|
 
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| REVIEW ARTICLE |
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| Year : 2021 | Volume
: 1
| Issue : 1 | Page : 1-8 |
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The under-explored side of diabetes mellitus: Rheumatic manifestation
Sukdev Manna1, Ravi Kant2
1 Department of Clinical Immunology and Rheumatology, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
2 Department of Internal Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
| Date of Submission | 22-Dec-2020 |
| Date of Decision | 09-Mar-2021 |
| Date of Acceptance | 30-Apr-2021 |
| Date of Web Publication | 18-May-2021 |
Correspondence Address:
Dr. Ravi Kant
Department of Internal Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand
India
 Source of Support: None, Conflict of Interest: None  | 1 |
DOI: 10.4103/JCDM.JCDM_7_20
Immune-mediated musculoskeletal (MSK) manifestation is one of the most prevalent phenotypes of rheumatic disorders. Diabetes Mellitus (DM), the modern epidemic, acts as a great mimicker of rheumatic diseases in terms of MSK involvement. Numerous attempts have been made in various strands of scientific research to identify the level of association of these disorders with DM but unfortunately, the results are not uniform. In daily clinical practice, it is sometimes difficult to differentiate diabetes-related joint and muscle problems from pure rheumatic disorders without proper background knowledge. Rheumatic manifestations often amplify the magnitude of diabetes-related morbidities. In the modern era, treating the primary disease is often not sufficient; we need to go further ahead to tackle its long-term complications also to mitigate the suffering of patients. The identification and management of diabetes-related rheumatic problems in the ocean of rheumatology needs sufficient evidence-based knowledge, expertise, as well as clinical experience. In our article, we intend to discuss various MSK problems related to diabetes, their pathogenesis, clinical features, important clues for diagnosis, and overall management strategies. Keywords: Diabetes mellitus, musculoskeletal manifestations, rheumatic manifestation
How to cite this article:
Manna S, Kant R. The under-explored side of diabetes mellitus: Rheumatic manifestation. J Cardio Diabetes Metab Disord 2021;1:1-8 |
| Introduction | |  |
The normal human body is an example of perfect homeostasis, and everything here lies in a controlled equilibrium. A minor alteration in this homeostasis is easily compensated, but significant alterations for a prolonged period lead to chronic organ-specific disorders. DM, with its complex interplay between chronic hyperglycemia, abnormal serum insulin level, and secondary metabolic abnormalities, can lead to various local and systemic disorders, of which rheumatic problems encompass a significant proportion. The spectrum of MSK disorders in rheumatology ranges from a mere single-joint problem to severe multi-organ dysfunction. Although a direct association between DM and rheumatic diseases is still a matter of debate, often these two disorders come closer in daily clinical practice. Diabetes contributes significantly toward the development of various MSK problems; similarly, therapy-related dysglycemia is a common happening in rheumatology. Fortunately, most of such rheumatic problems occurring in DM could easily be diagnosed with proper clinical evaluation through detailed history taking and a thorough clinical examination. The early recognition of such rheumatic problems when they are still reversible, to some extent, could help the clinician to start specific therapy for ongoing problems as well as to adopt preventive measures to tackle their long-term sequelae. Even in established disease, a prompt clinical diagnosis would help us to introduce appropriate supportive care as well as to avoid unnecessary costly investigations that are often required in rheumatology practice. In this article, we would like to describe various rheumatic problems in DM, their level of association, and the proposed treatment protocols.
| Pathogenesis of Rheumatic Diseases in DM | | |
Chronic hyperglycemia, the core feature of DM, occurs as a result of various genetic as well as immune-mediated mechanisms, leading to absolute or relative insulin deficiency. Rheumatic diseases occur mostly because of disordered immune regulations. Till today, the causal relationship between diabetes and rheumatic diseases has not been proven with hundred percent certainty. Although the exact pathophysiology of such manifestations is still unknown, a few theories have been postulated for this purpose. Suboptimal diabetes control for a prolonged duration can lead to enzymatic and nonenzymatic glycosylation of various molecules, with the final result of an accumulation of advanced glycation end products (AGEs). Collagen cross-linking of such products followed by deposition in tissues accompanied by microvasculopathy and nerve injury is supposedly the principal contributor toward the development of various MSK and cutaneous features of diabetes.[1],[2],[3] Since these AGEs also contribute to the microvascular as well as macrovascular complications of diabetes, it is assumed that there is some temporal relationship between these complications of diabetes. A few rheumatic complications are considered intrinsic complications of DM, whereas in others DM is merely a predisposing factor.
| Prevalence | | |
The exact prevalence of MSK problems in DM is unknown because of the heterogenous study population across the globe, incomplete data reporting, different survey policies, etc. Despite conflicting pieces of evidence regarding the relationship of MSK problems with diabetic control,[4],[5] most studies have concluded that rheumatic problems are more prevalent in patients with poorly controlled diabetes of a longer duration. The estimated prevalence of each disorder will be provided separately in subsequent sections of the article.
| Spectrum of Rheumatic Manifestations in DM | | |
Rheumatic manifestations of DM are not restricted to the joint cavity, as shown in [Table 1].
Diabetic sclerodactyly
Diabetic sclerodactyly is characterized by a thickened waxy skin affecting mostly the dorsum of the hand with or without adjacent joints’ involvement without Raynaud phenomena, typical tapering, ulceration, calcinosis, and autoantibodies.[6] It is also termed as “pseudoscleroderma diabeticorum” because of the superficial resemblance with cutaneous manifestations of systemic sclerosis.[7] Histopathology examination of the involved area shows plenty of cross-linked collagen in the reticular dermis with the resultant thick dermis and small amounts of mucin deposition.[8] The exact prevalence of this entity is not known but it can occur in both insulin-dependent and non-insulin-dependent DM.[8] Studies regarding its association with the duration of diabetes and microvascular complications show conflicting results.[7],[8],[9] Another dermopathy, scleredema, a well-defined entity of waxy, indurated skin involving the posterior neck and upper back is often associated with non-insulin dependent diabetes mellitus (NIDDM) and obesity.[10] Treatment results are often not very encouraging; the options available are improving glycemic control, topical and intralesional glucocorticoids, low-dose methotrexate, prostaglandin E, and physical therapy.[11]
| Limited Joint Mobility | | |
Limited joint mobility (previously known as cheiroarthropathy) is a common complication of both type 1 and 2 DM, with prevalence ranging from 8% to 58%.[12] The deposition of abnormally cross-linked, hydrated collagen in the connective tissue around joints leads to the limitation of joint movement that is most marked in the small joints of the hands, resulting in poor grip strength, difficulty in fine movements and hand function. The proximal interphalangeal and metacarpophalangeal joints of all four fingers commonly show contractures with or without coexisting diabetic sclerodactyly, trigger fingers followed by less frequent involvement in the order of distal interphalangeal joints, wrists, elbows, shoulders, knees, feet, and the axial skeleton.[13],[14] Proposed contributing factors are the duration of DM, HbA1c level, associated microvascular complications, and neuropathy. Diagnosis is usually clinical and is based on simple bedside tests: The “prayer sign” and the “table top test” facilitate the recognition of contractures in the metacarpophalangeal, proximal interphalangeal, and distal interphalangeal joints. Goniometers to assess the range of joint movement, USG MRI, sensors, and electromagnetic tracking devices are usually used for research purposes to assess the extent of involvement.[14],[15] Optimum glycemic control, passive physiotherapy, injection of palmar tendon sheath with corticosteroid,[16] and smoking cessation protocol are usually advocated but results are often not very satisfactory.
| Adhesive Capsulitis (Frozen/Painful Stiff Shoulder/Periarthritis) | | |
Adhesive capsulitis is characterized by insidious onset, and it is a gradually progressive painful global limitation of both active and passive shoulder movement in all planes without major radiographic abnormalities apart from osteopenia. The usual patient profile includes the age related to the fifth to sixth decade, female>male, nondominant side>dominant side, predominant unilateral involvement, and evidence of secondary predisposing factors, that is, DM, dyslipidemia, Parkinson disease, thyroid disorder, and use of protease inhibitor. The prevalence of frozen shoulder in the general population and in the patient with diabetes is estimated to be 2% to 5% and 10% to 20%, respectively.[17],[18] A correlation between frozen shoulder and type 1 DM is more established than type 2 DM.[19] Whether the underlying pathology is primarily an inflammatory, fibrosing, or algoneurodystrophic process is still to be understood fully; however, the arthroscopic evaluation has suggested an initial inflammatory stage in and around the axillary fold of the joint capsule, the anterosuperior joint capsule, the coracohumeral ligament, and the rotator cuff interval with the end result of the development of adhesions and fibrosis of the synovial lining, thereby restricting joint mobility.[20],[21] Commonly described phases of the frozen shoulder include an initial, painful phase with nighttime aggravation of symptoms, an intermediate phase with stiffness and severe loss of shoulder motion with relatively lesser pain symptoms, and a recovery phase with a gradual return of range of motion. Diagnosis is usually made by a comprehensive clinical evaluation and an injection test; joint imaging is usually performed to rule out other secondary pathologies. Apart from strict glycemic control, other treatment options are appropriate physiotherapy,[22] intra-articular injection of a corticosteroid, and surgical intervention in selected cases.[23]
| Calcific Periarthritis | | |
As the name suggests, calcific periarthritis is an inflammatory process involving periarticular structures (tendons, tendon sheaths, capsules, and bursae) resulting from local deposition of basic calcium phosphate. The factors responsible for such abnormal crystallopathy are local trauma, end-stage renal disease-associated metabolic abnormalities, genetic factors, altered estrogen level, thyroid disorder, and DM. In a controlled study involving 824 patients, calcific periarthritis was found to be three times more common in patients with diabetes than in those without diabetes.[24] Long-standing, poorly controlled DM leads to altered cellular biomechanics, with activation of the inflammatory and noninflammatory downstream pathway. The composite outcome of such a multifactorial process is local tissue deposition of calcium crystals. The process can affect larger joints such as the shoulder as well as smaller joints. Acute, subacute, and insidious onset pain is often felt in the surrounding areas but not at the true joint space and the associated limitation of movement is very common. Periarticular calcific cloud-like densities on the plain radiograph are diagnostic and in some difficult cases, we need to go for a USG scan, a CT scan, or an MRI for better delineation of crystal deposits at deeper tissues. Higher association of calcific periarthritis with DM, as described in previous literature, warrants investigations to rule out occult or symptomatic diabetes in such patients, especially in those with a strong family history. Management is usually supportive, that is, non-steroidal anti-inflammatory drugs (NSAID) for pain relief, physiotherapy and correction of underlying metabolic/endocrine abnormalities, and tight control of DM.
| Neuropathic Arthropathy (Foot and Ankle) | | |
Diabetic neuropathic (Charcot) arthropathy is a chronic, progressive, and destructive joint disorder. Although diabetes is the leading cause, a similar kind of arthropathy is seen in neurologic disorders, such as syringomyelia. Local trauma (major/minor) in a predisposed individual with diabetes-related micro- and macrovascular complications (neuropathy, vasculopathy) and metabolic bone disorders initiates a local inflammatory process (TNF alfa and IL 1 mediated), which together with abnormal weight-bearing leads to RANK-ligand-dependent and -independent bone resorption and osteoarthropathy. Accurate determination of the incidence of diabetic neuroarthropathy is often not possible because of biased study population sampling and lack of uniform diagnostic criteria. However, it seems to be rare in the general population with diabetes (<0.5% per year).[25],[26] Although variable, the usual clinical presentation is acute painless foot arthritis with unilateral warmth, redness, and edema, sometimes complicated with ulcerative skin lesions. In more rare instances, it may involve other joints such as the hand, wrist, and knee joint.[27] Classification of Charcot arthropathy by a modified Eichenholtz system has been described in [Table 2].
A high index of clinical suspicion in a patient with characteristic symptoms and physical and radiographic findings clinches the diagnosis easily after ruling out mimickers, that is, cellulitis, osteomyelitis, septic arthritis, gout, OA, and inflammatory arthritis. Apart from routine investigations and plain radiographs, some advanced investigations (CT, MRI, Bone Scan, and arthrocentesis) are sometimes necessary to establish the diagnosis in some special situation. A detailed evaluation of diabetic micro- and macrovascular complications is important in such patients. Management should involve a multidisciplinary team approach consisting of endocrinologist, rheumatologist, podiatrist, physiatrist, and surgeon. Treatment starts with optimal glycemic control, diabetic foot care, offloading through casting in the acute phase followed by gradual weight-bearing and surgical interventions in a selected group of patients.[28] Various agents have been tried to slow down bone turnover, such as bisphosphonates, calcitonin, etc., with limited success so they are not recommended for routine practice.
| Osteoarthritis | | |
OA is a degenerative, noninflammatory joint disorder that particularly affects weight-bearing large joints of our body, that is, knee joints, although it can occur as a generalized form in some cases. Much shreds of evidence are emerging day by day in favor of diabetes (type 2 > type 1) as a major contributing factor for cartilage damage in the pathogenesis of OA.[29],[30] Patients with OA are usually at the age of sixth to seventh decades, obese, and presenting with a noninflammatory type of arthritis, gelling phenomenon, and crackling sounds on joint movement. A plain radiograph of the affected joint in the weight-bearing position often demonstrates joint space asymmetric narrowing, osteophytes, loose bodies, and vacuum phenomenon. Altered pain sensation in diabetes due to peripheral neuropathy may sometimes complicate the natural course of OA, such as disproportionate symptom severity and accelerated disease progression. During the early stage, conservative management, that is, analgesics, quadriceps strengthening exercise, weight loss, and avoiding excess weight-bearing, suffices. Surgical interventions in the form of osteotomy, total knee replacement etc. are adopted in selected cases of severe disease or malalignment.[31] Intraarticular steroids and glucosamines are sometimes used for temporary symptom relief. Although the management plan is similar in a patient with or without diabetes, early aggressive glycemic control might provide a legacy effect in the prevention of early development of OA, at least theoretically.
| Dupuytren’s Contracture | | |
Dupuytren’s contracture is a progressive flexion deformity of digits because of fibrotic contracture and nodule formation in and around the palmar fascia. Various conditions have been reported to be associated with it, including racial and genetic factors, chronic liver disease, and diabetes. Diabetes is associated with 16–42% of the outpatient study population in various studies.[32] Long-standing diabetes in the elderly age group population has been more strongly linked to the development of Dupuytren’s contracture. It is important to differentiate it from similar-looking hand conditions, limited joint mobility [Table 3]. | Table 3: Differences between Dupuytren’s contracture and limited joint mobility
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The patient typically presents with a painful or painless thickening or a nodule in the palm and loss of motion of the affected finger. Treatment options are limited to modifying tools, intranodule corticosteroid injection, collagenase injections, percutaneous needle aponeurotomy,[33] prophylactic external beam radiation therapy, etc. which varies from patient to patient based on the facilities available.
| Trigger Finger (Stenosing Flexor Tenosynovitis) | | |
Tenosynovitis of the flexor tendon of the finger (trigger finger) is characterized by localized thickening of the flexor tendon or sheath, which thereby leaves a narrow space for the tendon to glide during the flexion and extension of fingers. The signature characteristics are localized palpable nodule formation and locking phenomenon. Females of the fifth and sixth decades are commonly affected. Systemic disorders commonly associated with trigger fingers are DM, rheumatoid arthritis, amyloidosis, etc. The fingers commonly affected are the ring finger, middle finger, and thumb. It can sometimes have bilateral involvement. Prevalence in people with diabetes is highly variable among studies: 5% of a series of 250 patients with type 1 diabetes aged 3 to 38 years,[34] 20% of 100 patients with type 1 or 2 diabetes aged 19 to 62 years,[32] and only 1.5% of 250,000 patients in a large insurance database.[32] The duration of diabetes is more strongly related to the prevalence of the trigger finger than overall metabolic control.[30] Multiple digital involvements were more common than nondiabetic controls.[35] The usual presentation includes painless or painful snapping, catching, or locking of one or more fingers during flexion or extension. Pain may be localized one over the volar aspect of metacarpophalangeal or sometimes radiate to the distal finger and palm. Gradually, the patient requires passive manipulation for finger movement, eventually leading to fixed flexion or extension posturing secondary to contracture. Typical history, demonstration of locking phenomenon, tenderness, and palpable localized nodules help to reach a clinical diagnosis. Treatment modalities usually offered to patients are activity modulation, NSAID for pain relief, splinting, local glucocorticoid injection into tendon sheath, and surgical release (USG-guided percutaneous or open).
| Rotator Cuff Tendinopathy | | |
Symptomatic rotator cuff tendon disorders, especially that due to supraspinatus tendinopathy, is a common cause of OPD visits for shoulder pain evaluation. It is more common among people with diabetes, and the prevalence increases steadily with age. Diabetes was found to be a major risk factor for rotator cuff tendinopathy in a case-control study of 5000 patients (adjusted odds ratios [OR] 1.77, 95% CI 1.20–2.61, and 1.66, 95% CI 1.48–1.87)[36] and a population-based study (hazard ratios [HR] 1.43, 95% CI 1.35–1.51, and 1.64, 95% CI, 1.53–1.75).[37] Surgical intervention is required early in people with diabetes than in the general non-diabetic population. The patient usually complains of localized pain over the lateral aspect of the deltoid during overhead activities. Evaluation starts with proper history taking, a local MSK examination of the shoulder joint, special provocative tests (The Neer and Hawkins-Kennedy tests), and supportive investigations (X-Ray, USG, MRI, etc.), which are performed to reach the diagnosis. Management strategy includes NSAID for pain relief, ROM exercise, physiotherapy, and local glucocorticoid injections. Patients with diabetes require early aggressive management to avoid operative interventions.
| Diabetic Muscle Infarction (Spontaneous Diabetic Myonecrosis) | | |
This is a rare vascular complication of long-standing, poorly controlled DM. It is characterized by acute or subacute onset of painful spontaneous ischemic necrosis of the skeletal muscle of the thigh and cuff region without any atheroembolism or occlusion of major arteries. Diabetes-related vasculopathic changes are often held responsible for such clinical conditions. However, the factors behind acute occlusion of arterioles and capillaries by fibrin are yet to be discovered. This condition can occur in both type 1 and type 2 DM, and multiple diabetes-related microvascular complications usually accompany diabetic muscle infarction.[38] The affected patient presents over weeks with acute onset of atraumatic unilateral or sometimes bilateral pain, swelling, and tenderness over the front of the thigh, back, and cuff area with or without constitutional symptoms. Usual laboratory investigation findings are elevated CPK-NAC, LDH, leukocytosis, and raised ESR. Gadolinium-enhanced MRI scans serve as diagnostic imaging tools of choice to differentiate infarcted muscle areas from surrounding healthy muscle. Spontaneous resolution of symptoms over weeks to months is a usual occurrence. During acute phase rest, analgesics (NSAID) and antiplatelet drugs have been tried with variable results.[38] Available limited data suggest that appropriate glycemic control is the best way to prevent such rare complications of DM.
| Carpal Tunnel Syndrome | | |
Carpal tunnel syndrome (CTS), the most common focal compressive mononeuropathy, is characterized by a constellation of signs and symptoms arising from compression of the median nerve at the carpal tunnel, which is usually due to secondary as well as numerous primary disorders such as obesity, diabetes, pregnancy, rheumatoid arthritis, hypothyroidism, connective tissue diseases, acromegaly, genetic predisposition, and drugs such as aromatase inhibitors, etc. Unilateral involvement is found to be more common than a bilateral presentation, with classical complaints of pain and paresthesia along with the distribution of the median nerve over the first three and radial aspect of the fourth digits. In advanced disease, a weakness for fine movement and sensory loss may be reported. Pain is often aggravated at nighttime, with sustained hand posture and repetitive wrist movement. Similar pathophysiology, by which limited joint mobility occurs due to diabetes-related connective tissue disorder, can also predispose to entrapment neuropathy. The duration of diabetes is much more important than metabolic control, nephropathy, and neuropathy for CTS to develop.[32] The reported prevalence of CTS in DM is around 20%, reaching up to 75% in those with limited joint mobility whereas diabetes is found to be associated with 6% to 17% of patients with CTS.[34],[39] According to a systematic review and meta-analysis, patients with both type 1 and type 2 diabetes were found to be equally at risk for the development of CTS.[40] Diagnosis is usually straightforward based on classical presentation. However, provocative tests are usually performed at the bedside, such as the Phalen maneuver, the Tinel test, the manual carpal compression test, and the hand elevation test. Digital X-ray wrist, USG wrist, and NCS EMG help the clinician to rule out various causes. Clinical and electrodiagnostic grading of CTS severity is given next[41] [Table 4].
Mild cases are managed conservatively with NSAID and wrist splinting. In moderate to severe cases, surgical decompression, local glucocorticoid injection into the carpal tunnel, etc. are often warranted.[42]
| Dish (Diffuse Idiopathic Skeletal Hyperostosis) (Ankylosing Hyperostosis, Forestier Disease, And Forestier-Rotes-Querol Disease) | | |
DISH is a noninflammatory symptomatic or asymptomatic spinal disorder associated with abnormal calcification and ossification of spinal ligaments and entheses. Although the cause of DISH is obscure till date, the hypothetical associations are mechanical factors, dietary contributions, drugs, environmental exposure, and metabolic conditions such as abnormal lipid profile, elevated IGF level, etc. Evidence on the association of DISH and diabetes is limited and conflicting. A recent review article described a positive association of DISH with metabolic abnormalities (abdominal obesity, type 2 DM, glucose intolerance, hyperinsulinemia).[43] A study involving 133 patients with diabetes and 133 nondiabetic controls showed an insignificant association of DISH with or without diabetes (12% versus 6.8%).[44] The thoracic spine is the most commonly affected site than the lumber or cervical area. Pain and spinal stiffness and restricted spinal mobility in DISH mimic inflammatory spondyloarthropathy. Flowing linear calcification and ossification along with the anterolateral aspects of the vertebral bodies, which continue across the disk space involving at least four contagious vertebral bodies without any evidence of sacroilitis, apophyseal joint involvement, are the usual findings on digital radiography of the spine. The NSAID for pain relief, graded physiotherapy, and the correction of underlying metabolic abnormalities are the mainstay of treatment. Surgical interventions are required in case of dysphagia due to cervical spur,[45] progressive myelopathy, and thoracic outlet syndrome. Although the association with diabetes is controversial, a good practice is to rule out diabetes, hyperinsulinemia, and abnormal lipid profile in patients with DISH.
| Bone Disorders | | |
Bony affection in diabetes is a multifactorial complex process that adds to the increased risk of fragility fracture. The bone mineral density (BMD) assessment by Dual Energy X-ray Absorptiometry (DEXA) scan may not reflect accurate results in a patient with diabetes; low in type 1 DM, normal or high in type 2 DM, yet increasing risk of fracture.[46] OHA such as thiazolidinediones and sodium-glucose co-transporter 2 (SGLT2) inhibitors are associated with increased fracture risk. In addition to an individualized approach to improve glycemic control, lifestyle modifications, anti-resorptive and anabolic therapy should be started in an appropriately selected patient.
| Pain Disorders | | |
Fibromyalgia syndrome (FMS) is a central pain processing disorder manifesting as bothersome and widespread MSK pain and tenderness. A systemic metabolic disorder such as diabetes can predispose individuals to such widespread myalgia. Lichtenstein et al. found a higher prevalence of diabetes in the FMS than the non-FMS group.[47] Pregabalin and duloxetine are approved medicines for the treatment of FMS.
DM and other endocrine disorders such as hyperthyroidism, hyperparathyroidism and metabolic disease such as IV hyperlipidemia have been described as important predisposing factors for complex regional pain syndrome (CRPS), a painful neuropathic condition with local dysautonomia.[48]
| Conclusion | | |
There is a scarcity of uniform data on rheumatic manifestations of DM. This article emphasizes the underlying pathogenesis, clinical spectrum, important clues for diagnosis, and the basic management plan of clinically relevant rheumatic manifestations of diabetes mellitus. This much of basic knowledge will help clinicians in their day-to-day clinical practice for better patient care. Although it is relatively easy to identify most of these disorders at bedside, management and overall prognosis is not very satisfactory. Additional scientific research and clinical discussions are needed to cope with such disabling manifestations of diabetes.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4]
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