ABSTRACT
Löfgren syndrome (LS) is a sarcoidosis subtype characterized by an acute disease course, bilateral hilar lymphadenopathy, erythema nodosum, and ankle arthritis. LS in Caucasians appears to be self-limiting; however, our patients required glucocorticoid (GC) treatment. Here, we present a case of LS and review the literature to identify the characteristics of the Japanese patients with LS. Sixty-six-year-old woman was referred to our hospital; she initially presented with an acute onset of low-grade fever and ankle arthritis, followed by erythema nodosum. Skin biopsy revealed a non-caseating granuloma, and chest computed tomography scan displayed bilateral hilar lymphadenopathy; she was diagnosed with LS. Her arthralgia ameliorated spontaneously, but erythema persisted, necessitating GC treatment. Literature review revealed that the Japanese LS patients showed more fever, were more frequently treated with GC and more patients seemed to relapse, which may be explained by the absence of human leukocyte antigen-DR isotype 3, a good prognostic allele in Caucasians. Japanese LS may cause severe symptoms after development because of the differences in human leukocyte antigen from foreign countries. For early diagnosis, it is important to evaluate erythema nodosum and bilateral hilar lymphadenopathy in patients with polyarthritis involving ankle arthralgia.
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We present the case of a 34-year-old Japanese man with anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer and brain metastases. After central nervous system (CNS) disease progression with alecintib and brigatinib, treatment with lorlatinib resulted in a good intracranial response. In this case, we investigated brain penetration ratio of brigatinib using cerebrospinal fluid and paired serum samples, and the ratio was 0.012. Further, we investigated resistance mechanisms via next-generation sequencing (NGS) using lung biopsy at lung cancer diagnosis and brain biopsy sample at progressive disease of brigatinib. No apparent resistance mechanism of known ALK resistance, such as ALK mutations, amplifications, epithelial-mesenchymal transition (EMT) and bypass pathway activation were detected. Taken together, we speculate that the low CNS penetration rate of brigatinib confers CNS progression. Further studies are warranted to reveal the resistance mechanism and propose a treatment strategy for CNS progression in ALK-positive patients.
Subject(s)
Adenocarcinoma of Lung , Aminopyridines , Anaplastic Lymphoma Kinase , Carbazoles , Drug Resistance, Neoplasm , Lactams, Macrocyclic , Lactams , Lung Neoplasms , Organophosphorus Compounds , Piperidines , Pyrazoles , Pyrimidines , Humans , Male , Organophosphorus Compounds/therapeutic use , Organophosphorus Compounds/pharmacology , Organophosphorus Compounds/administration & dosage , Lactams/therapeutic use , Adult , Aminopyridines/therapeutic use , Aminopyridines/pharmacology , Anaplastic Lymphoma Kinase/genetics , Pyrimidines/therapeutic use , Pyrimidines/pharmacology , Pyrimidines/administration & dosage , Lung Neoplasms/drug therapy , Lung Neoplasms/pathology , Lactams, Macrocyclic/therapeutic use , Lactams, Macrocyclic/pharmacology , Adenocarcinoma of Lung/drug therapy , Adenocarcinoma of Lung/pathology , Adenocarcinoma of Lung/genetics , Pyrazoles/therapeutic use , Pyrazoles/pharmacology , Carbazoles/therapeutic use , Carbazoles/pharmacology , Carbazoles/administration & dosage , Piperidines/therapeutic use , Piperidines/pharmacology , Brain Neoplasms/drug therapy , Brain Neoplasms/secondaryABSTRACT
Introduction: The role of iron in, and the prognosis of, pediatric Immunoglobulin A nephropathy (IgAN) with macrohematuria (MH)-induced acute kidney injury (AKI) (MH-AKI) have not been evaluated. Thirty percent of adults with MH-AKI, and especially those who are older, show progression to chronic kidney disease. Methods: We evaluated the immunohistopathologic characteristics of renal biopsy samples from pediatric patients with MH-AKI IgAN and controls, using Berlin Blue to identify iron, CD163 (a hemoglobin-scavenging receptor), and CD68 (a total macrophage marker), then compared the findings against the clinical characteristics of the patients. Results: We enrolled 44 children as follows: 19 with IgAN but no MH or AKI; 5 with IgAN and MH but no AKI (MH(+)AKI(-) IgAN); 11 with MH-AKI IgAN; and 9 with no IgAN, MH, or AKI, according to a renal biopsy. Berlin Blue staining was detected predominantly at the injured tubulointerstitium, and the areas of staining in children with MH(+)AKI(-) and MH-AKI IgAN were significantly more extensive. The areas of Berlin Blue and CD163 staining did not perfectly match; however, areas of Berlin Blue were surrounded by immunopositivity for CD163. No children with MH-AKI IgAN showed decreased renal function at their last visit. Conclusion: Children with IgAN and MH, with or without AKI, showed considerable iron deposition in their renal tubules. CD163-positive cells might scavenge hemoglobin in patients with MH-AKI IgAN, but not their roles as macrophages. The renal prognosis of pediatric MH-AKI IgAN is good.
Subject(s)
CD8-Positive T-Lymphocytes , Graft vs Host Disease , Hematopoietic Stem Cell Transplantation , Humans , Graft vs Host Disease/etiology , CD8-Positive T-Lymphocytes/immunology , Hematopoietic Stem Cell Transplantation/adverse effects , Male , Transplantation, Homologous , Female , Tissue Donors , Middle Aged , Adult , AllograftsABSTRACT
A 78-year-old woman presented with multiple pulmonary nodules, mixed with solid and ground-glass nodules. We pathologically confirmed that the multiple pulmonary nodules were a combination of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) and multiple pulmonary meningothelial-like nodules (MPMNs). This is the first case report of concurrent DIPNECH and MPMNs.
ABSTRACT
Japanese spotted fever is an emerging rickettsiosis caused by Rickettsia japonica and is characterized by high fever, rash, and eschar formation. Other symptoms are often vague and nonspecific and include headaches, nausea, vomiting, and myalgia. We present a case of a 46-year-old woman with Japanese spotted fever, complicated by transient bilateral sensorineural hearing loss and presenting cutaneous IgM/IgG immune complex vasculitis. The patient was admitted with a history of several days of high fever, generalized skin erythema, and hearing impairment. Laboratory findings revealed thrombocytopenia and elevated liver enzyme and C-reactive protein levels. Pure-tone audiometry revealed bilateral sensorineural hearing loss, and a skin biopsy revealed leukocytoclastic vasculitis with deposition of C3 and IgM on the vessel walls. Under the tentative diagnosis of rickettsiosis, scrub typhus, or Japanese spotted fever, the patient was treated with minocycline, and her symptoms improved within approximately 10 days. A definitive diagnosis was made on the basis of a serological test showing increased antibody levels against Rickettsia japonica. Japanese spotted fever can cause transient sensorineural hearing loss, a rare complication that presents with cutaneous IgM/IgG immune complex vasculitis.
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PURPOSE: Tubulointerstitial nephritis (TIN) has various etiologies, including IgG4-related disease (IgG4-RD), autoimmune diseases, antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), and others. IgG4-positive plasma cell infiltration can occasionally be found in TIN unrelated to IgG4-RD. Therefore, there may be problems with usage of IgG4 immunostaining to differentiate between TIN with and TIN without IgG4-RD. This study aimed to compare the proportion of plasma cells that are positive for each IgG subclass and to clarify the predominant IgG subclass trends and clinical characteristics associated with IgG4-RD and non-IgG4-related interstitial nephritis. METHODS: The study enrolled 44 cases of TIN: 6 of IgG4-RD, 8 of autoimmune disease, 9 of AAV, and 21 of unknown disease group. In addition to clinical characteristics, IgG subclass composition of interstitial plasma cells was evaluated among 4 groups by immunohistochemistry. RESULTS: IgG1 was the predominant IgG subclass in TIN unrelated to IgG4-RD. In the IgG4-RD group, the IgG subclass rate was high in both IgG1 and IgG4. The rate of average IgG4-positive cells was significantly lower in the autoimmune disease group and unknown disease group compared with the IgG4-RD group. CONCLUSION: The present study revealed IgG1-dominant immune profiles of TIN unrelated to IgG4-RD. Further investigation is required to elucidate the clinicopathological differences between IgG1-dominant and IgG4-dominant groups in IgG4-RD.
Subject(s)
Immunoglobulin G4-Related Disease , Immunoglobulin G , Nephritis, Interstitial , Humans , Nephritis, Interstitial/immunology , Nephritis, Interstitial/pathology , Immunoglobulin G/blood , Male , Female , Middle Aged , Immunoglobulin G4-Related Disease/pathology , Immunoglobulin G4-Related Disease/immunology , Aged , Adult , Immunohistochemistry , Immunophenotyping , Plasma Cells/immunology , Retrospective Studies , Aged, 80 and overABSTRACT
Histologic transformation is one of the mechanisms of resistance to EGFR tyrosine kinase inhibitor in patients with NSCLC with EGFR mutation. The transformation from adenocarcinoma to squamous cell carcinoma (SCC) has been recently recognized as a mechanism of resistance to osimertinib. The prognosis after transformation to SCC is considered to be poor, and the therapeutic strategy for these patients is unclear. Herein, we report a case of long-term response to pembrolizumab monotherapy for an SCC-transformed lesion in a patient with EGFR-mutated adenocarcinoma after osimertinib treatment. A 68-year-old man underwent right upper lobectomy and was diagnosed with lung adenocarcinoma, pathologic stage IIA, with EGFR L858R. Five years after the surgery, he was diagnosed with recurrence and administered osimertinib. Ten months after, biopsy for an enlarged subpleural lesion revealed SCC with EGFR L858R, leading to a diagnosis of histologic transformation. Notably, the programmed death-ligand 1 expression level of the transformed lesion was higher than that of the adenocarcinoma (90% versus <1%). The size of the SCC lesion had reduced with pembrolizumab monotherapy, and the reduction was maintained for over 47 months since transformation. Nevertheless, the original adenocarcinoma lesion progressed after pembrolizumab therapy and was controlled by other cytotoxic drugs and readministration of osimertinib. Immune checkpoint inhibitor therapy is generally ineffective against EGFR-mutated adenocarcinoma. Nevertheless, it may be promising for achieving a good prognosis when EGFR-mutated adenocarcinoma transforms to SCC after developing EGFR tyrosine kinase inhibitor resistance-particularly if the transformed lesion has high programmed death-ligand 1 expression.
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There is a close relationship between thyroid dysfunction and renal dysfunction. However, thyroid dysfunction can unfortunately result in inaccurate measurements of serum creatinine and cystatin C levels. The chronic decrease in cardiac output due to hypothyroidism can reduce renal plasma flow (RPF) resulting in renal dysfunction. We report the case of a 36-year-old male in whom renal dysfunction detected during a company health check-up was found to be caused by severe hypothyroidism. His serum creatinine levels showed poor results, but serum cystatin C levels were within the normal range. The physician thus prioritized serum cystatin C for assessing the patient's renal function, and concluded that his renal function was normal. He subsequently visited our hospital, aged 36 years, for a comprehensive examination. His serum creatinine level was 1.88 mg/dL and his serum cystatin C level was 0.75 mg/dL, indicating an unusual discrepancy between the two measurements. The patient also presented with fatigue, suggesting hypothyroidism, and we therefore evaluated his thyroid function. His free thyroxine level was below the sensitivity of the assay, while his thyroid-stimulating hormone level was > 100 µIU/mL. A renal biopsy was performed to further explore the underlying cause of his renal dysfunction, which suggested that reduced RPF could be the leading cause of his renal ischemia, with no indications of chronic glomerulonephritis or other abnormalities. His hypothyroidism and renal function improved after thyroid hormone replacement therapy. Given the limited reports of renal biopsy tissue examination during the acute phase of hypothyroidism, the current case provides important information regarding the diagnosis of renal dysfunction in patients with hypothyroidism.
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Pancreatic solid pseudopapillary neoplasm (SPN) is a low-grade malignant neoplasm with a good prognosis. Clinically aggressive SPNs have rarely been reported but have not been analyzed in detail. In this study, we referred to this highly malignant type of SPN as high-grade SPN (HG-SPN) and compared its clinicopathological and genetic characteristics with conventional SPN (C-SPN) using immunohistochemistry and gene panel analyses. Five HG-SPNs and 15 C-SPNs were evaluated in this study. HG-SPNs share many pathologic characteristics: macroscopically, solid/cystic appearances, microscopically, pseudopapillary/pseudorosette pattern (100%), tumor cell loose cohesiveness (100%), thin/delicate vasculature (100%), tumor cell cytoplasmic vacuolization (100%), immunohistochemical positivity for ß-catenin (nuclear expression) (100%), CD10 (80%), CD56 (80%), and vimentin (100%). Conversely, HG-SPNs showed distinct malignant features compared with C-SPNs: mean tumor size (11.7 vs. 2.9 cm, P <0.001); true necrosis (100% vs. 0%, P <0.001); high-grade nuclear atypia (100% vs. 0%, P <0.001); lymphatic and/or venous invasion (100% vs. 20%, P =0.004); mean mitotic count (4.38 vs. 0.05/high-power field, P <0.001); and mean Ki-67 labeling index (33.9% vs. 3.4%, P <0.001). All HG-SPN patients died of primary disease 3 to 36 months after surgery, while all C-SPN patients were alive without disease. Genetic studies have shown that all analyzed HG-SPNs have CTNNB1 mutations. Two HG-SPN cases showed RB1 mutations with altered immunohistochemical findings for RB1 and p16. Two HG-SPN cases had TP53 mutation and/or p53 overexpression. In conclusion, HG-SPNs show distinct malignant features and some genetic alterations that differ from C-SPNs, indicating the importance of differentiating between these 2 subtypes.
Subject(s)
Pancreatic Neoplasms , Humans , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/pathology , Pancreas/pathology , MutationABSTRACT
BACKGROUND: The tumour microenvironment (TME), which is modulated after immune-chemotherapy, is involved in tumour growth and metastasis. Programmed cell death 1 (PD-1) expressed on tumour-infiltrating non-malignant cells plays an important role in the TME through the PD-1/programmed cell death ligand 1 (PD-L1) signalling pathway. However, its impact in patients with relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL) remains unclear. METHODS: We conducted a retrospective study using tissue samples at relapse for patients with R/R DLBCL (n = 45) and evaluated the clinical impact of PD-1 expression on tumour-infiltrating non-malignant cells (microenvironmental PD-1, mPD-1). In addition, corresponding 27 samples at diagnosis were analysed to evaluate the changes in PD-1/PD-L1 expression in the TME after chemotherapy. RESULTS: Patients with mPD-1+ DLBCL showed significantly better overall survival compared with patients with mPD-1- DLBCL (hazard ratio, 0.30, p = 0.03). Among patients with mPD-1- DLBCL, those positive for neoplastic or microenvironmental PD-L1 (nPD-L1+ or mPD-L1+ ) showed significantly worse outcomes. Microenvironmental PD-1 and PD-L1 expression has high correlation at relapse, although none was found at diagnosis. CONCLUSION: We determined the clinical impact of microenvironmental PD-1 expression and its relationship with neoplastic or microenvironmental expression of PD-L1 in patients with R/R DLBCL. The expression of PD-1 and PD-L1 in the TME dramatically changes during the chemotherapy. Therefore, evaluating TME at relapse, not at diagnosis is useful to predict the outcomes of R/R DLBCL patients.
Subject(s)
B7-H1 Antigen , Lymphoma, Large B-Cell, Diffuse , Humans , Prognosis , B7-H1 Antigen/metabolism , Programmed Cell Death 1 Receptor/metabolism , Retrospective Studies , Neoplasm Recurrence, Local , Lymphoma, Large B-Cell, Diffuse/diagnosis , Lymphoma, Large B-Cell, Diffuse/drug therapy , Lymphoma, Large B-Cell, Diffuse/pathology , Recurrence , Tumor MicroenvironmentSubject(s)
IgA Vasculitis , Scalp , Humans , Edema/diagnosis , Edema/drug therapy , Edema/etiology , Immunoglobulins , MusclesABSTRACT
Corynebacterium striatum occasionally causes nosocomial infections, such as catheter-related bloodstream infection and pneumonia; however, C. striatum-related infective endocarditis or septic arthritis is uncommon. We present the case of an 85-year-old woman with infective endocarditis at the native valve and septic arthritis at the native shoulder joint caused by C. striatum. The patient was admitted for a 10-day history of fever and right shoulder pain. She had no history of artificial device implantation, injury, arthrocentesis, or hospitalization. A physical examination revealed conjunctival petechiae, a systolic heart murmur, and right shoulder joint swelling. C. striatum was observed in two blood culture sets. Transesophageal echocardiography revealed vegetation in the right aortic coronary cusp. Arthrocentesis at the right shoulder aspirated pyogenic fluid and C. striatum was detected in the culture. The patient was diagnosed with infective endocarditis and septic arthritis caused by C. striatum, and ampicillin was administered based on antimicrobial susceptibility test results. The patient's condition was initially stable; however, she developed pulmonary congestion on day 56 and eventually died. An autopsy demonstrated perforation of the aortic left coronary cusp with vegetation. C. striatum may cause native valve endocarditis and native joint septic arthritis.
Subject(s)
Arthritis, Infectious , Corynebacterium Infections , Corynebacterium , Endocarditis, Bacterial , Humans , Female , Arthritis, Infectious/microbiology , Arthritis, Infectious/diagnosis , Arthritis, Infectious/drug therapy , Corynebacterium/isolation & purification , Aged, 80 and over , Corynebacterium Infections/microbiology , Corynebacterium Infections/diagnosis , Corynebacterium Infections/drug therapy , Corynebacterium Infections/complications , Endocarditis, Bacterial/microbiology , Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/drug therapy , Endocarditis, Bacterial/complications , Fatal Outcome , Anti-Bacterial Agents/therapeutic use , Echocardiography, Transesophageal , Aortic Valve/microbiology , Aortic Valve/pathology , Aortic Valve/diagnostic imagingABSTRACT
A 34-year-old Japanese man presented with blurred vision, headache, nausea, anemia, thrombocytopenia, and severe renal dysfunction. Thrombotic microangiopathy was initially suspected to have been caused by malignant hypertension. Antihypertensive medications did not improve his thrombocytopenia or renal dysfunction, and other diseases causing thrombotic microangiopathy were ruled out. Therefore, the patient was diagnosed with atypical hemolytic uremic syndrome. A renal biopsy revealed an overlap of thrombotic microangiopathy and C3 glomerulopathy. Genetic testing revealed c.848A>G (p.Asp283Gly), a missense heterozygous variant in the gene encoding complement factor I. Overlapping atypical hemolytic uremic syndrome and C3 glomerulopathy with complement factor I mutation is very rare, especially in Japan.
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BACKGROUND: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a systemic autoimmune disease characterized by mononuclear cell infiltration and small and medium-sized blood vessel destruction leading to renal failure. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been shown to have the potential to induce the presentation or exacerbation of autoimmune disease. This report describes the clinical features of a case of newly diagnosed ANCA-associated vasculitis after COVID-19 Infection. CASE PRESENTATION: During the COVID-19 pandemic, a 67- year-old female Japanese was undergoing treatment for interstitial pneumonia, diabetes mellitus, and hypertension at her local doctor. About 2 months ago, she was diagnosed with COVID-19 and went to a hotel for treatment, and her condition improved. But a month later, after her COVID-19 infection, she presented with a fever and cough and visited Yodogawa Christian Hospital in Osaka, Japan. The reverse transcription-polymerase chain reaction was negative. She underwent extensive radiological and laboratory investigations. Serologies revealed a high perinuclear-ANCA titer with a specific anti-myeloperoxidase antibody titer of 31.7 units/mL. We suspected ANCA-associated vasculitis and performed a renal biopsy. Renal biopsy showed evidence of crescentic glomerulonephritis, which was consistent with ANCA-associated vasculitis. The patient was referred to the Department of Rheumatology and Clinical Immunology for steroid pulse and cyclophosphamide treatment. CONCLUSIONS: Delayed screening may lead to progression of the autoimmune disease, so prompt diagnosis is necessary. In this case, we could make an immediate diagnosis and refer the patient to the Department of Rheumatology and Clinical Immunology.
Subject(s)
Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis , Autoimmune Diseases , COVID-19 , Female , Humans , Aged , SARS-CoV-2 , Antibodies, Antineutrophil Cytoplasmic , Pandemics , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/complications , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/diagnosisABSTRACT
Monoclonal gammopathy of undetermined significance (MGUS) is a benign but precancerous condition that can progress to multiple myeloma. Patients with MGUS are typically monitored closely for signs of disease progression, but in some cases, they may also develop renal insufficiency, a condition known as monoclonal gammopathy of renal significance (MGRS). In MGRS, M-protein secreted by a nonmalignant or premalignant cell clone triggers renal damage by definition. Herein, we report a case of a 66-year-old Asian male with MGUS complicated by renal insufficiency. A kidney biopsy showed no evidence of renal injury mediated by M-protein; instead, the direct infiltration of clonal cells into renal tissues was observed. Although five similar cases have been previously reported, our case is unique in that the involvement of clonal cells was directly confirmed by fluorescence in situ hybridization. Our findings suggest the need to consider a novel disease concept, as this phenomenon appears to be reproduced.
ABSTRACT
BACKGROUND: Antibody-mediated rejection (ABMR), T-cell-mediated rejection (TCMR), BK polyomavirus nephropathy, and calcineurin inhibitor (CNI) toxicity are all common causes of kidney allograft dysfunction that can affect long-term allograft function. SUMMARY: The prevalence of various pathological diagnoses changes over time for both indication and protocol biopsies. Active ABMR and CNI toxic tubulopathy are the leading causes of kidney allograft dysfunction in the early posttransplant period. Active ABMR can also manifest as thrombotic microangiopathy. Acute TCMR, borderline for acute TCMR, and BK polyomavirus nephropathy will occur, then comes a causal peak of renal allograft dysfunction, followed by chronic active ABMR. Active ABMR in the late posttransplant period would progress to chronic active ABMR, indicating sequential evolution from the incipient to advanced phase of chronic active ABMR. CNI toxicity also manifests as chronic lesions of arteriolar hyalinosis. Interstitial fibrosis and tubular atrophy are the result of multiple insults and are linked to underlying diseases, particularly in the late posttransplant period. Even with established pathological criteria of the Banff scheme, it can be still challenging to clearly delineate the causes of the allograft dysfunction, especially in the complicated cases. Understanding the chronological causes of renal allograft dysfunctions improves comprehension of renal allograft pathology. KEY MESSAGES: Identifying the time-dependent prevalence of renal allograft dysfunction can be a critical and effective approach to pathological diagnosis.
Subject(s)
Kidney Transplantation , Polyomavirus Infections , Humans , Kidney Transplantation/adverse effects , Kidney Transplantation/methods , Transplantation, Homologous , Kidney/pathology , Antibodies , Allografts , Graft Rejection/etiologyABSTRACT
Angiofibroma of soft tissue (AFST) is a recently described benign fibroblastic neoplasm composed of uniform bland spindle cell proliferation in fibrous and fibromyxoid stroma with prominent thin-walled small branching vessels. A major recurrent genetic abnormality in AFST is t(5;8)(p15;q13), which results in the rearrangement of AHRR and NCOA2 . Owing to a lack of discriminatory IHC markers and potential overlap with other mesenchymal neoplasms, it may be difficult to confirm the diagnosis of AFST in some cases. Triggered by a recent gene expression profile study of AFST, which showed the significant upregulation of AhR/AHRR/ARNT downstream genes (including CYP1A1 ), we used a mouse monoclonal antibody to explore the diagnostic significance of CYP1A1 expression in histologically confirmed AFST cases along with 224 control cases, consisting of 221 neoplastic mimickers and 3 non-neoplastic lesions. We found moderate to strong cytoplasmic expression of CYP1A1 in 13 of 16 AFST cases (sensitivity, 81.3%). In contrast, the vast majority of other examined histologic mimickers exhibited no expression of CYP1A1 (specificity, 97.3%), except for 3 myxofibrosarcomas (3/31), 2 solitary fibrous tumors (2/22), and 2 neurofibroma (1/27). Our results indicate that CYP1A1 immunohistochemistry may aid in the diagnosis of AFST by distinguishing among various kinds of tumors, particularly those harboring prominent vasculature.