Patient with a rare display of Granulomatosis

Granulomatosis with Polyangiitis (Wegener’s granulomatosis)

ABSTRACT

the Granulomatosis Polyangiitis ( Wegener’s granulomatosis), an autoimmune disease is characterized by necrotizing, and granulomatous inflammation of small to medium-sized vasculitis. This rare disease affects approximately 3 out of every 100,000 people, affecting men and women equally ^[1]. GPA can occur at any age, but most often between the ages of 40 and 65 ^[1]. Granulomatosis with polyangiitis classifies as ANCA-associated small-vessel vasculitis ^[3]. The Clinical triad consists of upper airway involvement, lower respiratory tract involvement (sinusitis, otitis, nasal mucosa ulcers, subglottic stenosis, recurrent cough, chest pain and hemoptysis) and glomerulonephritis. If untreated, this disease carries a high mortality. Diagnosis bases on obtaining an extensive clinical history, imaging, laboratory tests, and histology. Computed Tomography (CT) evaluates upper airway and lungs, because of its high sensitivity detecting anomalies of paranasal sinuses, bronchial tree and lungs ^[5].  PET/ CT scan is the preferred method of choice to evaluate renal manifestation. The treatment of GPA includes a combination of cytotoxic agents like cyclophosphamide, corticosteroids and immunosuppressive therapy. These patients require long term care and follow up due to the relapsing nature of the diseases.

 Introduction

Granulomatosis Polyangiitis (GPA) is a rare disease characterized by necrotizing granulomatous vasculitis of small vessels. GPA annual incidence is 5-10/million, with a prevalence of 24-157 cases per million^[2]. Although it can occur at any age, it most common manifest at 65-74 years of age and affects both sexes equally. GPA  an antineutrophil cytoplasmic antibody (ANCA) associates with necrotizing granulomatous inflammation that affects multiple system organs in the body. It distinguishes by its preference for upper and lowers respiratory tracts, glomerular of the kidney, and other systemic organs and tissues. In approximately 90% of patients, these antineutrophil cytoplasmic antibodies attack proteinase 3(PR3), a neutrophil protease. Antineutrophil cytoplasmic is responsible for the necrotizing granulomatous inflammation seen the vessels. The presence of such antibodies has reasonable specificity and is a reliable indicator for a diagnosis of WG but not sensitivity. Therefore, a tissue biopsy needs for a definite diagnosis of GPA.

Approximately 70-100 % of patient have lung involvement (epistaxis, nasal discharge, nasal ulcers, granulomatous lesions and deformation of the nasal bridge, recurrent sinusitis, chronic otitis media, dyspnea, bronchial obstruction, pleuritis, pleural effusion) at the time of diagnosis. PET/CT has high sensitivity in the detection of thoracic involvement in active GPA, with 100% sensitivity in a respiratory and vascular thoracic relationship ^[13]. MRI usually does not add extra information to that provided by CT and PET/CT in the upper respiratory tract ^[13]. The most frequent pulmonary radiological findings are peripheral pulmonary nodules and masses, which is present in 70-90% of patients ^{[14, 15]}. These nodules and masses tend to cavitate with consolidation areas and ground-glass opacities.

Approximately 80-90% of patients with GPA present with renal involvement characterized by segmental necrotizing glomerulonephritis. In most of these cases, there is the formation of pauci-immune growth which manifest as hematuria, proteinuria and renal failure. Most patients with renal involvement develop ESRD within a median of 2 months after starting therapy [19]. Female sex, black ethnicity and severity of renal involvement were identified as predictors of treatment resistance.  PET/CT is the most sensitive imaging to detect non-mass participation due to its functional and not purely anatomical nature [16]. Orbital manifestation is present in 60% of patients with GPA and even as an initial manifestation [17]. The patient presented here had a rare cardiac sign of GPA.  Only 3.3-15% of patients with GPA have cardiovascular involvement. Transthoracic echocardiography, followed by contrasted cardiac MRI is the most sensitive tools for detecting cardiovascular anomalies in patients with GPA [18]. MRI findings include granulomatous myocarditis, left ventricular dysfunction (EF<45) and Pericarditis [12]. There is also involvement in gastrointestinal, skin lesions, central nervous system and salivary glands.  It is essential to diagnose and treat this disease early. GPA is untreated has 1-year mortality of up to 80% and a 2-year rate of 90% [11].  The purpose of this case report is to discuss the presentation, clinical manifestations and treatment of a patient that had a rare display of Granulomatosis with Polyangiitis with cardiovascular involvement.

Methods

PubMed was used to search for articles related to the case. Keywords search in PubMed included “Granulomatosis with Polyangiitis,” “granulomatous inflammation,” “C-ANCA-associated vasculitis,” “antineutrophil cytoplasmic antibodies -associated,” and “pauci-immune glomerulonephritis.” A combination of twenty-two research articles, four case reports were reviewed that spanned twenty-six years (from 1991 to 2017) of academic knowledge and reported data. All items in written languages other than English were excluded from the review, and those used are cited in the reference section. All clinical information specific to this patient’s presentation was obtained from patient medical records and clinical encounters.

Case Report

The patient is a 69-year old Caucasian male with a past medical history of anemia secondary to hemorrhoids, Gastroesophageal Reflux diseases who presented to the Emergency Department with shortness of breath, and dyspnea.  The patient received flu shot earlier in the year and denied any sick contact at home. He is a non-smoker with no secondhand smoke exposure. The patient had no history of asthma. Of note, he has had progressive fatigue for the last few months and was worked up for iron deficiency anemia. He was placed on oral iron supplements by his primary care provider. He had a colonoscopy two years prior with no abnormal findings. Two weeks earlier, the patient developed cough and dyspnea on the exhaustion that was diagnosed with bronchitis. He was placed on Doxycycline antibiotics. His fatigue progressed to shortness of breath at rest which prompted him to come to the Emergency department.

In the Emergency Department, he was found to be hypoxemic with oxygen saturation of 85%. He was given 4 l/min of Oxygen and was admitted with an oxygen saturation of 99%.  On admission, his temperature was 100.3 F (37.9C), blood pressure was 76/51 mm Hg, pulse was 76 beats/ min, respiratory rate was 20 breaths/min, and his BMI was 27. On physical exam, he had decreased breath sounds bilaterally at the base of his lungs and rhonchi was heard at mid to lower right lung. He was alert and oriented to person, place, and time. He had transparent tympanic membranes with positive light reflex. His eyes were sclerae anicteric. The neck was supple with no meningeal sign and trachea was midline. He had regular rhythm; healthy S1/S2 heart sounds with no murmur, no rubs. He had active bowel sounds, soft nontender, non-distended abdomen and no organomegaly was detected. His musculoskeletal exam showed no dynamic joint deformities. The integumentary review showed stable rash on the trunk and no induration on extremities.

His labs showed acute kidney injury on with creatine of 3.2. Chest X-ray findings included extensive bilateral pulmonary infiltrates present, more extensively noted on the right. With a history of elevated white blood cell count and fever, it is likely extensive pneumonia. Laboratory studies are included in the table below.

Table 1: Laboratory studies

Result Value Ref Range               WBC 14.98 (H) 4.80 – 10.80 10*3/µL               Hemoglobin 7.9 (L) 13.5 – 17.1 g/dL               Hematocrit 24.4 (L) 41.0 – 51.0 %               Platelets 276 150 – 350 10*3/µL               BUN 63 (H) 5 – 25 mg/dL               Glucose, Bld 102 65 – 140 mg/dL               Creatinine 3.2 (H) 0.5 – 1.5 mg/dL               Calcium 8.0 (L) 8.1 – 10.2 mg/dL               Total Protein 5.6 (L) 6.4 – 8.2 g/dL               Albumin 2.0 (L) 3.2 – 5.0 g/dL             Troponin I             Result Value Ref Range               Troponin I <0.015 0.000 – 0.045 ng/mL             Result Value Ref Range               BNP 199.6 (H) 0 – 100 pg/mL

 

 

 

EKG showed normal sinus rhythm, no ST elevation, anterior Q waves and T wave inversion in aVL. Negative hepatitis B and HIV test. The differential diagnosis was admission diagnosis was Pneumonia and Acute Kidney Injury (AKI). The patient was started on Amoxicillin/clavulanate two g/125 mg twice daily in addition to doxycycline. He was given fluids and monitored closely. For the next three days, the patient’s renal and pulmonary condition deteriorated. The patient developed hematochezia and thrombocytopenia with a platelet of 66 10*3/µL.  Nephrology and gastroenterology were consulted.

On the fourth day, the patient had laboured breathing and reported dyspnea at rest — respiratory rate 29 per minute. Physical exam revealed Basilar crackles on auscultation noted throughout the lungs — reports occasional cough with blood-tinged phlegm output. PRN Nebulizer treatment given was given, which provided dyspnea relief at the time. Oxygen Saturation was 92% on 6L Oxygen. He had a BUN of 118, and creatinine of 6. Physical examination revealed +2 pitting edema in his bilateral lower extremities, regular rhythm, normal S1/s2 heart sounds, no murmurs, no rubs. He developed Atrial fibrillation with RVR, and he became tachycardic with a heart rate of 150 BPM. An IJ tunnelled dialysis catheter was placed for hemodialysis dialysis due to worsening renal function (creatine of 6). He received IV metoprolol 5 mg and then- 25 mg twice daily. Cardiology consultation was requested due to new onset of Atrial fibrillation with a rapid ventricular response. His CHADS-2 VASC score is 2 (due to age/ HTN). However, given his severe anemia, and unexplained bleeding (rectal bleeding) thrombocytopenia – he was not a candidate for anticoagulation. The patient was given one dose of IV Lopressor 5 mg and metoprolol 25 mg every 12 hours of withholding parameters. 2-D Echocardiogram revealed mildly reduced LV function (EF- <35%), mid and distal anteroseptal hypokinesis (Not seen in the previous echo). Mild LVH, moderately enlarged left atrium, mild MR, aortic valve sclerosis without aortic stenosis or regurgitation. Mild TR, RVSP is 38. No evidence for pericardial effusion. His Troponin I was 0.096 then increased 0.125, which may be due to renal insufficiency/ demand ischemia.

On the seventh day, he developed epistaxis. The hematocrit of 20.9 and Hemoglobin of 6.7. He had a positive POBT. He receives two units of packed RBC. His BNP increased to 572.7 pg/mL, Albumin decreased to 1.9 g/dL, and his oxygen saturation was 95% on 4L nasal cannula. Troponin <0.015, BNP: 572.7, PROTIME: 16.4, INR: 1.4. EKG showed A fib with RVR, heart rate of 128 BPM, delayed R wave progression, low voltage QRS, with nonspecific ST T changes. His physical exam showed +2 pitting edema, basilar crackles in lower lobes and stable rash on his trunk. Neck JVP was <8cm, and no masses were palpated. His chest had central line present (for dialysis) with clean and patent portal of entry. Cardiovascular auscultation has an irregularly irregular rhythm with S1 and S2. A systolic murmur, 2/6 was heard at the apex. Other physical exam findings were within normal limits. Repeat CT of the chest showed persistent extensive bilateral alveolar and interstitial pulmonary opacities with some areas improving and some other areas worsening. There were persistent extensive bilateral centrilobular mixed alveolar and interstitial pulmonary opacities with some interval improvement in the right upper lobe but with worsening in the lingula and left lower lobe. CT guided kidney biopsy and cultures were obtained. Serum cytoplasmic antineutrophil cytoplasmic autoantibody (C-ANCA) levels and other biological markers were ordered.   The serum PR3-ANCA level was elevated to 27.0 U/mL (normal, <3.5 U/mL). Urine analysis showed hematuria (3+) and proteinuria (2+). Renal biopsy histopathological revealed pauci- immune crescentic glomerulonephritis, ANCA positive vasculitis (Figure 1). Based on these findings and patient clinical manifestations (renal involvement, pulmonary involvement and cardiac involvement), he was diagnosed with Granulomatosis with Polyangiitis.

Figure 1: Lionaki, S., &Boletis, J. N. (2015). Glomerulus from a patient with PR3-Anca pauci-immune crescentic glomerulonephritis showing remarkable fibrinoid necrosis surrounded by crescent formation. Retrieved fromhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4934804/#B51

Treatment/ Patient Management

Following the diagnosis of GPA, he was treated with intravenous pulses of methylprednisolone (7 mg/kg body weight for three consecutive days), followed by 40 mg of prednisone for two weeks. Within days of treatment, the dramatic improvement was seen. For the acute kidney failure with fluid overload in the setting of newly diagnosed crescentic glomerulonephritis, he started hemodialysis. Rheumatology was consulted, and he was placed on Rituximab, a chimeric monoclonal antibody directed against the CD20 antigen of B lymphocytes. The two indications that warrant the use of plasma exchange in the inductive phase of treatment include pulmonary hemorrhage and severe renal dysfunction at clinical presentation (serum creatinine >500 μmol/l) [10]. The patient had severe renal dysfunction and received of Plasmapheresis and Epogen. He had iron infusion and folate supplement for his anemia. He had blood transfusion throughout his admission with Hemoglobin goal >7. Gastroenterology followed the patient for anemia and a history of hemorrhoid rectal bleeds. He was placed on Protonix 40 mg BID. For his cardiac involvement, he continued metoprolol 25 mg twice daily. He was discharged on the 13th day of admission. The patient was placed on a disease-modifying therapy regimen, including azathioprine and prednisone, and would be followed by rheumatology, pulmonology, cardiology, nephrology and his primary care provider.

Discussion and Conclusion

The IgG class ANCA activity on proteinase 3 (PR3) of neutrophils and monocytes is responsible for the vascular damage by activating excessive neutrophil and facilitating the destruction of the vessel wall [7]. This damage leads to glomerular sclerosis, fibro cellular crescents and interstitial fibrosis. PR3-ANCA is associated with granulomatous inflammation, more extensive extrarenal involvement, and a higher relapse rate. There are various environmental factors related to the pathogenesis of GPA. Microbial factors through mimicry of host antigens can initiate an autoimmune response [8]. Also, T cell-mediated immune response plays a role in the pathophysiology of GPA. CD4+ helper T cells with interferon-gamma secretion and T cell-mediated response are involved in granuloma formation [8]. Also, TH17 cells are critical in the creation of granulomatous inflammation and vascular injury in PR3 AAV [9]. The pathophysiology of these diseases is multifactorial, involving environmental factors and cell-mediated responses.

The standard of care in patients with GPA includes an induction phase with high dose corticosteroids, Rituximab, a chimeric monoclonal antibody directed against the CD20 antigen of B lymphocytes, and Cyclophosphamide. Patients with pulmonary hemorrhage and severe renal dysfunction at clinical presentation (serum creatinine >500 μmol/l) may require Plasmapheresis, as seen in this patient [10]. High dose glucocorticoid therapy is associated with glucose intolerance, infection, and osteoporosis. Myelosuppression, Myelodysplasia, lymphoma, skin cancer and hemorrhagic cystitis can occur in 10% of patients on cyclophosphamide. Also, long term cyclophosphamide use is associated with bladder cancer rate has been estimated at 5% in 10 years and at 16% in 15 years [19].

The diagnosis of Granulomatosis with Polyangiitis is often tricky and challenging. It is crucial to have detailed patient history, thorough physical exam, organ biopsies, imaging and other histological findings to make a proper diagnosis. The patient who presents with constitutional symptoms or inflammation with antibiotic failure should prompt a high degree of suspicion for vasculitis. It is essential to identify this disease early and give adequate treatment. Although upper respiratory, lower respiratory and renal involvement is the most common, it is necessary to watch out for other less common organ involvement and the manifestation of the disease.

These patients would need an interdisciplinary medical team approach to manage and maintain this disease.  The Interdisciplinary team should include Nephrology, Cardiology, Rheumatology, Pulmonology and Primary care. Other specialists may be required in cases that involve vascular, ear, nose, and throat for more focused management.

  References:

1. Falk RJ, King Jr TE, Stone JH. Clinical manifestations and diagnosis of granulomatosis with polyangiitis (Wegener’s) and microscopic polyangiitis. 2013:15. Available at:

www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-granulomatosis-with-polyangiitis-wegeners-and-microscopic-polyangiitis?.

2. Frankel SK, Cosgrove GP, Fischer A, Meehan RT, Brown KK. Update in the diagnosis and management of pulmonary vasculitis. Chest, 2006; 129(2): 452–465. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16478866
3. Berden AE, Ferrario F, Hagen EC, Jayne DR, Jennette JC, Joh K. et al. Histopathologic classification of ANCA-associated glomerulonephritis. J Am Soc Nephrology. 2010;21(10):1628–36. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20616173
4. Kosovsky PA, Ehlers KH, Rafal RB, Williams WM, O’Loughlin JE, Markisz JA. MR imaging of cardiac mass in Wegener granulomatosis. J Comput Assist Tomogr. 1991;15(6):1028–30.
5. Lutalo P, Cruz D. Diagnosis and classification of granulomatosis with polyangiitis (aka Wegener’s granulomatosis). J Autoimmune 2014; Volume 48-49: 94-98. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24485158
6. Comarmond C, Cacoub P. Granulomatosis with polyangiitis (Wegener): Clinical aspects and Conference Autoimmun Rev 2014; 13: 1121-1125. Available at: https://www.ncbi.nlm.nih.gov/pubmed/25149391
7. Van der Woude FJ, Rasmussen N, Lobatto S, et al. Autoantibodies against neutrophils and monocytes: a tool for diagnosis and marker of disease activity in Wegener’s granulomatosis. Lancet. 1985;i:425–429. Available at: https://www.ncbi.nlm.nih.gov/pubmed/2857806
8. Kain R., Exner M., Brandes R., et al. Molecular mimicry in pauci-immune focal necrotizing glomerulonephritis. Nature Medicine. 2008;14(10):1088–1096. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18836458
9. Lamprecht P., Wieczorek S., Epplen J. T., Ambrosch P., Kallenberg C. G. M. Granuloma formation in ANCA-associated vasculitides. APMIS. 2009;117(127). Available at:

https://www.ncbi.nlm.nih.gov/pubmed/19515137

10. Nachman PH, Hogan SL, Jennette JC, et al. Treatment response and relapse in antineutrophil cytoplasmic autoantibody-associated microscopic polyangiitis and glomerulonephritis. J Am Soc Nephrology. 1996;7:33–39. Available at:

https://www.ncbi.nlm.nih.gov/pubmed/8808107

11. Gal AA, Velasquez A. Antineutrophil cytoplasmic autoantibody in the absence of Wegener’s Granulomatosis or microscopic polyangiitis: implications for the surgical pathologist. Modern Pathology. 2002;15(3):197-204. Available at:

https://www.ncbi.nlm.nih.gov/pubmed/11904336

12. Puget G, Gouya H, Puéchal X, Terrier B, Kahan A, Lehmann P, et al. Cardiac involvement in granulomatosis with polyangiitis: A magnetic resonance imaging study of 31 consecutive patients. Rheumatology 2017; 56(6): 947-956
13. Lynch JP, Tazelaar H. Wegener Granulomatosis (Granulomatosis with Polyangiitis): Evolving Concepts in Treatment. Semin Respir Crit Care Med 2011; 32: 274.297. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21674414
14. Martinez F, Chung JH, Digumarthy SR, Kanne JP, Abbott GF, M, Jo-Anne O, Shepard J-A O, et al. Manifestations of Wegener Granulomatosis at Chest CT: Radiologic- Pathologic Correlation. Radio Graphics 2012; 32: 51-69. Available at:

https://www.ncbi.nlm.nih.gov/pubmed/22236893

15. Soussan M, Abisror N, Abad S, Nunes H, Terrier B, Pop G, et al. FDG-PET/CT in patients with ANCA associated vasculitis: Case-series and literature review. Autoimmunity Reviews 2014;13: 125-131.
16. Muller K, Lin JH. Orbital granulomatosis with polyangiitis (Wegener granulomatosis): Clinical and pathologic findings. Arch Pathol Lab Med 2014; 138: 1110-1114. Available at: https://www.ncbi.nlm.nih.gov/pubmed/25076302
17. Puget G, Gouya H, Puéchal X, Terrier B, Kahan A, Lehmann P, et al. Cardiac involvement in granulomatosis with polyangiitis: A magnetic resonance imaging study of 31 consecutive patients. Rheumatology 2017; 56(6): 947-956. Available at: https://www.ncbi.nlm.nih.gov/pubmed/28339663
18. Lee T, Gasim A, Derebail VK, et al. Predictors of treatment outcomes in ANCA-associated vasculitis with severe kidney failure. Clin J Am Soc Nephrol. 2014;9:905–913.

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