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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 2  |  Issue : 4  |  Page : 80-85

Extrapulmonary inflammatory myofibroblastic tumor at different sites with histopathology and immunohistochemical analysis: A case series


1 Department of Pathology, Oncquest Laboratories, New Delhi, India
2 Department of Pathology, Ruby Hall Clinic, Pune, Maharashtra, India

Date of Web Publication26-Dec-2018

Correspondence Address:
Dr. Swati Saxena
Department of Pathology, Oncquest Laboratories, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/oji.oji_38_18

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  Abstract 


Background: Inflammatory myofibroblastic tumor (IMT) is a rare entity and has wide anatomical sites of origin. Because of overlapping clinical and radiological features, histopathology study followed by immunohistochemistry (IHC) analysis is necessary for confirmation of the diagnosis. Aim of the Study: This study aimed to present the demographic, histopathological, and IHC analysis of patients diagnosed with extrapulmonary IMT. Materials and Methods: Patients diagnosed with extrapulmonary IMT were analyzed from January 2017 to July 2018. Results: A total of six cases were included in our series, with the mean age of presentation being 37 years. Male-to-female ratio was 1:2. The primary site of origin was distributed as follows: two cases of face and neck (one mandible and one naso-orbital), three cases of abdominal location (one spleen, one periaortic node, and one paraaortic node), and one case of cervix. There was no local invasion or metastasis found. Microscopically, all the cases revealed a common pattern of finding of the presence of intersecting fascicles of spindle cells with intervening collagenous to myxoid matrix along with infiltration of plasma cells and aggregates of lymphocytes. There were no atypical cells or mitosis in all the cases. All six cases were smooth muscle actin and vimentin positive and S100, desmin, and cytokeratin negative on IHC study. All the cases were anaplastic lymphoma kinase (ALK) negative, except one case with cervical primary where it was positive for ALK-1. Conclusion: Extrapulmonary IMT is a rare entity with diagnosis by exclusion on histopathological examination, and IHC should be done for confirmation of the diagnosis as well as ALK expression status.

Keywords: Extrapulmonary, histopathology, immunohistochemical examination, inflammatory myofibroblastic tumor


How to cite this article:
Saxena S, Dhal I, Mohanpuria A, Garg J, Karnik S, Khedkar B. Extrapulmonary inflammatory myofibroblastic tumor at different sites with histopathology and immunohistochemical analysis: A case series. Oncol J India 2018;2:80-5

How to cite this URL:
Saxena S, Dhal I, Mohanpuria A, Garg J, Karnik S, Khedkar B. Extrapulmonary inflammatory myofibroblastic tumor at different sites with histopathology and immunohistochemical analysis: A case series. Oncol J India [serial online] 2018 [cited 2019 May 19];2:80-5. Available from: http://www.ojionline.org/text.asp?2018/2/4/80/248534




  Introduction Top


Inflammatory myofibroblastic tumor (IMT) is a rare heterogeneous group of tumor and comprises differentiated myofibroblastic spindle cells with various inflammatory cell infiltrates in a myxoid stromal background.[1] IMT can originate in different anatomical sites, with the lung being the most common site, followed by other extrapulmonary sites such as head and neck, spinal meninges, digestive system, heart, soft tissues, mesothelial membranes, bladder, lymph nodes, liver, spleen, and female genital tract.[2],[3],[4],[5],[6]

The etiopathology of IMT is not clear, and the biologic behavior of IMT either as reactive lesion or true neoplasm is doubtful. However, IMT can undergo a rare malignant transformation with occasional distant metastasis.[1] Because of the various doubtful histologic appearances, immunohistochemistry (IHC) should be performed to confirm the diagnosis.[2] IMT should be ruled out from other infectious, granulomatous, autoimmune, and malignant lesions on the basis of histopathologic and IHC analysis. Based on the pattern of recurrence, location, extent and behavior of the tumor, steroid therapy, surgical excision, and radiotherapy alone or in combination are the treatment modalities.[7],[8]

In the present case series, we have tried to focus on the demography and the pathological details (including IHC) of extrapulmonary IMT with the intention to understand the biological behavior of this rare entity.


  Materials and Methods Top


The study was conducted in the department of pathology of a tertiary care center from January 2017 to July 2018. Patients with IHC-confirmed extrapulmonary IMT were included in the study. Demographic, histopathology, and IHC profiles were analyzed. Age, sex, and primary site of origin for the tumor were the parameters taken for the patient's demographic profile. Specimens received at histopathological department were routinely grossed, processed, and stained with hematoxylin and eosin stains, and IHC panel was run. The IHC panel included smooth muscle actin (SMA), vimentin, desmin, cytokeratin (CK), S100, and anaplastic lymphoma kinase 1 (ALK1) markers as common for all the six cases along with few other markers as per the requirement. The histopathological diagnosis was compared with the final IHC confirmation for the cases, and the different histopathological differential diagnoses were discussed. The data were collected and recorded in the structured pro forma. The patients of IMT diagnosis with primary pulmonary were excluded from the study.


  Results Top


A total of six cases of IHC-confirmed extra-pulmonary IMT were included during the study period. The age at presentation in our series ranged between 22 and 57 years. 50% of patients presented at the age group of 30–39 years, with the mean age group of presentation being 37 years. Female patients were affected more as compared to males, with the male-to-female ratio of 1:2. The primary site of origin were two cases for face and neck (one mandible and one naso-orbital), three cases at abdominal location (one spleen, one periaortic, and one paraaortic), and one case of cervix. After radiological investigations, all the six cases in our series had no distant metastasis.

Preoperative biopsy was performed for the three cases, i.e., cases with head and neck primaries and cervix primary (punch biopsy: mandibular primary, incisional biopsy: naso-orbital primary, and punch biopsy for cervix primary). Histopathological features revealed possible diagnosis of benign spindle cell tumor with the presence of inflammatory cells in the head and neck primaries and the possibility of leiomyoma, IMT, or fibroma in case of cervix IMT.

For splenic IMT, contrast-enhanced computed tomography (CECT) scan of the abdomen was done, showing a nonenhancing hypodense mass at central portion of the spleen without any calcification or the presence of locoregional extension and suspected as possibility of hamartoma. As per the record, chest X-ray and ultrasonography of the abdomen were done as metastatic workup for two head and neck primaries, splenic primary, and cervix primary. Instead of benign-looking features of both lymph node primaries on ultrasonography, CECT scan of the thorax and whole abdomen was done to rule out the presence of other regional or distant nodes or any other possible lesions. In periaortic IMT, CECT scan revealed a well-defined periaortic lymphadenopathy of size around 2.5 cm × 3 cm with the absence of any other significant lymph nodes. In paraaortic IMT, CECT scan revealed a well-defined paraaortic lymphadenopathy of size around 3.5 cm × 3.8 cm long with few small periportal, periaortic, aortocaval, and perihilar lymph nodes. The possibility of tuberculosis or low-grade malignancy was suspected for both the cases.

Three cases with preoperative pathological diagnosis of benign tumor underwent surgery. Two nodal IMT cases underwent excisional biopsy for pathological diagnosis. Splenic IMT underwent splenectomy for both treatment and pathological diagnosis. The types of surgery for the cases are highlighted in [Table 1].
Table 1: Demographic characteristics, surgical procedure, and histopathological result

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Gross examination of the operated specimen for the six cases of IMT was mentioned.

Mandibular IMT

Hemimandibulectomy specimen showed a irregular, gray-white infiltrative tumor of size approximately 4 cm × 3 cm along the alveolar arch of mandible [Figure 1]a and [Figure 1]b.
Figure 1: Gross picture showing (a) left hemimandibulectomy specimen with a relatively well-circumscribed, gray-white tumor of size around 4 cm × 3 cm along the lower alveolar arch and (b) the cut surface showing a gray-white firm tumor without any necrosis

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Nasolabial IMT

The operated specimen showed a gray-white nodular mass of size approximately 1.5 cm × 1.8 cm with areas of hemorrhage.

Splenic IMT

Splenectomy specimen showed gray-white, irregular areas of size around 8 cm × 5 cm × 5 cm.

IMT of cervix

Gross specimen for IMT of cervix showed a circumscribed gray-white lesion in the stroma of cervix of size approximately 3 cm × 2.5 cm, and the cut surface was solid, whitish-yellow appearance with areas of hemorrhage. There was an indistinct border between tumor and healthy cervix.

Periaortic IMT

The excised node showed a gray-white, relatively spherical tumor of size 2 cm × 2.5 cm. The cut surface was smooth with grayish-pink for both the cases.

Paraaortic IMT

The excised node showed a gray-white, nodular mass of size 3 cm × 3 cm. The cut surface was smooth with grayish-pink for both the cases.

The histopathological possible differential diagnoses and final histopathological diagnosis for all the six cases are highlighted in [Table 1]. Microscopic examination of all the six cases of IMT revealed a common pattern of finding, i.e., composed of intersecting fascicles of spindle cells with much intervening collagenous to myxoid matrix, moderate infiltrate of plasma cells, and aggregates of lymphocytes with many blood vessels [Figure 2]a. In case of mandibular IMT, there was presence of bony bit inside the proliferative spindle cells [Figure 2]b. Individual tumor cells were having oval to elongated nuclei and moderate tapering cytoplasm [Figure 2]c. Splenic IMT revealed infiltration into splenic red pulp and white pulp. IMT with cervix primary revealed infiltration of tumor cells into cervical stroma and both the parametrium were free of tumor cells. Microscopically, there was complete effacement of architecture, loss of well-preserved lymphoid follicles with germinal centers, and significant sclerosis of the lymph node parenchyma for both the lymph node IMT cases.
Figure 2: Photomicroscope (H and E stain) showing (a) the presence of spindle cells arranged in sheets and vague whorls interspersed by mixed inflammatory infiltrate (×10), (b) the presence of entrapped bony bit within the proliferative spindle cells (×10), and (c) the presence of tumor cells with oval to elongated nuclei and moderate tapering cytoplasm (×40)

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In our study, all six cases were SMA and vimentin positive, and S100, desmin and CK negative on IHC examination [Figure 3]. All the cases were ALK negative, except one case with cervix primary where it was positive for ALK-1 [Table 2] and [Figure 4]. Epithelial membrane antigen (EMA) was negative in mandibular, naso-orbital, and splenic primaries. For lymph node primaries, leukocyte common antigen, CD68, CD15, and CD30 markers were negative. For splenic primary, CD21 was done to rule out the possibility of follicular dendritic cell sarcoma (FDCS) and found negative [Figure 5].
Figure 3: Immunohistochemistry analysis showing (a) smooth muscle actin positive, (b) vimentin positive, (c) S100 negative, and (d) cytokeratin negative

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Table 2: Immunohistochemical analysis

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Figure 4: Immunohistochemistry analysis showing anaplastic lymphoma kinase 1 negative (a) and anaplastic lymphoma kinase 1 positive (b: ×10 and c: ×40)

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Figure 5: CD21 marker negative on immunohistochemistry analysis

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  Discussion Top


IMT is a rare tumor. The first case was reported by Brunn in 1939, with the lung primary having an uncertain pathogenesis, a wide range of clinical and histological presentations, and a potential for recurrence.[9] In 1954, Umiker and Iversin designated IMT as an inflammatory pseudotumor due to its similar clinical and radiological manifestations with malignant tumors.[10] Due to histopathological diversity, IMT is also known as inflammatory pseudotumor, plasma cell granuloma, and inflammatory myofibroblastic hyperplasia. Finally, according to the WHO classification, IMT is an intermediate malignant entity with a risk of metastatic spread below 5%.[11],[12]

The etiopathogenesis and biology of IMT is unclear. The relation of Epstein–Barr virus (EBV) with this tumor, the hypothesis of vascular, traumatic, and immunologic cause for this tumor, and the existence of chromosomal abnormality for the neoplastic nature are the possible factors.[2] ALK gene rearrangements may be positive in more than half of the cases. Viral infections such as EBV, human immunodeficiency virus and human herpesvirus-8, IgG4-related disease, trauma, chronic inflammation, and autoimmune diseases are the possible factors for the etiopathogenesis of IMT.[13]

The prevalence rate of IMT is 0.04%–0.7%.[14] According to the primary site of origin, IMT can be divided into the more common pulmonary variant and the less common extrapulmonary variant. The pulmonary variant was commonly seen in children and young individuals with a more benign clinical course. Whereas, the extrapulmonary variant affects older individuals with a more aggressive clinical course.[15]

Head and neck region comprises 11% of all extrapulmonary IMT cases, and larynx is the most common site among these.[7] Among head and neck primaries, epiglottis, endolarynx, parapharyngeal spaces, maxillary sinus, orbits, mandible, submandibular region, and oral cavity were the different sites to be reported for IMT.[16] IMT of oral cavity primary is very rare with an incidence of 0.0012% and has been reported in different locations of oral cavity such as gingiva, tongue, hard palate, mandible, buccal mucosa, and submandibular salivary gland.[7],[15],[16] We reported two cases of IMT with head and neck primary: one with nasolabial primary and another one with mandible primary. Primary benign splenic tumors are a rare entity, with the most common primary being hamartomas, hemangiomas, and lymphangiomas. Splenic IMT is an extremely rare finding and only few cases have been reported in the literature.[17],[18] The first case of IMT with spleen primary was described by Cotelingam and Jaffe in 1984.[19] Most of the cases have a benign course of the disease. We reported one case of IMT with spleen primary in a 22-year-old female having a benign course. Female genital tract is a rare primary site for IMT. IMT of cervix is an extremely rare entity with only few cases reported in the literature. Fuehrer et al. in a series reported eight cases of IMT of female genital tract primary, with four cases of myometrium and one case each for endometrium,  Fallopian tube More Details, cervix, and cervical polyp.[5] We reported a case of IMT of cervix primary in a 35-year-old female.

IMT of lymph nodes is a rare finding for lymphadenopathy. It can occur in any lymph node groups. Single node involvement is common, but multiple nodes may be found at diagnosis either in a single nodal group or at different sites.[20],[21] In our series, the periaortic IMT involved as single node whereas paraaortic IMT involved multiple nodes as well as two nodal groups.

Macroscopically, IMT are well-circumscribed, nonencapsulated, multiple or single firm masses, and the cut surface appears as tan or yellow-white color which may contain necrotic or hemorrhagic area.[22]

Microscopically, IMT shows proliferation of bland spindle cells admixed with variable inflammatory cells such as polymorphonuclear leukocyte, plasma cells, histiocytes, and lymphocytes. Majority of these lymphocytes are T cells, with few being B cells.[3] Three different patterns of growth may be seen in IMT such as cellular compact spindle cell pattern, hypocellular collagenous pattern, and xanthogranulomatous pattern.[22]

The possible histological differential diagnosis of IMT includes nodular fasciitis, solitary fibrous tumor, benign fibrous histiocytoma, calcifying fibrous tumor, fibrosarcoma, follicular tumor, myofibroma, dendritic cell tumor, leiomyoma, leiomyosarcoma, and odontogenic tumors of mesenchymal origin (odontogenic fibroma, odontogenic myxoma, and odontogenic fibromyxoma).[16] The final diagnosis of IMT is based on exclusion by histopathology and requires further confirmation on immunohistochemical staining. There is no imaging technique for definitive preoperative diagnosis of splenic IMT and can only be made after surgical removal of the spleen with histological evaluation.[18]

Although overlapping histologic features of IMT with nodular fasciitis and fibrous histiocytoma exist, features such as storiform pattern, lack of necrosis, and pronounced chronic inflammatory component are inconsistent for the last two diagnoses.[15],[23]

Cytologic atypia and nuclear hyperchromasia present in spindle cells of sarcomas, but absent in IMT. IHC analysis should be used to confirm the myofibroblastic phenotype of the tumor spindle cells in IMT. Spindle cells are typically reactive to vimentin (99%), SMA (92%), muscle-specific actin (89%), and desmin (69%). Furthermore, spindle cells may be focally positive to epithelial markers such as CK, EMA, and CD68. Myoglobin and S100 protein are typically negative in IMT. Only few splenic and liver IMTs may be positive to EBV-latent membrane protein and human herpesvirus-8.[16],[24] Interleukin (IL)-1 and IL-6 are the constant constituents of IMT, and major cellular sources for these two are monocytes and macrophages.[16]

In our case series, we found SMA and vimentin positive in all the cases, whereas desmin, S100, and CK were negative in all the cases. EMA was performed in three cases (mandible, naso-orbital, and splenic primaries), and CD68 was performed in two cases (periaortic and paraaortic node primaries), showing no expression for all these cases.

The IMT at head and neck region clinically mimics with malignancy. Biopsy followed by IHC helps in confirmation of the diagnosis. It is difficult to distinguish IMT of the spleen from fibroblastic reticulum cell (FBRC) tumor, which normally behaves more aggressively than IMT. There may be a common origin of these two entities.[25] Cytologic atypia is usually greater in FBRC tumor, which was negative in our case. Moreover, keratin or desmin is positive in almost all the FBRC tumors, whereas these markers were negative in our case. CD21 was performed on splenic tissue which came negative, and the possibility of an FDCS was ruled out. A variety of tumors in the female genital tract may have a myxoid appearance on the IHC staining. Immunostains for smooth muscle markers, including SMA, caldesmon, and desmin, are strongly expressed in leiomyoma and leiomyosarcoma. Whereas, CD10 marker is usually strongly present in endometrial stromal sarcoma, though it is a relatively nonspecific marker in this region. In suspicious case of embryonal rhabdomyosarcoma, skeletal muscle markers such as myoD1 and myogenin can be of value. In IMTs of female genital tract, the presence of bland to atypical spindle cells in a myxoid background with occasional mitotic activity and even necrosis is highly suggestive of leiomyosarcoma. The overexpression of ALK-1 protein establishes the diagnosis of IMT in this situation.[5] IMT of lymph node has marked morphological heterogeneity depending on the extent of fibrosis and inflammatory response. For IMT of lymph node, tuberculosis, other forms of reactive proliferation, Hodgkin's disease, and non-Hodgkin's lymphoma may be considered in the differential diagnosis. The absence of Langhans giant cells and granulomas in our case ruled out the possibility of tuberculosis.[20] Kimura's disease of lymph node may mimic IMT due to sclerosis and infiltration of plasma cells and eosinophils in the medullary cords and paracortex. However, the absence of florid germinal centers, vascularization, proteinaceous material, and polykaryon formation in our cases ruled out the possibility of Kimura's disease. The polymorphic cell proliferation in IMT may be found in Hodgkin's disease, but the absence of Reed–Sternberg and Hodgkin's cells in our cases ruled out the possibility of Hodgkin's disease. Fibroblastic element is not a feature of most of the non-Hodgkin's lymphoma. The presence of occasional immunoblasts in the infiltrate may lead to overdiagnosis of malignancy.[21]

ALK expression indicates the proliferation potential of malignant tumors. ALK overexpression is found in approximately 50% of cases and depends on the site of primary for IMT.[2],[26] Adult IMT may originate from an inflammatory process, whereas pediatric IMT may result from a tumorous process, i.e., due to chromosomal abnormalities that include ALK gene rearrangement in children.[27] In our series, one case with the age of 35 years presented as ALK positive, demonstrating a neoplastic response for adult IMT.

Among IMT cases, ALK expression is seen in 45% of cases with lung primary, 60% of cases with gastrointestinal tract primary, 62%–71% of cases with urinary bladder primary, and 100% cases of peritoneum primary.[5] ALK expression is usually negative for the reticuloendothelial organs such as spleen and lymph nodes.[28] In our case series, IMT with splenic, periaortic, and paraaortic primaries also came negative for ALK expression, supporting the literature. Fuehrer et al. in a case series for IMT of female genital tract found overexpression of ALK expression in 7 out of 8 cases, including cervix primary. In our series, the case with cervix primary also revealed ALK overexpression, supporting the literature.[5]

The site of primary, multinodularity, and vicinity of vital structure are the important parameters for aggressiveness of the IMT. Abdominal and sinonasal IMTs have more aggressive behavior in comparison to others.[2] The presence of vesicular nuclei, prominent nucleoli, and mitosis indicate malignant transformation of IMT. In our cases, the tumor had no atypical cells and mitosis, and there was no metastasis or local invasion. In spite of good prognosis, complete resection of IMT may not be always possible due to incomplete capsule and involvement of surrounding important structures, resulting in recurrence. The recurrence rate for ALK-negative extrapulmonary IMT was 31%, whereas it was 69% for ALK-positive cases.[26] Malignant transformation occurs in 8%–18% of cases whereas metastasis has been observed in < 5% of the cases.[15] However, truth regarding the reported cases of metastatic IMT is confusing and may be multicentric IMTs instead of a true metastasis.[16]

Extrapulmonary IMTs has mortality rate of 4%.[13] Surgical excision, curettage, steroid therapy, radical surgery, and radiotherapy are the treatment options for IMT. Surgical excision is the common modality of treatment with a local recurrence rate of up to 15%. Due to their vague biological behavior, IMT patients should be kept under close observation after treatment to rule out local recurrence and malignant transformations.[15] Radiotherapy, chemotherapy (cyclosporine, azathioprine, methotrexate, and cyclophosphamide), ALK molecular-targeted therapeutic drugs (crizotinib), and steroid therapy are used in invasive, nonresectable, recurrent, malignancy/metastatic IMT or when surgical margins are positive.[13] In splenic IMT, splenectomy is the best method of obtaining histopathologic specimen and has been used for both diagnosis and treatment purpose.[17],[18]

ALK gene rearrangement gives an opportunity to perform targeted therapy on this rare tumor when required. However, due to inert biological behavior, the role of ALK-mediated target therapy for IMT treatment is limited.


  Conclusion Top


Extrapulmonary IMT is a rare entity with diagnosis by exclusion on histopathological examination and IHC should be done for confirmation of the diagnosis as well as ALK expression status. In our series on extrapulmonary IMTs, the mean age group of presentation was 37 years and only the case with cervix primary reveals ALK-1 overexpression. The number of ALK negativity in our case series is possibly due to different sites of the primary. However, due to less number of cases in the study, it needs further evaluation with larger series or study on primary extrapulmonary IMT.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

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