Rarely seen is Retroperitoneal fibrosis (RPF), which presents with anomalous tissue that has both inflammatory and fibrous features. This oddity typically arises near the sub-renal segment of the abdominal aorta and iliac arteries causing ureter obstruction. Significantly, RPF may be associated with IgG4 disease as one its manifestations. Diagnostic imaging proves invaluable in identifying PRF cases. Glucocorticoids remain at forefront treatment either alone or combined alongside other medications while surgery comes secondary if non-surgical means prove ineffective; more recently though, minimally invasive procedures have become feasible options for therapy too.

• Retroperitoneal fibrosis ; Abdominal aorta ; Ureter obstruction ; Minimally invasive procedures

Maachi Y, Zerda I, Fouimtizi J, Slaoui A, Karmouni T, et al. (2024) Retroperitoneal Fibrosis: Review of the Literature. J Urol Res 11(2): 1149.

Retroperitoneal fibrosis (RPF) is an uncommon ailment identified by the presence of abnormal inflammatory tissue that often develops near the sub-renal area of both iliac arteries and the abdominal aorta. It typically envelops proximate structures such as inferior vena cava and ureters [1]. The condition was initially referenced in 1905 by French urologist Albarran, but it gained clinical recognition after Ormond’s two-case report in 1948 [2,3]. RPF has no known cause for about two-thirds of cases while remaining third can be linked to infections, medication, malignancy or previous surgeries on abdomen. Notably, IgG4 disease may also contribute to idiopathic RFP affliction these days according to recent reports highlighting this association claim explicitly.

This study’s objective is to examine recently published articles regarding the pathophysiology, diagnosis, and treatment of RPF.

We conducted a literature search using pertinent keywords such as retroperitoneal fibrosis, Ormond’s disease, chronic periaortitis and IgG4 disease-related retroperitoneal fibrosis from an electronic database called PubMed. The majority of references used in our research were published within the past ten years.

The differentiation between idiopathic and secondary RPF forms lacks clarity due to the uncertain causal relationship with its underlying cause. Certain factors such as surgery, radiotherapy, and drugs are viewed by some authors as potential contributing elements to these conditions [4].

The development of Secondary RPF can occur due to a variety of factors including aortic aneurysm, prior radiotherapy or surgery in the abdominal region, traumatic injury, as well as primary or metastatic retroperitoneal tumors. Infections such as tuberculosis and histoplasmosis along with certain medications like ergotamine, methyldopa,beta-blockers,methysergide,bromo criptine,and hydralazine may also lead to this condition as listed in Table 1 [5].

Table 1: Main causes of secondary retroperitoneal fibrosi

Additionally,situations that involve fibroinflammatory reactions caused by Primary retroperitoneal tumors including lymphoma and sarcoma;and Metastatic Tumors from organs like the breast and colon could be mistaken for symptoms associated with RPF itself [6]. Malignant cases are particularly serious since their estimated frequency is around 8% resulting in poor prognosis [7].

The origin of PRF’s development remains unclear, although in 1980 Parums and Mitchinson proposed that it results from an amplified inflammatory reaction to aortic atherosclerosis. This response is activated by lipids found within the plaque, including ceroids and oxidized LDL [8].

Patients diagnosed with PRF frequently display symptoms that are general in nature, alongside heightened levels of inflammatory markers and positive autoantibodies. There is also often evidence of autoimmune diseases affecting other organs within the patient’s body. Immunossupressants tend to be highly effective at treating this condition as it appears to stem from a systemic disease rather than any overly exaggerated local response simply caused by atherosclerosis alone [6-9].

According to certain studies, PIF may have originated from a primary inflammation of the aorta leading to an inflammatory response in surrounding fibrous tissue. This theory suggests that vascular inflammation might affect additional arterial sections such as gastrointestinal arteries and branches of the thoracic artery with adventitia being predominantly affected; vasa varum vasculitis could also be evident based on this hypothesis [10,11].

In recent times, several writers have proposed that there is a correlation between idiopathic RPF and IgG4 disease - an inflammatory condition affecting the systemic [12]. This has been detected in nearly half of patients previously diagnosed with idiopathic RPF (47-58%) [13,14]. Inflammatory aneurysms of the abdominal aorta also show around 50% association with this disorder [15]. Nevertheless, limited knowledge exists regarding its pathogenesis as well as the connection between non-IgG4- related and IgG4-related forms of RPF.

The condition known as IgG4-associated systemic disease or Hyper-IgG4 syndrome is a newly identified ailment that presents with one or more fibro-inflammatory organ dysfunctions, frequently accompanied by heightened serum levels of IgG4. The hallmark of this disorder involves tissue damage characterized by an inflammatory lymphocytic and plasma cell invasion leading to extensive fibrosis. In such cases, the predominant type of infiltrating cells are those expressing high amounts of IgG4 protein markers.

Several organs disorders have been   documented   and may overlap in the same individual. These ailments consist of sclerosing pancreatitis, sialadenitis, dacryoadenitis, polyadenopathy, aortitis, sclerosing cholangitis, interstitial nephritis retroperitoneal fibrosis as well as inflammatory pseudotumors. The evolution is predominantly characterized by heightened corticosensitivity levels. In 2011 two Japanese teams introduced more inclusive diagnostic guidelines for IgG4 disease [12] [Table 2].

Table 2: Diagnostic criteria for IgG4 diseases

Only 50% of FRPI cases are attributed to IgG4 disease [13,14].

Thelikelihoodofapredisposinglandscapeorgeneticinfluences has been contemplated. Examination of genetics discloses strong correlation connecting FRPI and HLA-DRB1*03, an allele related to numerous IAMs like type 1 diabetes, myasthenia gravis, and autoimmune thyroiditis [16]. Additionally variation in the CCR5 gene heightens patient susceptibility towards developing FRPI - particularly its manifestation as aneurysms [17].

Clinical

Clinical manifestations of the disease are not specific, show high variability and usually arise due to mechanical influence of PRF on neighboring structures such as abdominal pain, lumbar discomfort (observed in 80%of cases), renal colic, DVT,cases indicative testicular pain along with hydrocele. The intermittent IM claudication is also prominent. Accompanying signs like fatigue or anorexia have a higher occurrence rate indicating inflammation commonly associated with this disorder.

Typically, the initial clinical symptoms do not distinguish idiopathic PRF from secondary types. Thus, it is crucial to thoroughly examine potential instances of occupational asbestos exposure or smoking habits as well as any use of drugs that may induce fibrosis. Additionally, previous radiotherapy or surgery and signs of IgG4 disease in other body regions should be investigated systematically [12,15-18].

Biology

Upon conducting a biological examination of PRF, it is common to detect heightened inflammation-related markers that are linked with inflammatory anemia and compromised renal function. Taking note of these results is crucial as they serve as benchmarks for monitoring the progress made in treating the disease. In a significant study involving 58 patients with PRF, nearly two-thirds had increased SV and CRP levels - at 66.7% and 64.9%, respectively [20]. Depending on how severe ureteral obstruction may be, creatinine level readings can differ accordingly; whereas renal failure occurs consistently between eighty to one hundred percent instances [1].

Positive anti-nuclear antibodies (ANA) are found in 5-60% of patients [9-21], and other autoantibodies such as rheumatoid factor, anti-neutrophil cytoplasmic antibodies, anti-smooth 

muscle cell antibodies and anti-thyroid antibodies may also be present [1,9-22]. Nevertheless, the presence or onset of clinical disease manifestations associated with these autoantibodies cannot necessarily be predicted by positive antibody results [6].

An increase in serum IgG4 levels may be observed in patients who experience PRF related to IgG4 disease [13]. However, this elevation of the protein is not unique and has been found among 5% of individuals with conditions such as Churg-Strauss syndrome, eosinophilic pneumonia, and systemic Castleman’s disease [23,24].

CT SCAN / MRI

The role of imaging cannot be overstated in diagnosing PRF and differentiating between favorable benign cases and unfavorable malignant ones, as well as monitoring the evolution of the condition under therapy.

The primary radiological exam frequently conducted is ultrasound, which has limited sensitivity in detecting PRF but can quantify obstructive uropathy [25,26].

CT and MRI are the preferred diagnostic tests to differentiate between benign and malignant forms of fibrotic plaque. These examinations can reveal important information such as the morphology, location, and spread of the disease to adjacent structures [26,27]. Additionally, these exams may uncover other types of IgG4 associated diseases like chronic pericarditis with mediastinal fibrosis or autoimmune pancreatitis. The typical appearance is an irregular mass located in the region surrounding aorta that extends from RA level down towards iliac vessels while progressing into retroperitoneum enclosing ureters and IVC [22,28,29], but sparing its posterior aspect [22- 28]; however appearances vary greatly based on individual cases- sometimes presenting itself in different areas including pelvis downward extension or upward over renal hilum leading up till rare occurrences where it might even invade duodenum [30], renal hilum or kidney [31,32].

Several characteristics can aid in discerning: Malignant PRF frequently presents with anterior displacement of the aorta and inferior vena cava. One possible explanation for this is hypertrophy of lymph nodes located posterior to these vessels. However, it should be noted that although this finding has been observed, its application cannot always be universally applied due to limitations in sensitivity and specificity.

Location of the head in retroperitoneal region. Lymphomas tend to occur more towards the upper part of the retroperitoneum, while benign RPF is mostly found below the renal hilum [27]. However, it’s not unusual for benign RPF to spread cranially above the renal hilum as well. Therefore, knowing about extent of mass may not be very useful clinically either way [26].

Neighbouring organs are affected due to the presence of nodules.

The early   stages   of   benign   PRF   and   malignant   PRF may experience an increase in enhancement following the administration of contrast medium [29]. Consequently, using enhancement as a diagnostic tool to differentiate between these two conditions is not beneficial.

Assessing the size of the mass is where follow-up CT or MRI hold significant value.

PET has already become a functional imaging technique that is widely employed in the field of oncology. Moreover, its popularity continues to grow as it becomes increasingly valuable for diagnosing inflammatory conditions such as PIF with more frequent usage being reported [33-35].

One benefit is that it allows for a comprehensive evaluation of the entire body, consequently detecting additional inflammatory sites such as multifocal fibrosclerosis, PIF resulting from neoplastic or infectious causes and more [36-38].

Biopsy

If the radiological features indicate RPF, biopsy may not be necessary in all cases. Nevertheless, if there are diagnostic uncertainties or a potential malignancy is suspected, or initial treatment fails to show improvement, undergoing a biopsy becomes crucial for confirming the diagnosis. This procedure can either be carried out surgically or under imaging control [1-39].

Treatment

There are multiple therapeutic objectives

Treat obstructive complications such as unilateral and/or bilateral hydronephrosis.// Reduce inflammatory syndrome// Limit fibrosis progression.// Prevent recurrence.// Treatment for medical ailments.

Medical treatment

The management of idiopathic PRF is currently based on the modes of treatment for autoimmune or inflammatory conditions, without a concrete scientific basis.

Follow-up may only be necessary for asymptomatic patients with no effects on neighboring structures, as anecdotal instances of natural healing have been documented [40].

The primary treatment for symptomatic patients is corticosteroid therapy, yet there is no agreement regarding the dosage (0.5-1 mg/kg/day) or length of time it should be administered.

The prevailing procedures found in literature are: The dosage started at 60 mg per day for a duration of two months (1D/2). It was then slowly decreased over the course of two more months until it reached a daily intake amounting to only 5 mg. This dose level was maintained throughout the following two years [41]. totaling an overall time span that added up to forty- one months in total.

The suggested dosage is 40-60 mg per day for a period of six weeks, followed by a gradual decrease to 5-10 mg over the course of two to three months. This treatment plan lasts from six to twelve months [39].

The prescription is for a maximum of 80 mg per day, to be taken over the course of four weeks. After that initial period, the dosage should gradually decrease until it reaches 10 mg per day within two or three months. The total treatment duration spans between twelve and eighteen months.

In conclusion, the authors found that corticosteroids are an effective induction treatment option as they quickly improve clinical symptoms, biological parameters and occasionally radiological images. Nonetheless, compared to tamoxifen, long- term use of corticosteroids is linked with a higher risk of adverse effects.Due to its anti-fibrosing abilities, Tamoxifen can serve as a substitute for corticosteroids without the need for high doses of cortisone. However, only one trial has compared prednisone and tamoxifen in terms of their ability to prevent recurrence. The findings revealed that when facing recurrences, tamoxifen proved less effective than prednisone [42].

Numerous alternatives to cortisone have been explored, such as mycophenolate mofetil, cyclophosphamide and azathioprine [43-45]. Combining prednisone with mycophenolate mofetil or azathioprine has proven effective. However, the side effects from the biggest study involving combining cyclophosphamide and steroids are deemed unacceptable.

While different immunosuppressive drugs have demonstrated successful treatment of PRF [45,46], their effectiveness in relapsed patients has not been extensively researched. A recent study found that a combination therapy using methotrexate and prednisone effectively treated recurrent cases by inducing remission while minimizing negative side effects on renal function or inflammatory markers. However, it is crucial to monitor these individuals closely as they may be susceptible to future relapses after cessation of treatment. In addition, biotherapies are becoming increasingly popular for tackling stubborn PRF conditions.

Surgical treatment

During the acute phase, drug therapy is necessary along with double-J catheter debulking or percutaneous nephrostomy if there is dilation in the urinary excretory tract. The most prevalent drainage method is utilizing indwelling ureteral stents which are typically removed after three months of treatment.

If drug treatment successfully stabilizes the disease but overt urinary obstruction remains, surgery may be recommended. This procedure includes performing ureterolysis alongside deep biopsies of the plaque to protect and reposition the ureters with intraperitonealization or utilizing an epiploic or peritoneal flap. All these steps are critical for restoring renal function as well [1,46-48].

The surgical procedure can be conducted in two ways - open or laparoscopic, and with or without robotic aid. Minimally invasive methods have parallel rates of complications as the conventional surgery but are equally efficient. Furthermore, they offer a quicker recovery period and lessen the need for postoperative painkillers and blood transfusion compared to traditional techniques [49,50].

Despite their potential benefits, surgical procedures carry a notable risk for complications such as ureteral wounds, devascularization and strictures, urinary fistula formation, recurrent fibrosis and thromboembolic issues [26].

PRF is a disease that occurs infrequently and often without an identifiable cause. There isn’t a standardized diagnostic method, but performing biopsies indiscriminately seems impractical if clinical or paraclinical guidance is absent. Despite there being no agreement among medical professionals on how to treat the disease, corticosteroids used alongside urinary drainage are typically prescribed for patients who have excretory tract dilation as their primary symptom. Certain immunosuppressive medications also demonstrate positive outcomes as alternatives to cortisone due to its sparing effects

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