Abstract
Objective
To report a case series of three patients with septic arthritis of the acromioclavicular joint and a review of the literature for this condition. Additionally, we developed an algorithm for diagnosing and treating septic arthritis of the acromioclavicular joint.
Methods
A retrospective review of patients treated at our institution for septic arthritis of the acromioclavicular joint during the collection period was performed and three cases were identified. A review of the English literature on this rare condition was also performed with only 28 cases being identified.
Results
A series of three consecutive patients were treated for septic acromioclavicular arthritis with resolution of the infection. Two patients underwent open surgical debridement and one underwent aspiration. All patients were treated with a minimum of six weeks of tailored intravenous antibiotic therapy.
Conclusion
Septic arthritis of the acromioclavicular joint can be difficult to diagnose and requires a high index of suspicion. Surgical debridement, open or arthroscopic, with tailored antibiotic therapy is an effective means for the management of septic arthritis of the acromioclavicular joint. In patients who are unable to have surgical debridement, aspiration and tailored antibiotics have been shown to be effective.
Keywords: septic arthritis, acromioclavicular joint, acromioclavicular arthritis, septic shoulder
Introduction
Septic arthritis of the acromioclavicular (AC) joint is a rare condition which has been described sparsely in the literature mostly through case reports and small case series. The diagnosis of this condition can be difficult and may be confused with degenerative AC arthritis or glenohumeral pathology. This disease is most commonly seen in patients with a preexisting immunocompromised state; however, it has also been reported in patients without any predisposing comorbidities.1–15 With an increasing number of patients with compromised immune systems from etiologies such as diabetes, drug abuse, cancer, and chemotherapy, this disease process may become more prevalent in the future. We present a case series of three patients along with a review of the literature and propose an algorithm for diagnosing and treating septic arthritis of the AC joint.
Methods
A retrospective review of patients treated at our institution for septic arthritis of the AC joint during the collection period from January 1, 2011, to December 31, 2016, was performed, and three consecutive cases were identified and included in this series. Inclusion criteria consisted of patients with confirmed septic arthritis of the AC joint diagnosed either by surgery or by aspiration. No patients presenting with septic arthritis of the AC joint were excluded. From October 3, 2017, to October 10, 2017, a review of the English literature on this rare condition was performed utilizing PubMed and OVID databases using the combinations of the terms “septic arthritis,” “acromioclavicular joint,” “AC joint,” “shoulder.” We excluded any literature that did not specifically discuss the AC joint. We identified 28 cases in 26 patients in the literature.
Approval for this study was obtained from the University of Oklahoma Health Sciences Center Institutional Review Board (IRB approval number 15134). Patient consent was waived for this study as all patient information was de-identified, and given the retrospective nature of this review, no additional radiographic or follow-up commitments were requested of the patients enrolled.
Cases
Case 1
A 34-year-old man with a history of uncontrolled diabetes mellitus presented to an outside emergency room with a one-day history of left shoulder pain. He denied any history of trauma. He was discharged from the outside emergency room with no treatment after X-rays were negative. He then presented to our emergency room three days after the onset of his symptoms with worsening left shoulder pain. He was febrile on evaluation. Laboratory evaluation revealed a white blood cell (WBC) count of 10,800/mm3 (normal 4000–11,000/mm3), erythrocyte sedimentation rate (ESR) of 27 (normal 0–15 mm/h), and C-reactive protein (CRP) of 174.9 mg/L (normal < 3 mg/L). His blood glucose was 260 mg/dL and hemoglobin A1c 7.5. The patient was subsequently discharged home that evening by the emergency room physician after blood cultures were obtained. He returned to the emergency room the following day when blood cultures were positive for Gram-positive cocci in clusters. He was admitted to the hospital on a medicine service, and intravenous (IV) vancomycin was started initially and then transitioned to Nafcillin after his blood cultures speciated methacillin-sensitive Staphylococcus aureus (MSSA). Piperacillin-tazobactam was then added on hospital day 3 after he failed to improve clinically on Nafcillin alone. An orthopedic consult was obtained on hospital day 3 because of concern for septic arthritis of the glenohumeral joint. On physical examination, the patient's shoulder was erythematous and warm with diffuse tenderness to palpation along the entire shoulder girdle with the most significant pain over the AC joint. Active motion of the shoulder was limited due to intense pain, and the patient had severe pain with cross-body adduction testing localized to the AC joint. Radiographs revealed widening of the AC joint (Figure 1). Magnetic resonance imaging (MRI) with gadolinium contrast showed increased signal within the AC joint extending into the subacromial space. There was diffuse deltoid myositis and his rotator cuff was noted to be intact. There were no findings of synovitis or any significant effusion of the glenohumeral joint to indicate any glenohumeral pathology (Figure 2(a) and (b)). A computed tomography (CT) scan was also obtained, which showed diffuse soft tissue edema, widening of the AC joint, and small periarticular erosions of the clavicle. He was subsequently taken to the operating room and underwent open irrigation and debridement of the AC joint with open distal clavicle excision with irrigation and debridement of the subacromial space. Postoperatively, his pain and lab values improved. Cultures obtained intraoperatively also grew MSSA. He was eventually discharged home on IV Nafcillin for six weeks.
Figure 1.
AP X-ray of left shoulder showing widening of the acromioclavicular joint.
Figure 2.
(a)–(f): axial (a) and coronal (b) left shoulder MRI of case 1 showing fluid within the left acromioclavicular joint with extension into the subacromial and subdeltoid space. Axial (c) and coronal (d) left shoulder MRI of case 2 showing fluid within the acromioclavicular joint with osteomyelitis of the distal clavicle and deltoid/supraspinatus myositis. Axial (e) and coronal (f) left shoulder MRI of case 3 showing fluid within the acromioclavicular joint.
Postoperatively, he struggled to regain range of motion and eventually returned to the operating room several months later for an arthroscopic lysis of adhesions and capsular release. At the time of the surgery, he was found to have some periarticular adhesions but mostly a clinical picture of a classic adhesive capsulitis perhaps more related to his uncontrolled diabetes than his prior infection. His glenohumeral cartilage was normal. After this procedure and with better control of his diabetes, he regained full motion and strength returning to work and athletics at one-year final follow-up.
Case 2
A 58-year-old man with a history of uncontrolled diabetes mellitus, hepatitis C, and intravenous drug abuse presented to an outside emergency room with a one-day history of left shoulder pain. He was diagnosed with cellulitis of his shoulder and treated with oral antibiotics and a methylprednisolone taper. He presented to our institution 10 days later with worsening left shoulder pain and failure to improve on oral antibiotics at which point an orthopedic consultation was obtained. He was afebrile on presentation. His labs revealed a WBC count of 18,300 (normal 4000–11,000/mm3), ESR of 66 (normal 0–15 mm/h), and CRP of 0.6 mg/L (normal < 3 mg/L). His blood glucose was 443 and hemoglobin A1c 14.5. Upon evaluation, he was unable to actively range his shoulder and would only allow approximately 40° of abduction with minimal passive internal and external rotation due to pain. He had significant tenderness to palpation at the AC joint. An MRI was obtained which showed increased signal within the AC joint, distal clavicle osteomyelitis, and myositis of the deltoid and supraspinatus muscles (Figure 2(c) and (d)). His rotator cuff was intact, and there was no significant fluid collection within the glenohumeral joint. He was taken to the operating room that evening and underwent an open irrigation and debridement and distal clavicle excision. Postoperatively, he was started on broad spectrum antibiotics with IV vancomycin and piperacillin-tazobactam. Endocrinology was consulted, and the patient was admitted to the intensive care unit and started on an insulin drip. Once his blood glucose normalized, he was transferred to the floor on oral diabetic agents and an insulin sliding scale. On postoperative day 3, the intraoperative cultures and blood cultures subsequently grew MSSA, and he was transitioned to IV Nafcillin. On postoperative day 5, he developed purulent drainage from his wound and was taken back to the operating room for a second irrigation and debridement. He was treated with six weeks of IV Nafcillin and then with an additional month of oral trimethoprim/sulfamethoxazole. Postoperatively, his range of motion improved with aggressive physical therapy, and at his one-year final follow-up, he had regained full range of motion when compared to the contralateral side.
Case 3
A 48-year-old man presented to our emergency room with a one-day history of left shoulder pain. His medical history included diabetes mellitus and acute myelogenous leukemia treated with a bone marrow transplant and was on immunosuppressant therapy after developing graft-versus-host disease. He denied any history of trauma or injury. On examination of the left shoulder, he had severely limited active motion and painful passive range of motion, especially with cross-body adduction testing. He had significant tenderness to palpation of the AC joint. He was afebrile on examination. His WBC was 4800/mm3 (normal 4000–11,000/mm3). CRP and ESR were not obtained upon presentation. Plain radiographs did not reveal any abnormalities. An MRI was obtained which revealed increased signal intensity and fluid collection in the AC joint. There was no significant fluid accumulation in the subacromial/subdeltoid space and no evidence of associated myositis. The rotator cuff was noted to have small chronic partial thickness tears in the supraspinatus and infraspinatus tendons (Figure 2(e) and (f)). The orthopedic service was consulted at this time, and an aspiration was performed with approximately 2 cc of purulent fluid being aspirated. The blood cultures and aspirate grew methicillin-resistant Staphylococcus epidermidis (MRSE). After aspiration, he was started on IV vancomycin and improved significantly in the hospital in regards to pain and range of motion. The Internal Medicine team determined that he was not an optimal surgical candidate. Given his rapid clinical improvement after aspiration and IV vancomycin, surgical intervention was not performed. He was treated with six weeks of IV vancomycin. At the conclusion of his treatment and at final follow-up at one year, he had relief of pain and had full range of motion of the shoulder with no radiographic signs of postinfectious arthritis.
Discussion
Septic arthritis of the AC joint is a very rare entity, as there are only reports of 26 patients with 28 cases of septic AC arthritis with this condition in the English literature (Table 1). This condition has been shown to occur more commonly in patients who are immunocompromised or engaged with high-risk behavior such as IV drug abuse. In the current literature, over 75% (20 of 26) of cases have been in patients with an immunocompromised state or high-risk behavior.1–14 This is comparable to our study in which all three patients were either immunocompromised or engaged in high-risk behavior (Table 2). The average age of the patients is 49.7 years (range: 17–79).1–14 The average duration of symptoms prior to presentation was 21.7 days.1–14 High suspicion for this condition is necessary for correct and early diagnosis of this condition which is crucial to prevent morbidity and mortality, as septic AC arthritis can be rapidly destructive.10
Table 1.
Literature review of septic acromioclavicular arthritis.
| Patient age | Sex | Time to presentation | Comorbidities | Side | Labs | Febrile | Imaging studies | Bacteria (cultured from AC joint) | Blood cultures | Treatment | Outcome |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Hong et al.15 | |||||||||||
| 53 | M | 7 days | Hypertension | L | WBC, ESR, CRP-elevated | Yes | X-rays normal. Ultrasound and MRI diagnostic | Culture negative | Haemophilus parainfluenzae | Aspiration and 1 month of IV cefazolin and gentamicin | Healed |
| Chiang et al.4 | |||||||||||
| 55 | F | 3 days | Multiple myeloma renal insufficiency | L | WBC-normal ESR and CRP-elevated | Yes | MRI diagnostic | Not reported | Positive (Streptococcus pneumoniae) | Arthroscopic I&D and open AC resection and eight weeks of IV linezolid | Healed |
| 55 (same patient as above) | F | 1 day | Multiple myeloma, renal insufficiency | R | WBC, ESR, CRP-elevated | Yes | Normal X-rays. MRI diagnostic | Not reported | Positive (Streptococcus viridans) | Open I&D w/DCE and six weeks of IV Ceftriaxone | Healed |
| 79 | F | 4 days | Hypertension, dementia | R | WBC-normal ESR and CRP-elevated | No | Normal X-rays | Group B streptococcus | Not reported | Aspiration and six weeks of IV Ceftriaxone | Healed |
| 65 | M | 7 days | Diabetes mellitus, gout, renal insufficiency | L | WBC, ESR, CRP-elevated | Yes | Normal X-ray, MRI diagnostic | Negative | Negative | Aspiration and four weeks of IV Nafcillin and Zosyn | Healed |
| Battaglia1 | |||||||||||
| 17 | M | 3 months (90) | None | R | NA | No | MRI | Ochrobactrum antropi | NA | Open I&D w/DCE and PO Cipro + Bactrim × two weeks | Healed |
| Widman et al.12 | |||||||||||
| 44 | M | 2 days | IVDU, diabetes mellitus, hemodialysis | NA | WBC-elevated | NA | Ultrasound w/aspiration | Staphylococcus aureus | NA | NA | NA |
| 41 | M | 8 months (240) | Lymphoma | NA | WBC-elevated | NA | Ultrasound w/aspiration | Streptococcus pneumoniae | NA | NA | NA |
| 51 | M | 2 days | IVDU | NA | WBC-elevated | NA | Ultrasound w/aspiration | Staphylococcus aureus | NA | NA | NA |
| 44 | M | 1 month (30) | IVDU | NA | WBC-elevated | NA | Ultrasound w/aspiration | Staphylococcus aureus | NA | NA | NA |
| 40 | M | 5 days | IVDU | NA | WBC-elevated | NA | Ultrasound w/aspiration | Staphylococcus aureus | NA | NA | NA |
| Blankstein et al.2 | |||||||||||
| 48 | M | 8 hours (h/o trauma 8 hours prior to presentation) | None | R | WBC-elevated | No | Plain radiographs showed widening | Streptococcus viridans | Negative | I&D with open AC resection and Penicillin (did not specify length) | Healed |
| Iyengar et al.8 | |||||||||||
| 42 | M | 2 days | None | L | WBC, ESR, CRP-elevated | NA | X-ray showed superior clavicle erosion. MRI diagnostic | Staphylococcus aureus | Positive | Aspiration with 6 weeks of IV Flucloxacillin + 8 weeks of Fusidic Acid | Healed |
| Hammel and Kwon6 | |||||||||||
| 68 | M | 6 hours | Diabetes mellitus | R | WBC and ESR-elevated | Yes | MRI diagnostic | None Obtained (attempted aspiration) | Positive (group B streptococcus) | 6 weeks of IV ampicillin | Healed |
| Martínez-Morillo et al.10 | |||||||||||
| 73 | M | 7 days | Cirrhosis and chronic renal failure | R | NA | No | Ultrasound | Staphylococcus aureus | Positive | Open I&D w/IV cloxacillin and PO cipro × 6 weeks | Healed |
| 46 | F | 7 days | Chemotherapy for disseminated breast cancer | R | NA | Yes | Ultrasound | Staphylococcus aureus | Positive | IV cloxacillin | Death at day 9 |
| 72 | M | 10 days | Chronic renal failure and alcoholism | L | NA | Yes | Ultrasound | Staphylococcus aureus | Positive | IV cloxacillin and PO cipro × 6 weeks | Healed |
| 52 | M | 4 days | Chronic renal failure | NA | NA | Yes | Scan | Streptococcus pneumoniae | Positive | Penicillin G IV and PO amoxicillin 8 weeks | Healed |
| 53 | M | 2 days | Diabetes mellitus | NA | NA | Yes | Scan | Streptococcus agalactiae | Positive | Penicillin G IV and PO amoxicillin × 8 weeks | Healed |
| 71 | M | 5 days | Chronic renal failure | R | NA | Yes | None | Staphylococcus aureus | Positive | IV cloxacillin | Death |
| Corey et al.14 | |||||||||||
| 42 | F | 11 days | Obesity | L | WBC, ESR-elevated CRP-normal | No | MRI and CT | Staphylococcus aureus | Negative | Sugical I&D and IV vanc, transition to PO clinda × 5 weeks | Healed |
| Noh et al.11 | |||||||||||
| 63 | M | 3 days | Diabetes mellitus | L | WBC, ESR, CRP-elevated | Yes | X-ray showed widened AC w/bony erosion. MRI diagnostic | Staphylococcus aureus | NA | Scope I&D and DCE. IV ceftriaxone × 6 weeks | |
| Carey et al.3 | |||||||||||
| 60 | F | 7 days | Hypertension | L | WBC-normal ESR and CRP-elevated | No | X-ray w/AC degenerative change, MRI diagnostic | Haemophilus parainfluenzae | NA | Surgical I&D. PO levofloxacin × 2 weeks | Healed |
| Hashemi-Sadraei et al.7 | |||||||||||
| 43 | M | 5 days | Endocarditis | Bilateral | WBC, ESR, CRP- elevated | No | Normal X-ray. Ultrasound diagnostic | Streptococcus pneumoniae | Positive | Surgical I&D and ceftriaxone × 4 weeks | Healed |
| Zimmerman et al.13 | |||||||||||
| 25 | M | 4 months (120) | AIDS | L | WBC-normal | Widening and bone loss on X-ray. Increased uptake on gallium scan | Staphylococcus aureus | NA | Surgical I&D and ciprofloxacin × 3 months | Healed | |
| Cone et al.5 | |||||||||||
| 63 | M | 7 days | Diabetes mellitus | L | NA | Ultrasound, MRI diagnostic | Staphylococcus aureus | Positive | I&D and DCE × 2 with oxacillin × 6 to 9 weeks | Healed | |
| Laktasic-Zerjavic et al.9 | |||||||||||
| 44 | M | 6 days | Diabetes mellitus | L | WBC-elevated | Yes | Ultrasound and Tc99 scan | Staphylococcus aureus | Positive | IV cloxacillin and gentamicin × 6 weeks | Healed |
I&D: irrigation and debridement; WBC: white blood cell; IV: intravenous; CRP: C-reactive protein.
Table 2.
Case series of septic acromioclavicular arthritis.
| Age | Sex | Time to presentation | Comorbidities | Side | Labs | Febrile | Imaging studies | Bacteria (culture from AC joint) | Blood cultures | Treatment | Outcome |
|---|---|---|---|---|---|---|---|---|---|---|---|
| 34 | M | 3 days | Diabetes mellitus | L | WBC, ESR, CRP-elevated | Yes | X-rays showed widening. CT showed periarticular erosions. MRI diagnostic for septic AC arthritis | MSSA | Positive | Open surgical I&D with DCE. IV Nafcillin × six weeks | Healed. Required arthroscopic lysis of adhesions several months later |
| 58 | M | 10 days | Diabetes mellitus, hepatitis C, IVDU | L | WBC, ESR-elevated, CRP-normal | No | X-rays normal. MRI diagnostic for septic AC arthritis, distal clavicle osteomyelitis, deltoid/ supraspinatus pyomyositis | MSSA | Positive | Open surgical I&D with DCE. Required repeat open I&D on postoperative day 2. IV Nafcillin × 6 weeks followed by one month of trimethoprim /sulfamethoxazole | Healed |
| 48 | F | 1 day | Diabetes mellitus, acute myelogenous leukemia on immunosuppressants | L | WBC-normal | No | X-rays normal. MRI diagnostic for septic AC arthritis | MRSE | Positive | Aspiration and 6 weeks of IV vancomycin | Healed |
AC: acromioclavicular; MSSA: methacillin sensitive Staphylococcus aureus; MRSE: methacillin resistant Staphyococcus epidermidis; IVDU: intravenous drug use; WBC: white blood cell; DCE: dual channel endoscope; I&D: irrigation and debridement; ESR: erythrocyte sedimentation rate; CRP: C-reactive protein.
Physical examination findings for AC septic arthritis can be difficult to differentiate from glenohumeral septic arthritis, as patients will often have restricted painful shoulder motion with both active and passive motion. Patients will often have significant tenderness to palpation over the AC joint but may have diffuse tenderness because of surrounding myositis.3 Physical examination maneuvers that localize to the AC joint such as the cross-body adduction test are often strongly positive.1,3,4,8,13 Fever was documented in 13 of 19 cases in which it was reported.1–6,7,9–11,14
Laboratory studies play a key role in assisting with the diagnosis of an infection. The WBC count was elevated in 83% (19 of 23) of cases in which the WBC was reported. CRP level was elevated in 94% (15 of 16) of the cases in which it was reported. ESR was elevated in 94% (15 of 16) of the cases in which it was reported.2–4,6–14 Laboratory values should not be the primary diagnostic tool used, but rather should supplement other diagnostic criteria.
When concerned about AC septic arthritis, arthrocentesis is the gold standard for diagnosis as it provides rapid diagnosis and cultures of the infectious source.16 Often times, patients with septic AC arthritis present in a delayed manner and have received antibiotics which may affect the accuracy of arthrocentesis. The most common pathogen was Staphylococcus aureus (14 of 21). The second most common pathogen was Streptococcus pneumoniae (3 of 21). Other pathogens that have been reported include methicillin-resistant Staphylococcus epidermidis, Streptococcus pneumonia, Streptococcus viridans, Group B streptococcus, Ochrobactrum anthropi, and Haemophilus parainfluenzae.1–15 Patients with septic AC arthritis have been shown to have a high percentage of positive blood cultures.10 This suggests that there is often hematogenous spread and therefore we recommend blood cultures should be obtained.
In addition to arthrocentesis, imaging also plays a very important role in the diagnosis of this condition. Widening of the AC joint and erosion of the surrounding bone have been shown to be associated with this condition on X-rays.2,5,11 Ultrasound and MRI are imaging modalities that are more sensitive and specific than plain X-rays and provide an earlier diagnosis. As shown by Widman et al., ultrasound can be an effective tool for the diagnosis of septic AC arthritis.12 Widman et al. showed that distension of the AC joint is consistently seen on ultrasound in patients with this condition.12 Additionally, ultrasound can help guide aspiration of the AC joint which can be challenging to aspirate. MRI has been shown to be a key diagnostic tool in the literature. MRI has been shown to detect septic arthritis as early as 24 h after the onset of infection.17 MRI with gadolinium has been shown to have a high sensitivity and specificity for diagnosing septic arthritis, 100% and 77%, respectively; however, this study does not look specifically at the AC joint.18 MRI also provides detailed information about the involvement of the glenohumeral joint and surrounding myositis. MRI also can provide information on the presence or absence of concurrent osteomyelitis which can affect treatment and antibiotic management. We believe that MRI should be obtained in any patient for whom there is uncertainty about the diagnosis, as it can provide the physician with a correct differential diagnosis.
Once the diagnosis has been made, the appropriate treatment regimen must be determined. Septic AC arthritis has been effectively treated with surgical irrigation and debridement or aspiration of the AC joint followed by a course of IV or oral antibiotics.1–11,13–15 There have also been reports of successful treatment with IV antibiotics alone without surgery or aspiration.6,9,10 Surgical debridement, either arthroscopic or open, offers the most complete debridement of the AC joint and any subacromial or subdeltoid extension or associated pyomyositis. There is not adequate literature to determine if arthroscopic or open debridement is a better option. Distal clavicle excision at the time of surgery should be performed if osteomyelitis of the distal clavicle is suspected or if there is co-existent osteoarthritis. In patients who are not suitable surgical candidates, aspiration of the AC joint may be a good option. If aspiration is performed, the patient should be monitored, and if no improvement is seen clinically or with laboratory markers, then surgical irrigation and debridement should be considered. IV antibiotics should be used, as this provides better tissue penetration and after adequate control of the infection is obtained, transition to oral antibiotics is appropriate.19 The average duration of successful antibiotic management in the current literature is 5.9 weeks. This is comparable to our patients who were all treated with six weeks of IV antibiotics with resolution of the infection. There are currently no specific guidelines for the duration of treatment for septic arthritis.19 Given that a majority of patients with AC septic arthritis are immunosuppressed at baseline or present with co-existing osteomyelitis, we feel as though this constitutes a more complicated picture and therefore we recommend at least four to six weeks of antibiotics in patients with this condition.20 We prefer consulting infectious disease for recommendations on the choice of antibiotic and duration of treatment in order to maximize quality of patient care. Patient's comorbidities, such as glycemic control in diabetics, should also be managed to help eradicate the infection.
Based on our experiences and the current literature, we have developed an algorithm for the management of this condition which we believe would help physicians correctly diagnose and effectively treat this condition and hopefully prevent delay in diagnosis and treatment (Figure 3). This algorithm is based on our experience with a small case series and select group of patients; thus, further research utilizing our proposed algorithm in a larger patient population should be taken to confirm the effectiveness in the management of this condition.
Figure 3.
Algorithm for treating septic acromioclavicular joints.
Conclusion
In summary, septic AC joint arthritis is an infrequently diagnosed and rarely discussed disease process. It requires a high index of clinical suspicion coupled with laboratory values and advanced imaging studies to make the diagnosis. Treatment can consist of irrigation and debridement or aspiration of the AC joint followed by antibiotic management for at least four to six weeks with guidance from infectious disease if available. Management of the patient's predisposing comorbidities is imperative in eradicating the infection.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
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