Society for Peritoneal Dialysis Ad Hoc Committee on

Ultrafiltration Management in Peritoneal Dialysis

The utilization of the peritoneal cavity for dialysis creates the opportunity for alterations in the function and structure of the peritoneal membrane. The peritoneal membrane has proven, however, to be a remarkably resilient organ. Indeed, several studies have documented the functional stability of the membrane in short and midterm evaluations (1_5). One is reminded of the spectacular observations in a small number of patients examined at autopsy who had minimal structural changes despite recurrent infectious complications (6). These isolated observations illustrate the fact that the response of the peritoneal membrane to potentially modifying factors can be diverse, and generalizations on both the immunity to change or the proclivity to widespread change err in their extremism. Further, despite notable attempts at various time points in the history of peritoneal dialysis (PD) to examine the peritoneum of patients on PD (6_12), the scope of changes and the natural history of the peritoneal membrane during dialysis have not been fully elucidated. This is clearly due to the limitation of clinical material to examine and the possibly biased nature of samples that are examined. Further, the techniques of morphologic analysis have been gradually maturing; the targets of examination have also evolved.

One structural modification of the peritoneum that has caused significant concern over the fate of dialysis patients is what has been labeled sclerosing encapsulating peritonitis. This entity is not unique to dialysis patients, it occurs in a variety of other clinical conditions discussed below. The multiplicity of suspected etiologies and the confusion over its pathophysiology are reflected in the variety of terms that have been used indiscriminately and interchangeably to describe this complication, such as peritoneal fibrosis, peritoneal sclerosis, sclerotic thickening of the peritoneal membrane, sclerotic obstructive peritonitis, calcific peritonitis, abdominal cocoon, and sclerosing peritonitis (13_34). The most common term used in the nephrology literature in recent years has been sclerosing encapsulating peritonitis, but the popularity of the term does not necessarily validate its continued use, as it is marred by its morphologic inaccuracy, particularly in its reference to an inflammatory component that is frequently absent in the developed syndrome (peritonitis). A more accurate description would be encapsulating peritoneal sclerosis (EPS), which is more descriptive of the morphologic changes.

Incidence

There is no satisfactory estimate of the comparative incidence of dialysis-related and non dialysis-related EPS. The best limited survey comes from a survey of 18 surgical centers in France that encountered 32 operated cases during a 16-year observation period (35). The results of this survey are shown in Table 1.

It is clear from these data that, from a surgical perspective, EPS is rare and that non dialysis-related causes exceed those resulting from dialysis. These results, however, cannot be generalized because they reflect only operable cases and may be subject to the confounding variables of differing medical practice. Another report from France also highlights the preponderance of non dialysis-related etiologies, with intraperitoneal chemotherapy contributing as many cases as PD (16).
TABLE 1
Comparative Incidence of Encapsulating
Peritoneal Sclerosis by Etiology
EtiologyNumberPercentage
Idiopathic515.6
Post surgical1959.4
Beta blockers412.5
Cirrhosis with ascites412.5
Generalized peritonitis39.4
Peritoneal dialysis

39.4
Total casesa32100
a Some patients had more than one etiology.

Two types of reports on the incidence of severe sclerosing peritonitis related to PD have been published. While the literature is replete with single-case studies and small series descriptions from high-risk patients exposed to acetate or chlorhexidine, a few more recent single-center experiences are useful to examine. The results from these are summarized in Table 2. The highest frequencies are observed in the Japanese reports, with very low frequencies in the U.S.A., Canada, and Europe. Of note is that the single-center frequencies in Japan are higher than the national frequencies from that country (see below).

Another type of report based on large national or multinational samples offers similar estimates. A study of the Registry of the European Dialysis and Transplant Association, conducted in 1985 at a time when acetate use and chlorhexidine use were still common, reported on 214 cases from 112 centers in 19 countries (42). They estimated a frequency range from a low of 0.3 per 1000 in Spain to a high of 3.1 per 1000 in Belgium (42). Two recent reports have the benefit of very large sample sizes with few or no patients having been exposed to acetate dialysis solution or lavage fluid. Rigby and Hawley (43) reported 54 cases of sclerosing peritonitis in 7374 Australian patients treated with PD over the years 1978 to 1994. This is an overall prevalence of 0.7%. The prevalence of confirmed EPS was 0.6%. Prevalence of sclerosing peritonitis, but not necessarily EPS, was 1.9, 6.4, 10.8, and 19.4% for patients on PD for longer than 2 years, 5, 6, and 8 years, respectively. Presumably, most of this was EPS, as EPS was diagnosed in 87% of all cases, and small bowel obstruction in 92% of all cases of sclerosing peritonitis. Yearly incidence rates for Australia were 1.9 per 1000 PD periods from 1980 to 1989, and 4.2 per 100 PD periods for 1990 to 1994. In a report by the Japanese Sclerosing Encapsulating Peritonitis Study Group, Nomoto et al. (44) reported 62 cases of EPS in 6923 patients treated between 1980 and 1994 (0.9%). In a recent re-evaluation of this frequency in a survey of 35 centers in Japan, 106 cases were identified in 3760 patients (2.8%) (H. Kawanishi et al., personal communication).

This is not a widespread syndrome in dialysis patients, but it is extremely serious when it does occur.

Etiology

A variety of etiologies are involved, with some overlap between the dialysis-related and non dialysis-related causes or suspected causes (Table 3). There are a number of agents or factors that contribute to or predispose the patient to the development of EPS; in fact, EPS is commonly referred to as being "multifactorial." For our purpose, the contributing factors can be divided into those that are related to PD and those that are not. A common thread among all causative factors and conditions, however, is that they all disrupt normal peritoneal membrane physiology. It is this disruption that starts a series of events that may eventually lead to the development of EPS. It should be pointed out that not all patients with these conditions develop EPS. There must therefore be some factor that prevents the majority of patients from proceeding to EPS, and something that makes a small minority more susceptible, even if they have been exposed to only one of the predisposing conditions.

The etiologies of EPS secondary to PD include severe and/or nonresolving peritonitis, especially that due to Staphylococcus aureus, fungi, and Pseudomonas sp, and especially in the long-term patient. Increased duration of PD has been assumed by some to be a risk factor for EPS, but the first reported correlation between increased time on dialysis and increased risk for EPS comes from the Australian study. According to Rigby, the prevalence of EPS increased from 1.9% at longer than 2 years, to 19.4% at longer than 8 years on PD. Whether the latter prevalence is reflected in the cause of death of patients on long-term PD remains to be shown. Some practices, mostly now discontinued, have been associated with EPS in the past, including acetate-buffered PD solutions, certain b-blocking agents, the use of in-line bacterial filters, and exposure to certain antiseptics or disinfectants. Of all of the above factors, the most convincing is the use of chlorhexidine as a spray disinfectant for PD connectors and severe/nonresolving peritonitis.

TABLE 2
Prevalence of Encapsulating Peritoneal Sclerosis: Single-Center Studies
Country (Ref.)Observation period (years)CasesPeritoneal dialysis patients (N)Frequency (%)
Netherlands (23)16104072.45
Japan (36)1471973.7
Japan (37)1492034.4
Canada (38)20712880.54
Germany (39)1001040
U.S.A. (40)1031881.6
U.S.A. (41)1124240.47

TABLE 3
Factors Implicated in the Etiology of Encapsulating Peritoneal Sclerosis
Unrelated to peritoneal dialysis (PD)
Primary
Idiopathic or unknown etiology (45_54)
Secondary
b-blockers (17,34,55_80)
Autoimmune disease (Lupus, etc.) (81_83)
Peritoneal sarcoidosis (34,56_75,79_81,84,85)
Peritoneovenous shunt (86)
Ventriculoperitoneal shunt (87_89)
Diseases of reproductive organs
Luteinized thecoma of the ovary (90_93)
Other ovarian disease (94)
Endometriosis (95_101)
Peritoneal and intra-abdominal malignancies (102)
Gastrointestinal diseases (14,15,18,29,35,103_127)
Intraperitoneal chemotherapy (16,128_134)
Other chemicals (69,130,135_138)
Particulate matter
Talc (139_141)
Exposure to asbestos (119,124,126,141_147)
and silicosis (148)
Familial Mediterranean fever (142)
Abdominal surgery (35)
Intra-abdominal infections (tuberculous) (101,149,150)
Peritoneal lavage using certain disinfectants (17,77,151_154)
Miscellaneous
Hemodialysis (155)
Related to PD
Duration of PDa
Peritonitisa (6,156_162)
Acetate dialysis solutiona (17,77,163,164)
Chlorhexidineb (42,153,154,165_167)
Plasticizersc (24,136,168_171)
Glucose/hypertonic solutiona (157,172_174)
a Association only.
b Based on epidemiological study and supported with animal models.
c Speculated.

There is a possibility that some people are genetically predisposed to sclerosing syndromes when exposed to one or more of the etiologic agents. For example, the incidence of EPS after more than 8 years on PD was 19.4%; more than 80% of these long-term patients were free of clinical signs or symptoms of sclerosing syndromes.

Diagnosis

In the diagnostic approach to ESP, four aspects need to be evaluated: (1) the clinical diagnosis, (2) the radiologic diagnosis, (3) the pathologic diagnosis, and (4) predictive tests.

Clinical Diagnosis: The starting point of clinical diagnosis is the determination of whether clinical symptomatology of the disease is indicative of definite underlying pathology. The symptoms related to EPS are based on interference of the pathologic process in intestinal function and peritoneal integrity. The encapsulating process is responsible for the disturbances in intestinal function that are manifested primarily as disorders of motility with resultant impairment of reabsorptive functions. The encapsulation results in reduced to absent motility, which manifests clinically as an obstructive ileus. Clinically, it is difficult to distinguish the obstructive ileus of EPS from that resulting from other causes of disturbances of intestinal motility on presentation, and elimination of other causes (adhesions, infections, other intra-abdominal pathology, etc.) is required. This caveat stems from the similarity that can occur between the clinical manifestations of different disease processes interfering with a common final pathway: intestinal motility. The presenting signs and symptoms of EPS are often vague and nonlocalizing. Nausea, vomiting, fullness, absent bowel sounds, abdominal pain, abdominal or pelvic mass, and other clinical aspects may be observed in a variety of conditions. Similarly, the anorexia and weight loss observed with EPS are the result of the disturbed intestinal motility, and any cause of the latter can result in a similar clinical picture. What may be a distinguishing feature of EPS, however, is the insidious nature and chronicity of the developing clinical syndrome. Other causes of alterations in intestinal motility and its consequences may tend to have more acute manifestations.

It should also be remembered that a few of the conditions with overlapping clinical symptoms could coexist. There are reports of independent abdominal pathologies occurring in conjunction with EPS (175). Additional caveats are in order: the presentation of the disease need not be uniform and the extent of symptomatology and pathology need not be correlated. Occurrence of signs and symptoms of disturbed intestinal motility may result not only from the rigid entrapment of the intestines by the encapsulating process, but also by involvement and destruction of the myenteric plexus by the fibrotic changes (17,176). In this case the disturbed motility is secondary to denervation.

Another aspect of the clinical profile of EPS is the not uncommon presentation as a recurring or nonresolving peritonitis (38). Patients with EPS may be first suspected of having the syndrome because of nonresolving peritonitis or symptoms suggestive of an indolent peritonitis in the absence of positive cultures. These patients may be subjected to procedures of catheter removal and the detection of EPS may be coincidental. The relationship between peritonitis and EPS is likely complex. Recurrent infections have been suspected of contributing to the development of peritoneal injury that may progress to EPS, and the development of EPS may be associated with greater predisposition to peritonitis. The latter aspects remain speculative but may explain the clinical observations related above. The recurrent or persistent bloody effluent that is occasionally observed in EPS may suggest neoangiogenesis or may be related to the process of adhesion formation. Bloody effluent, however, is not pathognomonic of either EPS or angiogenesis.

Alterations in peritoneal transport functions have been debated. Reference has been made to the occurrence of ultrafiltration failure and reduced small solute clearance as distinctive signs of EPS (37,38,44). While it is true that such disturbances do occur, formal transport evaluations in patients with EPS have shown a diverse picture. Progressive loss of fluid removal capacity is found in many patients. Its absence, however, should not discount the diagnosis, and the presence of declining ultrafiltration capacity cannot on its own be used as a diagnostic criterion for EPS because of the multiple causality of ultrafiltration failure (see "Evaluation and Management of Ultrafiltration Problems in Peritoneal Dialysis," the first article in this supplement). In contrast to the frequency of declining ultrafiltration capacity, other measurements of peritoneal transport (glucose, creatinine, etc.) do not show a uniform pattern (2,177,178). All variants of glucose and creatinine transport have been described with EPS.

It is important not to underestimate the value of clinical acumen in the detection of EPS. A high index of suspicion is required for the early diagnosis of the condition, early diagnosis may influence eventual outcome. This high index of suspicion, however, has to be coupled with rigor in pursuing a documented diagnosis. This can be achieved by coupling clinical presentation with radiologic and pathologic confirmation. The use of other laboratory tests in confirming the diagnosis of EPS still requires further scrutiny. Tests for anemia and high C-reactive protein levels have been suggested as adjunct tests (44). It should be remembered that more-common clinical conditions can alter these tests and they should be considered as minor criteria for the diagnosis and be properly weighted.

Radiologic Diagnosis (23,179_188): The elements in the radiologic diagnosis that are pertinent to confirmation of the diagnosis of EPS include verification of peritoneal thickening and encapsulation, identification of intestinal obstruction, recognition of cocooning, and detection of calcification. The presence of these findings in an individual patient can be variable, as is the suitability of various radiologic techniques; some are more reliable in detecting some of these changes than are others. Ultrasonography (183) and computerized tomography are the most widely used methods. They play a significant role in confirming a suspected diagnosis and, in some cases, the constellation of clinical profile and radiologic findings may be sufficient for diagnosis confirmation. The managing physician should remain alert to the possibility of false-negative and false-positive tests. Whether these tests can be used in screening programs has not been established and, considering the rarity of the condition and the high cost of the tests, indiscriminate screening is not likely to be beneficial. In the presence of clinical suspicion, however, the contribution of radiologic exploration may be rewarding (184). Typical or suggestive findings for each of the tests are listed in Table 4, and relative roles of each have been examined in a few small series (181,183).

Water-soluble contrast media studies of the small bowel are characteristic, showing varying lengths of intestine tightly enclosed in a "cocoon" of thickened peritoneum, proximal small bowel dilatation, and an increased transit time. Computed tomography scans demonstrate peritoneal thickening and can reveal loculated ascites, adherent bowel loops, and bowel luminal narrowing. Ultrasound demonstrates a characteristic trilaminar appearance, but requires peritoneal fluid in situ. Additional abnormalities seen on ultrasound comprise increased small bowel peristalsis, tethering of the bowel to the posterior abdominal wall, intraperitoneal echogenic strands, and, in the late stages of the disease, membrane formation. Optimal visualization of these features requires that dialysis fluid be present in the abdomen.

Pathologic Diagnosis: The data available on structural changes (7,9,12,15_17,20,23,31,35,38,44,156, 186,189_192) suggest massive alterations in the morphology of the peritoneal membrane. Although precise definitions are not currently available, a common feature appears to be complete loss of mesothelium accompanied by gross interstitial thickening within the membrane. This thickened interstitium can be cellular (presumably activated fibroblasts) or acellular in nature (presumably interstitial collagen deposition). Inflammatory cells are variably present although ongoing leukocyte infiltration is not necessarily a characteristic hallmark of the condition. Any blood vessels present have abnormal morphology, but this may be a reflection of changes seen during PD per se rather than related specifically to the development of EPS.

TABLE 4
Radiologic Findings in Encapsulating Peritoneal Sclerosis
TestFindings
Plain abdominal filmDilated small bowel loops
Air fluid levels
Peritoneal calcifications
Contrast studiesBowel motility disturbances
Separated rigid dilated bowel loops
Varying degrees of obstruction accompanied by hypermotility
UltrasoundDilated fixed loops matted together and tethered posteriorly
Intraperitoneal echogenic strands
Echogenic "sandwich appearance" membrane
Computed tomographyVariable diameter of bowel segments
Adherent dilated bowel loops
Air fluid level
Loculated ascites
Thickening intestinal wall and peritoneal membrane
Increased density of mesenteric fat
Entrapped fluid collections

Predictive Testing: The diagnosis of true EPS relies on clinical findings, radiologic tests, and tissue samples obtained during attempted corrective surgery. While many of the described radiologic features of EPS are helpful in the diagnosis of established cases, there are no studies examining these tools in predictive testing. Most studies evaluating the values of different radiologic techniques have been done on patients already diagnosed with EPS. Radiologic screening to detect sclerosing peritonitis early in high-risk patients requires further study. Effluent studies have yet to prove their value and there are no reproducible and reliable tests to identify patients at high risk of developing this complication.

Treatment

A variety of treatments have been used in EPS (Table 5). Considering the sporadic nature and low frequency of the disease, these treatments have been limited to case reports or small series. None of the clinically applied treatments was universally successful, and purported success has been countered by reported failures. In view of the "drawer syndrome" (failed therapies are not reported but filed in investigators' drawers), it can be stated with confidence that no uniformly successful therapy for EPS exists at this time. Even withdrawal from PD may not be considered therapeutic, but is likely done for presumed removal of pathogenic factors, although there is reason to believe that leaving the peritoneum "dry" may indeed exacerbate the condition.

A major limitation to the success of therapy is delayed diagnosis; a heightened index of suspicion is important for early intervention. The presence of a constellation of clinical findings suspicious for the condition should elicit a noninvasive radiologic work-up as an initial screen. The application of regular screening has not been tested because of the lack of predictive identifiers of high-risk groups.

There is no agreement in the literature on whether the treatment of choice is surgical (including complete release of the small bowel from the inflammatory process) or conservative therapy, consisting of steroids and/or immunosuppressive drugs with or without total parenteral nutrition (TPN) and possibly discontinuation of continuous ambulatory PD (CAPD) with subsequent transfer to hemodialysis (35,38,43,46,67,165,166,189,190,193_200). It is well accepted that TPN, sometimes for a prolonged period of time (194), forms an integral part of both conservative approach and surgical intervention, as good results have been reported for sclerosing peritonitis patients on TPN.

TABLE 5
Therapeutic Approaches in Encapsulating Peritoneal Sclerosis
TherapyType of evidence
CorticosteroidsCase reports
TransplantationCase reports
Immunosuppressive therapy
+ transplantation
Small series
PhosphatidylcholineCase reports
Peritoneal restCase reports
Long-term home parenteral
hyperalimentation
Case reports
Antifibrotic agentAnimal model
Surgical viscerolysisSmall series

Although there are isolated reports of successful outcomes after surgical intervention, especially in patients in whom the peritoneal cocoon is related to severe peritonitis, the prognosis after surgery is usually poor (35,38,50,67,189,190,193,195,196,200). Surgical attempts to free the small bowel from the constricting fibrous tissue are hazardous unless one can find a clear plane of cleavage between the membrane and the small bowel. An alternative approach is to make multiple releasing incisions in the thickened membrane to free the underlying bowel. Surgery under these circumstances is difficult, with many postoperative complications and a high mortality. Complications after surgical intervention include persistent recurrent intestinal obstruction, malnutrition, formation of fistulas, intraperitoneal abscesses, sepsis, and death.

Conservative Approaches: In the absence of small bowel obstruction, EPS may improve and become asymptomatic following the removal of the peritoneal catheter and cessation of CAPD. It has been shown that even extensive new membrane formation may disappear without surgical intervention (38,43,44, 189).

The basic strategy for the conservative treatment of EPS is cessation of CAPD (23,44,197), transfer to hemodialysis, and sustained rest of the bowel with TPN administration (44,201). However, cessation of CAPD does not always halt or reverse the progression of peritoneal fibrosis, except perhaps at an early stage (17). With the cessation of CAPD, the lack of free fluid between the bowel loops brings the bowel surfaces closer together and may hasten adhesion formation and the onset of intestinal obstruction. Under these conditions, EPS may even be accelerated after discontinuation of CAPD (36,76,155,156). Furthermore, dialysis may act to continuously remove fibrin, thus preventing further deposition and organization. Despite these risks, if the diagnosis has been made at the stage of irreversible intraperitoneal damage, discontinuation of CAPD and a switch to hemodialysis seems to be the only option. Patients with a constellation of symptoms and signs suggestive of EPS (severe ultrafiltration failure, calcified peritoneum, or persistent bloody effluent or intractable peritonitis) should be evaluated promptly, and if the diagnosis is confirmed, management initiated.

Immunosuppressive in EPS: Administration of immunosuppressive agents, alone or in combination with adhesion lysis, has been beneficial in the treatment of some patients with EPS, especially in the absence of peritoneal inflammation, although not universally confirmed (38,43,46,114,166,197_199, 201). Immunosuppressive therapy has been associated with prolonged survival in patients suffering from EPS (201) by slowing its progression and thus enhancing the chances of remission. Immunosuppressive therapy (prednisone 30 _ 50 mg, azathioprine 100 _ 125 mg), alone or in association with a renal transplant, may lead to prolonged remission and/or survival in EPS patients (15,23,38,43,46,166,193, 197_199,201).

Bhandari et al. (198) have suggested that preoperative immunosuppression in CAPD-related sclerosing peritonitis improves patient outcomes and should be considered as initial treatment with a view to subsequent surgery. Although in most reports patients had combination therapy with steroids and cytotoxic agents, Mori et al. (197) have successfully treated a sclerosing peritonitis patient with steroid therapy alone. More recently, anecdotal evidence of the successful use of tamoxifen in one case of EPS has been reported (202). Further exploration of this versatile agent may be warranted.

Prognosis/Outcome: Once symptoms of EPS have appeared and the diagnosis has been made, mortality is extremely high and varies between 20% and 93% (38,43,44). Death occurs in more than 60% of patients within 4 months of diagnosis, almost invariably due to illness related to bowel obstruction or complications of surgery.

Prevention

Our lack of understanding of the processes that lead to the development of EPS severely limit our ability to prevent its occurrence. In a situation where patients are receiving PD therapy for longer periods, the only way to understand how to prevent EPS is to better understand those factors important to its etiology. At this time, prevention may be unrealistic and we must identify which of the treatment regimes will be most effective and apply them at the earliest possible stages. Identification of early signs of EPS is a major goal, as earlier intervention, surgically or with immunosuppressive therapy, is theoretically more effective.

Summary

Current definitions of encapsulating peritoneal sclerosis are practical and clinically relevant. It is important to adhere to a more uniform use of the proper terminology, and it is the recommendation of the authors that EPS be adopted as the more appropriate term. The best literal definition of EPS is based on clinical_pathologic criteria. Differentiation of EPS from the general category of ultrafiltration failure is required. Further, better appreciation of the diverse pathways that can lead to the same final common clinical_pathologic picture should not be overshadowed by the requirement of uniform terminology.

Incidence and prevalence of the syndrome have been defined in some large populations and a few single-center experiences. The former show an incidence of less than 1%, while higher percentages are reported in the latter. The reported increased incidence with duration on therapy requires validation. The epidemiology of the syndrome offers limited insight into its pathogenesis.

A list of factors, both dialysis-related and non dialysis-related, has been accumulated. Except in a few categories where agents are clearly related to the development of EPS, the majority of the listed factors for dialysis-related EPS remain, at best, associations and at worst, simple conjecture.

The same limitations that plague the issue of etiology apply in the area of pathogenesis. More basic, focused work is required.

The diagnosis of EPS remains based on clinical suspicion confirmed with, primarily, radiologic findings. Pathologic confirmation is obtained in cases that come to surgery for management or for catheter removal. Radiologic studies are precise enough for confirmation, but none have been evaluated for early diagnosis for possible early intervention or prevention. Studies based on transport characteristics or effluent dialysate constituents are not useful for EPS. At present, there are no reliable predictive tests for EPS that can be used in individual patients.

Therapy of EPS is based on anecdotal evidence. The possible variable etiologies and probable distinct pathways leading to the syndrome may make a uniform therapeutic approach unlikely. Further, the limited number of cases and the sporadic pattern of occurrences make therapeutic trials not readily feasible. This is distinct from the case of ultrafiltration failure, where significant advances in mechanism elucidation and rationale-based interventions have been made.
Correspondence to: Y. Kawaguchi, Kangawa Prefectural Hospital, 1-6-5 Shiomidai, Isogo-ku, Yokohama, Kanagawa 235-0022 Japan.

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