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Back to Journal »International Journal of Medical Case Reports» Volume 14

Chronic pulmonary aspergillosis and type 2 diabetes in Saudi adult males with granulomatous polyangiitis: a case report

Authors Eldaabossi S, Saad M, Alabdullah M, Awad A, Alquraini H, Moumneh G, Mansour A

Published on December 20, 2021, Volume 2021: 14 pages, 829-837 pages

DOI https://doi.org/10.2147/IMCRJ.S340231

Single anonymous peer review

Editor approved for publication: Professor Ronald Prineas

Safwat Eldaabossi,1,2 Mustafa Saad,1 Mohammed Alabdullah,1 Amgad Awad,1,2 Hussain Alquraini,1 Ghada Moumneh,1 Ali Mansour1 1 Almoosa Specialist Hospital, Al Ahsa, Saudi Arabia; 2 Al Azhar School of Medicine, Al Azhar University , Cairo, Egypt. Chronic pulmonary aspergillosis (CPA) is a rare fungal infection with high morbidity and mortality. It usually affects normal or mildly immunosuppressed patients with underlying respiratory diseases. Antifungal drugs (voriconazole, itraconazole) are the main treatments. Intravenous drug therapy (amphotericin B or echinocandin) alone or in combination with azoles is the last resort in special situations, such as azole failure, drug resistance, or serious illness. Sometimes CPA and GPA coexist, because the symptoms are not specific, the clinical and imaging features are similar, and it is difficult to distinguish, so a high degree of suspicion is needed to make a correct diagnosis. Case introduction: We reported that a 28-year-old man from Saudi Arabia was diagnosed with GPA. The patient complained of cough, fatigue, polyarthralgia, and red eyes 40 days before admission. The diagnosis of GPA was confirmed by clinical and radiological examinations and pathological reports of lung biopsy, and immunosuppressive drugs were given. The patient's condition is complicated by chronic pulmonary aspergillosis and type 2 diabetes. The initial treatment included systemic glucocorticoids, methotrexate, then rituximab and voriconazole, and finally intravenous cyclophosphamide and amphotericin B, but there was no complete remission. The thoracic surgery team postponed the debridement of significant lung lesions until the active fungal infection was controlled. Conclusion: The clinical and imaging features of GPA are similar to those of tuberculosis, chronic pulmonary aspergillosis, and lung cancer. The lack of clear clinical symptoms of GPA requires a high degree of suspicion for early diagnosis. This case illustrates the dilemma of diagnosis and treatment of GPA and superimposed fungal infection. When immunosuppressive agents cannot control GPA, secondary infections, especially fungal infections, must be considered. Keywords: granulomatous polyangiitis, pulmonary aspergillosis, lung abscess, vasculitis

Granuloma with polyangiitis (GPA) (formerly known as Wegener's granulomatosis) is an extremely rare autoimmune, necrotizing granulomatous disease with unknown etiology, involving small and medium blood vessels in multiple organs, but the most common It is the upper respiratory tract, lungs (more than 90%), kidneys, as well as skin, eyes, muscles and nervous system. 1,2 The treatment of GPA depends on its severity and whether it causes organ damage. For patients with active, non-severe GPA (GPA has no life-threatening or organ-threatening manifestations), start induction therapy with methotrexate and glucocorticoids. For patients with active and severe GPA, rituximab and cyclophosphamide are recommended to induce remission and increase the survival rate by 20% to 80%. If liver or kidney dysfunction or repeated relapses occur during methotrexate treatment, rituximab may be preferable. 3,4

Chronic pulmonary aspergillosis (CPA) is a rare fungal infection with high morbidity and mortality. CPA usually occurs in patients with underlying lung diseases, such as previous tuberculosis, COPD, sarcoidosis, or lung cancer. The diagnosis of CPA depends on whether there are consistent clinical symptoms and imaging examination results, a positive serum Aspergillus precipitation test or the isolation of Aspergillus from respiratory specimens (ie, sputum or bronchial aspirate). Oral triazole therapy for CPA is now considered the standard therapy. Oral voriconazole is also effective for CPA, and has been accepted as first-line treatment in several studies or after itraconazole (due to failure or intolerance)5.

Sometimes CPA and GPA coexist. Because the symptoms are not specific and the clinical and imaging features are similar, it is difficult to distinguish, so a high degree of suspicion is needed to make a correct diagnosis. 6

The prevalence of fungal infections in Saudi Arabia is unclear, as there is no data on the burden of fungal diseases in Saudi Arabia. 7 The prevalence of CPA in Saudi Arabia is estimated to be 3.4 per 100,000. 8 Less cases of CPA are associated with superimposed pulmonary Aspergillus infection, especially in Saudi Arabia. We reported this case in eastern Saudi Arabia. This is a case of GPA in which multiple pulmonary nodules have developed into multiple cavities and have been refined due to chronic pulmonary aspergillosis.

In this report, we describe a 28-year-old Saudi man who was in good health before. His medical history dates back to January 2020, when he had 40 days of dry cough, fever, fatigue and red eyes, and abnormal chest X-rays. He smokes 10 packs of cigarettes a year. In August 2019, he underwent a lumbar laminectomy due to left sciatica. Before admission, he had a dry cough, red eyes, blurred vision, knee joint pain and low back pain. His chest X-ray revealed an isolated lung nodule in the upper right lobe, so he was referred to a pulmonary clinic (Figure 1A). Figure 1 (A) X-ray of consolidation of nodule in the upper right lobe with internal cyst formation. (B) X-ray of a hollow mass in the upper right lobe, if opaque, nodules in the lower left lobe. (C) Chest radiograph, with multiple bilateral cavity lesions with gas and fluid levels, the largest being in the upper right lobe.

Figure 1 (A) X-ray of consolidation of nodule in the upper right lobe with internal cyst formation. (B) X-ray of a hollow mass in the upper right lobe, if opaque, nodules in the lower left lobe. (C) Chest radiograph, with multiple bilateral cavity lesions with gas and fluid levels, the largest being in the upper right lobe.

Since tuberculosis is very common in our area, we carried out an outpatient tuberculosis screening to detect acid-fast bacteria through sputum smears and PCR. The test result is negative. The second chest X-ray examination 2 weeks later showed nodules in both lungs, the largest being in the upper right lobe.

He was taken to another hospital where he was examined and soft bronchoscopy, and a transbronchial biopsy of the right upper lobe was performed. No intraluminal lesions were found.

Denies fever, rash, numbness, headache, joint swelling, nasal congestion or mucus, or changes in urine color. His examination showed a body mass index of 30.5 kg/m2, a body temperature of 37.0*C, a blood pressure of 130/80 mmHg, a heart rate of 110 beats per minute, and an oxygen saturation of 95%. Binocular redness and swelling, no discharge. We found no nasal polyps or deformities. Auscultate the chest on both sides with equal air intake. His abdomen was neither tender nor swollen, and there was no evidence of organ enlargement. The patient has no palpable lymphadenopathy, rash, or arthritis. The ophthalmologist noticed bilateral episcleritis.

Subsequent chest radiographs showed that the upper right lobe nodule enlarged, forming a large amount of turbidity, and the left lower lobe nodule enlarged (Figure 1B).

The imaging examination on February 10, 2020 showed that there were multiple nodules of varying sizes on both sides of the chest, an enlarged right upper lobe lung mass, and multiple mediastinal lymph nodes (Figure 2A and B). Infectious causes include bacterial infections, tuberculosis, and even fungal diseases. Sarcoidosis and granuloma with polyangiitis are other differential diagnoses. The possibility of tumor process cannot be ruled out. His examination revealed microscopic hematuria and proteinuria and mild eosinophilia in the blood (Table 1). Table 1 Laboratory results of admission and follow-up Figure 2 (A) CT thoracic mediastinal window: central cavity like a mass in the upper right lobe, size 7.3×7 cm. (B) CT thoracic lung window, multiple nodules on both sides showed the lower lobe dominated, and the bronchial walls were slightly thickened on both sides. (C) CT thoracic mediastinal window: CT-guided needle biopsy of the right upper lobe mass with central cavitation. (D) CT thoracic lung window. Cavitation in the upper right leaf. (E) CT thoracic lung window, October 1, 2021: The size of the cavity lesion in the right upper lobe is 3.8×2.4 cm, which was 3.8×3 x 2.8 cm before. The interior contains solid components and crescent signs, adding potential fungi Possibility of the ball. (F) CT thoracic lung window, October 1, 2021: showing bilateral lung cavity lesions, 1 in the lower right lobe, 1 in the lingual side, and 2 in the lower left lobe.

Table 1 Laboratory results of admission and follow-up

Figure 2 (A) CT thoracic mediastinal window: a mass-like central cavity in the upper right lobe, 7.3×7 cm. (B) CT thoracic lung window, multiple nodules on both sides showed the lower lobe dominated, and the bronchial walls were slightly thickened on both sides. (C) CT thoracic mediastinal window: CT-guided needle biopsy of the right upper lobe mass with central cavitation. (D) CT thoracic lung window. Cavitation in the upper right leaf. (E) CT thoracic lung window, October 1, 2021: The size of the cavity lesion in the right upper lobe is 3.8×2.4 cm, which was 3.8×3 x 2.8 cm before. The interior contains solid components and crescent signs, adding potential fungi Possibility of the ball. (F) CT thoracic lung window, October 1, 2021: showing bilateral lung cavity lesions, 1 in the lower right lobe, 1 in the lingual side, and 2 in the lower left lobe.

He was admitted to the hospital on February 15, 2020 and underwent a CT-guided lung biopsy under local anesthesia. There were no complications caused by a cavity in the upper right lobe (Figure 2C and D). In addition to intravenous steroids (methylprednisolone 1), we also started using ambulatory steroids (prednisolone 50 mg/day) and methotrexate 25 mg once every two weeks for five days.

The histopathology of the cavity lesion in the upper right lobe is as follows: medium-sized blood vessels (arteries and veins) are usually missing due to inflammation, replaced by scattered necrosis, which contains nuclear ruptured neutrophils and eosinophils, accompanied by Fibrinoid necrosis (probably the focus of leukocyte fragmentation vasculitis)). The lesion consists of a collection of granulomas and epithelioid granulomas, with occasional small central necrosis and multinucleated giant Langerhans cells. An overlap syndrome between GPA and eosinophilic granulomatous polyangiitis has been reported in the literature. Based on the clinical history (no asthma, no atopic and no significant peripheral eosinophilia), eosinophilic granuloma with polyangiitis was ruled out in this case (Figure 3A and B). Figure 3 (A and B) The histopathology of the right upper lobe lung biopsy found that medium-sized blood vessels (arteries and veins) are rare and may be destroyed by inflammation, replaced by scattered relatively small necrosis, caused by basophils Increased degenerative nuclear rupture neutrophils compose eosinophils with fibrinoid necrosis (may be the focus of leukoblastic vasculitis). 8. There are collections of small epithelioid granulomas, small central necrosis, and a few multinucleated giant Langerhans type cells.

Figure 3 (A and B) The histopathology of the right upper lobe lung biopsy found that medium-sized blood vessels (arteries and veins) are rare and may be destroyed by inflammation, replaced by scattered relatively small necrosis, caused by basophils Increased degenerative nuclear rupture neutrophils compose eosinophils with fibrinoid necrosis (may be the focus of leukoblastic vasculitis). 8. There are collections of small epithelioid granulomas, small central necrosis, and a few multinucleated giant Langerhans type cells.

His immunological characteristics showed positive for anti-neutrophil cytoplasmic antibody (ANCA) C and rheumatoid factor, but negative for p-ANCA, antinuclear antibody (ANA) and anti-cyclic citrulline antibody (CCA). Since he has no children and is single, he rejected cyclophosphamide.

He received intravenous (IV) methylprednisolone 3 times for 3 months, oral prednisolone 50 mg, combined with weekly methotrexate 25 mg, and sometimes mycophenolate mofetil (daily 2 grams). Three months later, his clinical and radiological conditions still did not improve, so he was given 2 grams of rituximab 500 mg intravenously every 2 weeks for a total of 4 doses, but a severe allergic reaction occurred after the fourth dose.

On September 17, 2020, in addition to fever, he also experienced worsening cough, yellow, sometimes bloody sputum, fatigue and shortness of breath. He had joint pains and his eyes turned red again. Clinically, the body temperature is 39℃, the pulse is 140 beats/min, and the respiration is 28 beats/min. Red eyes, no edema of lower limbs, no rash, no arthritis, normal heart murmur, no murmur. The dullness of the air inlets at the bottom on both sides of the chest and in the distance. Repeated chest X-rays showed that the size of multiple cavities progressed with gas and liquid levels (Figure 1C). Blood and sputum cultures were negative for bacteria, but 3 sputum cultures were positive for Aspergillus. In many cases, the serum galactomannan test is negative. His inflammatory markers were elevated, and COVID -19 was repeatedly negative. He was recently diagnosed with type 2 diabetes and is taking basal insulin and normal insulin. According to experience, intravenous antibiotics were started, but after the culture results, voriconazole 200 mg/8 hours was intravenously injected for two weeks, and then orally administered.

During the treatment period, prednisolone 20 mg and voriconazole 200 mg were administered three times a day, while azathioprine 100 mg pod and trimethoprim and sulfamethoxazole 480 mg were administered daily. He has symptoms of suppuration (cough, sputum, sputum and fever, myalgia and fatigue, elevated inflammatory markers, negative sputum and blood cultures. Multiple courses of intravenous broad-spectrum antibiotics, each lasting three weeks, are hospitalized and outpatient.

In March 2021, his clinical condition was stable and his radiology was partially improved.

He suffered from bilateral cataracts and underwent two bilateral cataract surgeries under local anesthesia.

In June 2021, he developed suppuration (cough and excessive sputum), accompanied by fever, myalgia and fatigue, increased inflammation markers, and negative sputum and blood cultures. The fungal culture in the sputum was positive for Aspergillus fumigatus. Cyclophosphamide 500 mg intravenously for 3 months, and Ambisome b (Ambisome) intravenously 200 mg per day for 12 weeks. He became asymptomatic and improved in clinical, radiology and laboratory tests. Oral steroids were reduced to 10 mg of prednisolone per day. With trimethoprim and prevention of gastritis and osteoporosis.

After receiving IV Ambisome treatment for 12 weeks and restarting oral voriconazole (200 mg, 3 times a day), there was no sufficient response. He was admitted to King Faisal Specialist Hospital in Riyadh and passed soft bronchoscopy (BAL) in July 2021. ) And CT-guided lung biopsy for evaluation. The lower left leaf. BALF is negative (by staining) for malignancies, viruses, and fungi, but is positive for galactomannan (8,3). Serum galactomannan was negative (0.09).

Cardiothoracic surgeons, pulmonary rheumatology, and infectious disease teams recommend continuing medical treatment for fungal infections because the patient has multiple lung cavity lesions, some of which have air fluid (active infection?), and reduce oral corticosteroids to daily 10 mg. Lung biopsy showed non-specific inflammation.

Follow-up CT on October 1, 2021 showed a reduction in the size of bilateral lung cavity lesions and a significant increase in wall thickness (Figure 2E and F).

On October 26, 2021, he was reviewed by a multidisciplinary team at the King Faisal Specialist Center. It is recommended to continue medical treatment and surgical intervention after the accumulation of water, until the fungal infection is controlled or complications occur.

Granulomatous polyangiitis is a systemic vasculitis that can cause necrotizing granulomatous vasculitis of the respiratory tract, kidneys, skin, peripheral nervous system, joints and other organs. The incidence of 1-3 GPA is approximately 10 cases per 1 million people, and although there are no published data on the incidence of GPA in Saudi Arabia, men are more common than women. 4 The diagnosis of GPA depends on clinical, laboratory, radiological, and histopathological evaluations. GPA usually involves (a) upper respiratory tract (sinusitis, scleroderma, saddle nose) and lower respiratory tract (pulmonary nodules, cavities and alveolar hemorrhage), (b) systemic vasculitis and (c) glomerulonephritis- ANCA-positive results (82% to 94%) support but not confirm the diagnosis of GPA. 9 A biopsy of the affected organ is usually required to confirm the diagnosis and rule out infection or malignancy (scattered multinucleated giant cells, necrotizing granulomas with non-specific inflammation, and tissue necrosis with necrotizing vasculitis. 2 In active and non-active In severe GPA (GPA without life-threatening or organ-threatening manifestations), induction therapy starts with methotrexate and glucocorticoids; methotrexate is equivalent, but may be related to a higher recurrence rate. For mobility In patients with severe GPA, it is recommended to use rituximab instead of cyclophosphamide to induce remission. In the case of liver or kidney dysfunction or repeated relapses during treatment with methotrexate, rituximab may be more effective It is desirable. Long-term treatment with trimethoprim/sulfamethoxazole can prevent and prevent recurrent Pneumocystis carinii infection and induce remission of non-serious diseases. 3

Our patient has multiple organ involvement, including episclerositis, polyarthralgia, pulmonary nodules and cavities, microscopic hematuria, blood eosinophilia, c-ANCA and rheumatoid factor positive, ESR and CRP are elevated. Lung biopsy showed positive GPA and c-ANCA, excluding the diagnosis of tuberculosis and lung cancer. Initial treatment includes systemic glucocorticoids, methotrexate, followed by rituximab and cyclophosphamide, and prophylactic doses of trimethoprim.

Infections, especially lung infections, can also be a complication of immunosuppressive therapy. In some clinical situations, it may be difficult to recognize symptoms of worsening GPA or infection. Differential diagnosis requires clinical pictures, laboratory findings and chest radiographs, especially high-resolution computed tomography (HRCT). The most complex issue in the management of GPA patients is finding the right balance between the immunosuppression required to treat the disease and minimizing the risk of bacterial infection. 10

Aspergillosis is a lung infection caused by Aspergillus (mainly Aspergillus fumigatus and Aspergillus flavus) and can be chronic or acute. Usually, chronic infection or colonization occurs in patients with lung disease. Chronic pulmonary aspergillosis has many forms, including chronic cavitary pulmonary aspergillosis and chronic fibrotic pulmonary aspergillosis, aspergilloma and aspergillus nodules. 5 The prevalence of fungal infections in Saudi Arabia is unclear, as there is no data on the burden of fungal diseases. Saudi Arabia. 7 The prevalence of CPA in Saudi Arabia is estimated to be 3.4 per 100,000. 8

The current criteria for determining chronic pulmonary aspergillosis are (i) the clinical symptoms (fever, fatigue, sputum production, hemoptysis or shortness of breath), and (ii) the radiological findings (one large cavity or two or more small cavities, regardless of Yes or 1-3 months without aspergilloma), and (iii) positive serum Aspergillus precipitation test or isolation of Aspergillus species from respiratory specimens (ie, sputum, tracheal aspirate or bronchial aspirate). 5,11

The presence of fungal balls strongly suggests that aspergilloma is a manifestation of CPA. To confirm the diagnosis, microbiological confirmation is needed to rule out other diagnoses, such as tuberculosis, and to determine the presence of fungi. X-ray photographs showing holes may raise suspicion, but a positive Aspergillus IgG test is required to confirm the diagnosis. 12,13 In a small number of patients with chronic pulmonary aspergillosis, Aspergillus fumigatus culture is positive, and serum galactomannan is usually negative. If the sputum culture is negative, bronchoscopy and bronchoalveolar lavage may be required. The sensitivity and specificity of the BALF-galactomannan test for the diagnosis of CPA are 38-50% and 87-100%, respectively. 14 Elevated inflammatory markers, such as C-reactive protein and/or erythrocyte sedimentation rate, are very common in patients with chronic diseases. 5,13 Current drug treatments for invasive aspergillosis include voriconazole and liposomal amphotericin B combined with surgical debridement. 5,13,​​15

Chronic cavitary pulmonary aspergillosis requires life-long antifungal treatment. Oral triazole therapy for CPA is now considered the standard therapy. Oral voriconazole (200 mg twice a day; may increase to 300 mg twice a day based on therapeutic drug monitoring) is also effective in CPA and has been used as first-line treatment in several studies or after itraconazole (200 mg twice a day) The tolerance is acceptable. Currently, the choice between the two drugs depends on cost, availability, toxicity, and tolerability; therefore, they can be used interchangeably as first-line treatments. 5,15 Intravenous drug therapy, alone or in combination with azoles, is the last resort in the case of clinical failure, panazole resistance or drug toxicity, but it can also be used in the case of severe disease progression. Drugs administered intravenously include amphotericin B or echinocandin 5,13.

Surgery has two important purposes for CPA patients: it can relieve disabling or life-threatening symptoms, and if the local disease does not respond to antifungal therapy, it can even cure some patients. Because the prevalence of CPA is low and there are a large number of health conditions that prevent surgery, the evidence for surgical intervention is limited to large series of cases compiled over a long period of time. 4,16,17

The patient’s condition was complicated by type 2 diabetes and chronic Aspergillus infection, leading to other diseases. The patient’s diabetes was treated with basal insulin combined with immunosuppression and antifungal therapy. Therefore, he planned to perform surgical debridement on the two large cavities of the right upper lobe and lower lobe. However, the multidisciplinary team recommended to continue medical treatment until the fungal infection was controlled or complications occurred. .

GPA is extremely rare, and the occurrence of aspergillosis is also extremely rare. Few cases of pulmonary Aspergillus infection have been reported as complications of GPA. In both cases, lung cavities or nodules may occur. Detection of overlapping mycosis requires repeated sputum culture for fungal testing and serum galactomannan (positive predictive value 25-62%). In patients with diffuse lung involvement, bronchoalveolar lavage (BAL) is often helpful in the diagnosis of invasive pulmonary aspergillosis. Due to the risk of bleeding, transbronchial biopsy is not recommended. Diagnosis of invasive pulmonary aspergillosis also requires histopathological examination. 11, 13, 16

Arfaj et al. encountered 23 cases of GPA between 1990 and 2001, and reported that the proportion of lung involvement was 65.2%, and the proportion of ANCA test positive was 78.9%. The chest CT results were pulmonary nodules (80.0%) and cavities (53.3%). Lung biopsy revealed chronic granulomatous inflammation with vasculitis and necrosis. 63% of patients received intravenous cyclophosphamide, and 10.5% required rituximab treatment. 4Al-Harbi et al. studied the etiology of pulmonary granulomas (transbronchial or endobronchial biopsy, CT-guided core biopsy, or surgical specimens) from 2005 to December 2013, and GPA was detected in 18 of 158 cases . 18 He et al. report: A patient with GPA suffered from pulmonary mycosis (sputum culture showed Candida albicans 3+ and Aspergillus), and subsequently received immunosuppressant and antifungal therapy. 19 Richter et al. examined the bronchoalveolar lavage fluid (BALF) of 33 GPA patients to determine the main pathogen and only reported the growth of 1 case of fungal disease. 20 Invasive mycosis is considered to be rare, and preventive antifungal treatment should be considered for immunocompromised hosts. 11 Yagi et al. reported that an adult diagnosed with A. lentulus-induced invasive pulmonary aspergillosis (IPA) by bronchoscopy 3 weeks after starting systemic corticosteroid therapy for ANCA-related vasculitis and was taking antifungal drugs Improved after voriconazole treatment. 21 7 157 patients with ANCA-related vasculitis were found to have IPA. Two patients were classified as Wegener's granulomatosis and 5 patients were classified as microscopic polyangiitis. Despite intensive antifungal treatment, only 3 patients survived. 22 Le Thi Huong et al. 23 and Martens 24 reported a case of pulmonary aspergilloma as a complication of Wegener's granulomatosis.

The typical differential diagnosis of pulmonary cavities has a wide range and may include infection (bacteria, tuberculosis, fungus), malignancy, septic embolism, infectious cysts, necrotizing rheumatoid nodules, or GPA. Our case illustrates the dilemma of diagnosing and treating GPA and CPA in atypical patients. This case is one of the few cases described in the literature as GPA and CPA.

The clinical and radiological characteristics of GPA are similar to those of tuberculosis, chronic pulmonary aspergillosis, and lung cancer. The lack of clear clinical symptoms of GPA requires a high degree of suspicion for early diagnosis. This case illustrates the dilemma of diagnosis and treatment of GPA and superimposed fungal infection. When immunosuppressive agents cannot control GPA, secondary infections, especially fungal infections, must be considered. Targeted diagnostic tests and appropriate early antifungal treatment should be carried out as soon as possible, and the use of immunosuppressive drugs should be minimized.

ANCA, anti-neutrophil cytoplasmic antibody; ANA, antinuclear antibody; AIDS, acquired immunodeficiency syndrome; BALF, bronchoalveolar lavage fluid; CPA, chronic pulmonary aspergillosis; RF, rheumatoid factor; ASP, Aspergillus ; CT, computed tomography; GPA, granulomatous polyangiitis; IPA, invasive pulmonary aspergillosis; WBC, white blood cell count; MCV, mean red blood cell volume; CS, culture and sensitivity; PCR, polymerase chain reaction; IV , Intravenous injection; ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; anti-CCA, anti-cyclic citrulline antibody; RBCS, red blood cell.

All data generated or analyzed during this research period are included in this article.

Ethical approval and consent to participate, applicable disclosure request.

Ethical approval has been obtained from the Almoosa Specialty Hospital Review Board to publish detailed information on the case.

The patient has signed a written informed consent form to release the information in this case report. The consent form is available for review.

To the patient because he agreed to disclose his condition, to the Research Center, King Faisal Specialist Center, Rheumatology, Pulmonary and Thoracic Surgery and Infectious Diseases Department of Almoosa Hospital.

All authors have made significant contributions to the work of the report, whether in terms of concept, research design, execution, data acquisition, analysis, and interpretation, or in all these areas; participating in drafting, revising, or critically reviewing articles; final approval requirements Published version; agreed on the journal to which the article was submitted; and agreed to be responsible for all aspects of the work.

Almoosa Specialty Hospital Research Center will provide funding.

The authors declare that they have no competing interests in this work.

1. Singer O, McCune WJ. Update on maintenance treatment of granulomatous polyangiitis and microscopic polyangiitis. Curr Opin rheumatism. 2017;29(3):248-253. doi:10.1097/BOR.0000000000000382

2. Garlapati P, Qurie A. Granuloma with polyangiitis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021. Available from https://www.ncbi.nlm.nih.gov/books/NBK557827/. Visited on December 9, 2021.

3. Chung SA, Langford CA, Maz M, etc. 2021 American College of Rheumatology/Vasculitis Foundation Anti-neutrophil cytoplasmic antibody-related vasculitis management guidelines. Arthritis and rheumatism. 2021; 73(8): 1366–1383. PMID: 34235894. doi:10.1002/art.41773

4. Al Arfaj AS, Khalil N, Al Mogairen SA, Al Arfaj H, Al Khalaf A, Al Bedaiwi M. Pulmonary manifestations and imaging manifestations of patients with granulomatous polyangiitis in a university teaching hospital in Saudi Arabia. J Nat Sci Med. 2019; 2(2). doi:10.4103/JNSM.JNSM_38_18

5. Patterson TF, Thompson GR, Tannin DW and so on. Practice guidelines for the diagnosis and management of aspergillosis: 2016 update of the American Academy of Infectious Diseases. Clinical infection. 2016;63:e1-e60. doi:10.1093/cid/ciw326

6. Berden A, Göçeroglu A, Jayne D, etc. Diagnosis and treatment of ANCA-related vasculitis. BMJ. 2012;344:e26. doi:10.1136/bmj.e26

7. Albarrag AM, Al-Abdely HM, Khalid NFA, Denning DW. The burden of severe fungal infections in Saudi Arabia. Available from: http://life-worldwide.org/assets/uploads/files/ICAAC%202014_%20Fungal%20BurdenSaudi.pdf. Visited on June 5, 2017.

8. Wadi J, Denning DW. Burden of severe fungal infections in Jordan. J fungus. 2018;4(1):15. PMID: 29371507; PMCID: PMC5872318. doi:10.3390/jof4010015

9. Seo P, Stone JH. Anti-neutrophil cytoplasmic antibody-related vasculitis. It's J Med. 2004;117(1):39-50. doi:10.1016/j.amjmed.2004.02.030

10. Dadoniene J, Pileckyte M, Baranauskaite A, etc. Clinical features and long-term results of 35 patients with Wegener's granulomatosis followed in two rheumatology centers in Lithuania. medicine. 2010; 46: 256-260. doi:10.3390/medicina46040035

11. Denning DW, Cadranel J, Beigelman-Aubry C, etc. Chronic pulmonary aspergillosis: basic principles and clinical guidelines for diagnosis and management. Eur Respir J. 2016; 47:45-68. doi:10.1183/13993003.00583-2015

12. Desai SR, Hedayati V, Patel K, Hansell DM. Chronic Aspergillosis of the Lung: Unraveling Terminology and Radiology. Euro radio. 2015; 25: 3100-3107. doi:10.1007/s00330-015-3690-7

13. Denning DW, Page ID, Chakaya J, etc. Case definition of chronic pulmonary aspergillosis in a resource-constrained environment. Emergency infection. 2018;24:e1-e13. doi:10.3201/eid2408.171312

14. Maghrabi F, Denning DW. Management of chronic pulmonary aspergillosis: the method of the National Aspergillosis Centre in the United Kingdom. Curr Fungal Infect Rep. 2017;11(4):242-251. doi:10.1007/s12281-017-0304-7

15. Aspergillosis | About; May 10, 2021. It can be obtained from the following website: www.cdc.gov. Visited on June 1, 2021.

16. Barac A, Kosmidis C, Alastrue-Izquierdo A, etc. An update on chronic pulmonary aspergillosis: a year in review. Medicine Mycol. 2019;57(Supplement_2):S104–S109. doi:10.1093/mmy/myy070

17. Muniappan A, Tapias LF, Butala P, etc. Surgical treatment of pulmonary aspergilloma: 30 years of North American experience. An Thoracic Surgery. 2014; 97: 432-438. doi:10.1016/j.athoracsur.2013.10.050

18. Al-Harbi A, Al-Otaibi S, Abdulrahman A, etc. Pulmonary granuloma: a clinical pathological study of 158 cases. Ann Thorac Med. 2017; 12: 278-281. doi:10.4103/atm.ATM_1_17

19. He Y, Liu J, Gao B. Wegener's granuloma with pulmonary fungal infection: case report and brief review. J International Medical Research. 2012; 40: 383-392. doi:10.1177/147323001204000141

20. Richter AG, Stockley RA, Harper L, Dr. Thickett. Lung infections of Wegener's granulomatosis and idiopathic pulmonary fibrosis. Chest. 2009;64(8):692–697. doi:10.1136/thx.2008.110445

21. Yagi K, Ushikubo M, Maejima A, etc. Invasive pulmonary aspergillosis caused by Aspergillus lentilus in adult patients: case report and literature review. J infected Chemother. 2019;25(7):547–551. doi:10.1016/j.jiac.2019.02.003

22. Su Tao, Li Huicong, Chen Min, etc. Invasive pulmonary aspergillosis in patients with anti-neutrophil cytoplasmic antibody-related vasculitis. J Clinical Rheumatism. 2009;15(8):380–382. PMID: 19279506.doi: 10.1097/RHU.0b013e31819e67b1

23. Le Thi Huong D, Wechsler B, Chamuzeau JP, Bisson A, Godeau P. Pulmonary aspergillosis complicated by Wegener's granulomatosis. Scand J Rheumatism. 1995;24(4):260. PMID: 7481595. doi: 10.3109/03009749509100887

24. Martens J. Pulmonary Aspergilloma, an unusual complication of Wegener's granulomatosis. Postgrad Med J. 1982;58(675):55-56. PMID: 70887764; PMCID: PMC2426230. doi:10.1136/pgmj.58.675.55

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