Rheumatology

7 Rheumatology



The rheumatic diseases of childhood are a heterogeneous group of disorders usually manifested by signs and symptoms of inflammation. Although significant progress has been made in the understanding of the pathophysiology of these disorders, their etiologies remain largely unknown. Despite available laboratory markers, the cornerstones of diagnosis remain the history and physical examination. Knowledge of the natural history of these disorders is also helpful for diagnosis and management.


The majority of the common rheumatic diseases that occur during childhood are classified as inflammatory arthritis or enthesitis syndromes, connective tissue disorders, and vasculitides, although overlap does occur. Noninflammatory disorders that cause musculoskeletal pain include joint hypermobility syndromes and pain amplification syndromes. This chapter illustrates the more distinctive clinical features of these unique disorders.



Musculoskeletal History


A meticulous rheumatologic history is the foundation of accurate diagnosis (Table 7-1). The exact location that the patient complains about should be given careful attention. Muscle, bone, and tendon or ligament insertion pain (enthesitis) may be interpreted as joint pain unless the clinician asks specifically for the parent or child to describe the symptoms. Often it is helpful for the clinician to ask the child to point with one finger to the site of maximal discomfort.


Table 7-1 Distinguishing Features of the Rheumatologic History







The patient’s age and gender serve as initial guides to a possible etiology. The clinician must then try to discern whether musculoskeletal symptoms are inflammatory or mechanical. Pain that involves swelling, morning stiffness, warmth, redness, and improvement with movement is indicative of inflammation. Pain that is worse at the end of the day, worse with activity, and lacking persistent swelling is more mechanical in nature.


A history of prior illnesses, medications, immunizations, trauma, and bites, and the acuteness of symptoms, can be a clue to diagnosis. Joint pain (arthralgia) is a common symptom of childhood. However, the symptoms associated with inflammatory joint pain (arthritis) are uncommon in the pediatric population. In children with arthritis, the duration and pattern of the symptoms can be telling. Acute migratory arthritis affecting large and small joints is seen in acute rheumatic fever (ARF). Arthritis resolving within a few weeks is consistent with a reactive arthritis (i.e., Streptococcus, Epstein-Barr virus, parvovirus B19). An additive arthritis persisting for more than 6 weeks is consistent with a chronic form of arthritis (i.e., juvenile idiopathic arthritis [JIA]). The chronic arthritides cause indolent and persistent joint changes. Joint stiffness, or gel phenomenon, can be seen not only in the morning, but also after a child has napped or been immobile in a vehicle. As the day progresses, the child with chronic arthritis may become more limber and may even appear normal.


Differences in the quality and duration of arthritis exist among the various rheumatoid diseases. The arthritis in patients with systemic lupus erythematosus (SLE) may feature less swelling with more intense pain, whereas the arthritis of children with JIA is characterized by more stiffness and swelling and less pain. The joint pain of the patient with SLE may be intermittent in nature. The joint stiffness of JIA is usually a daily occurrence without treatment. The joints of ARF can also be distinguished from those of JIA by the presence of exquisite pain that is out of proportion to physical findings. A rapid response to nonsteroidal antiinflammatory drugs further supports a clinical impression of ARF.


A careful family history can be helpful. Children with an extensive family history of autoimmune diseases in their first-degree relatives are at slightly greater risk for developing a rheumatologic condition. Because these diseases are complex genetic traits, there is often little direct genetic linkage. Some diseases such as psoriasis, SLE, acute rheumatic fever, and autoimmune thyroiditis have a stronger genetic penetrance than other rheumatic diseases. Other conditions have little or no penetrance. A child with first-degree relatives with adult rheumatoid arthritis is not at increased risk for developing juvenile idiopathic arthritis.



Physical Examination of the Musculoskeletal System


The only way to confirm the diagnosis of JIA is to demonstrate arthritis by physical examination of the joints. The elucidation of joint inflammation by examination may be the only indication of a rheumatic disease. Because most joints are near the surface of the body, the examiner has an excellent opportunity to obtain significant information about many diseases. A rheumatologic diagnosis requires a thorough joint examination and meticulous general physical examination with special attention to the skin, mucous membranes, nail beds, and muscles.


The physical examination begins with observation of the child and parents walking from the waiting area to the examination room. The physician notes the general appearance of the patient and interactions among family members. Nutritional status and an incremental graph of height and weight must be carefully documented. Certain skin and mucous membrane changes provide valuable information (Table 7-2). Muscle strength must be evaluated first by attempting to elicit a Gowers sign (Fig. 7-1) and then by testing resistance capacity of individual muscle groups and grading them on a standard scale (Table 7-3).


Table 7-2 Mucocutaneous Signs of the Rheumatic Diseases







MCP, metacarpophalangeal; PIP, proximal interphalangeal.



Table 7-3 Standard Muscle Strength Grading
























Muscle Grade Description
5 Complete range of motion against gravity with full resistance
4 Complete range of motion against gravity with some resistance
3 Complete range of motion against gravity
2 Complete range of motion with gravity eliminated
1 Evidence of slight contractility; no joint motion
0 No evidence of contractility

The hallmark of a good physical examination of the musculoskeletal system is a careful examination of the joints, consisting of inspection, palpation, and measurement of each joint’s range of motion. The examiner should develop a standard order for examining joints and follow the same pattern so that no joints are missed. Large effusions are easily felt and often ballotable; synovial hypertrophy may be more subtle and has a doughy, spongy, boggy feel. Synovial outpouchings are common in children with arthritis and can resemble ganglion cysts, especially in the wrists and ankles. A ganglion cyst does not cause pain. In children with arthritis the findings may be subtle and often appreciated only because of pain or decreased range of motion.











Hip


The normal hip examination consists of 45 degrees of abduction and 20 degrees of adduction (Fig. 7-9) with the knee bent 20 degrees. The hip can extend 30 degrees, externally rotate to 45 degrees, and internally rotate to 35 degrees. An increase in lumbar lordosis may be the first sign of decreased hip flexion. Normally, hip flexion reaches to about 135 degrees (Fig. 7-10).







Leg Length


Leg length discrepancy (Fig. 7-14) is common in JIA because of hyperemia of an affected joint and subsequent overgrowth. Compensatory scoliosis may also develop.




Thoracic Spine/Lumbar Spine/Sacroiliac Joints


The entire spine including all spinous processes should be carefully palpated to elicit tenderness. Flexion, extension, and lateral motion of the spine should be measured, using S1 as the focal point. Thirty degrees of extension and 50 degrees of lateral motion are normal. Careful examination of the sacroiliac joints (Fig. 7-15) may give an important clue to the diagnosis of a spondyloarthropathy in an adolescent. Chest expansion, occiput-to-wall, and finger-to-floor measurements (Fig. 7-16) are useful in monitoring patients with inflammatory back disease. To detect limitation of forward flexion of the lumbar spine, the Schober test is quite useful. The patient is asked to stand erect, and the skin overlying the spinous process of the fifth lumbar vertebra (usually at the level of the “dimples of Venus”) and another point 10 cm above in the midline are marked. The patient is asked to maximally bend the spine forward without bending the knees. If the lumbar spine is mobile, the distance between the two points increases by 5 cm or more; that is, the distance between the two points becomes equal to or greater than 15 cm. An increase of 4 cm or less indicates decreased mobility of the lumbar spine.





Juvenile Idiopathic Arthritis


Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease in children. JIA is a broad term that is used to describe chronic arthritis in children. The group of diseases placed under the JIA rubric combines diverse entities, generally divided into seven categories: (1) oligoarthritis (persistent or extended), (2) polyarthritis (rheumatoid factor negative), (3) polyarthritis (rheumatoid factor positive), (4) enthesitis-related arthritis (ERA), (5) psoriatic arthritis, (6) systemic arthritis, and (7) undifferentiated arthritis. The JIA onset type is based on the disease presentation during the first 6 months of illness. The presenting subtype of JIA may differ from the child’s ultimate disease course. Of note, no laboratory tests, such as a positive anti-nuclear antibody or rheumatoid factor, are required to make a diagnosis of JIA.


The incidence of JIA is approximately 10 cases per 100,000 population per year. The prevalence of JIA is approximately 100 per 100,000 population. JIA in the United States is estimated to affect more than 300,000 children.


The first clear description of these entities was presented by George Still in 1897. He postulated multiple etiologies for childhood arthritis, and this concept is still supported today. All forms of JIA feature inflammation of the synovial tissue as one of the cardinal features. Synovium is usually hypertrophied, and joint effusions may occur. On physical examination (Fig. 7-17), joint swelling, loss of normal anatomical landmarks, tenderness, decreased joint mobility (Fig. 7-18), warmth, erythema, and joint deformity may be noted. It is typical for the child with JIA to have more joint stiffness than pain. Symptoms often develop gradually over a period of weeks or months before evaluation. Morning stiffness is often reported. The duration of morning stiffness correlates well with the degree of inflammation in children with JIA. Immobility and weather changes may exacerbate symptoms, although they have no impact on the underlying inflammatory component of the disease. Although arthralgia alone can be the initial presentation of JIA, the diagnosis cannot be confirmed without the presence of arthritis on physical examination.




Despite objective signs of arthritis, the patient with JIA may not experience pain. When inflammation persists for a long enough period of time, destruction of the articular surface and bony structures may occur (Fig. 7-19). Because of the poor regenerative properties of articular cartilage, these deformities are usually permanent. Fortunately, most cases of JIA are not associated with permanent joint deformity.









Systemic Arthritis


Systemic arthritis (Still disease) accounts for approximately 10% of all children with JIA. Fever, rash, irritability, arthritis, and visceral involvement dominate the clinical presentation. The patient’s temperature usually rises to greater than 39° C, and this often occurs twice daily in a double quotidian pattern. Chills are associated with fever, but rigors rarely occur. Although the late afternoon is a typical time for a temperature rise, many other patterns may occur. Other manifestations of systemic arthritis, such as rash and joint symptoms, may wax and wane during febrile periods. A helpful clinical feature during the febrile phase is one subnormal temperature during every 24-hour period, which suggests JIA.


The rash of JIA is macular, 2 to 6 mm in diameter, evanescent, and salmon or red in color, with slightly irregular margins (Fig. 7-21). An area of central clearing often exists. The rash usually occurs on the trunk and proximal extremities, but it may also be distal in distribution, with palms and soles affected. Although the rash generally does not produce discomfort, some older patients report pruritus. Superficial mild trauma to the skin, exposure to warmth, and emotional upset may precipitate the rash (Koebner phenomenon). Arthritis may not occur invariably at the onset of systemic arthritis, and thus the diagnosis may not be readily apparent. When fever of unknown origin is the sole initial presentation of systemic arthritis, it must remain a diagnosis of exclusion until the clinician observes inflammatory arthritis during the physical examination. Arthralgia and myalgia can be prominent early, as can hepatosplenomegaly and lymphadenopathy. Serositis, pleuritis, pericarditis, hyperbilirubinemia, liver enzyme elevation, leukocytosis, and anemia are supporting clinical features. About 50% of patients with systemic arthritis progress to having chronic inflammatory arthritis, which often is destructive (Fig. 7-22).





Extraarticular Manifestations


Patients with JIA are at risk of developing iridocyclitis (or uveitis). Although photophobia, eye pain, and erythema can occur, uveitis is often asymptomatic. For that reason, children with oligoarticular and polyarticular JIA must receive slit-lamp examinations frequently.


The first clinical sign of uveitis is cellular exudate in the anterior chamber. If the uveitis is left untreated, synechiae (adhesions) between the iris and lens may develop, leading to an irregular and poorly functioning pupil (Fig. 7-23). Further along in the clinical course, band keratopathy (calcium deposits in the cornea) (Fig. 7-24) may occur, as well as cataracts or glaucoma. For these reasons, strict adherence to the recommendations for eye examination outlined in Table 7-4 is necessary to help prevent visual loss in these children. Ophthalmologic complications do not parallel the activity of the arthritis.





Linear growth retardation may occur in the child with active JIA, especially with systemic or polyarticular disease. The degree of growth retardation and the ultimate prognosis for reaching adult height are related to the severity and duration of inflammation and the use of corticosteroids. Treatment with steroid-sparing agents such as nonsteroidal antiinflammatory drugs (NSAIDs), disease-modifying agents (i.e., methotrexate), and biologic agents (i.e., etanercept, adalimumab, and infliximab) is currently preferred compared with the heavy steroid usage of the past. Oligoarticular arthritis can present with bizarre growth abnormalities, usually confined to leg length discrepancy or an enlarged hand or foot related to refractory ankle or wrist involvement. During early illness, bony development may be advanced; later in the course of the illness the opposite may be true. Premature epiphyseal fusion may occur.


Cardiac involvement occurs in more than one third of patients with systemic arthritis. Pericarditis, myocarditis, and endocarditis occur, with pericarditis being the most common. Chest pain, a friction rub, tachycardia, dyspnea, and supportive chest radiograph, electrocardiogram, and echocardiographic findings may occur. These episodes may last for weeks to months and are usually associated with a generalized flare of disease. Various other extraarticular manifestations including hepatosplenomegaly and lymphadenopathy are particularly common in systemic arthritis.


Patients with systemic arthritis are at risk for developing a potentially fatal disorder called macrophage activation syndrome (MAS). Patients present with a toxic appearance, fever, hepatosplenomegaly, lymphadenopathy, and mucosal bleeding. If not recognized early, MAS can progress to hepatic failure, encephalopathy, and disseminated intravascular coagulation. Laboratory testing that supports a diagnosis of MAS includes evidence of hepatitis and coagulopathy. In addition, the white blood cell count, hemoglobin, and platelet counts are depressed with a normal or low sedimentation rate (Table 7-5). Diagnosis is confirmed by bone marrow aspiration demonstrating activated macrophages engulfing surrounding cells (Fig. 7-25).


Table 7-5 Characteristics of Macrophage Activation Syndrome in Patients with Systemic-onset Juvenile Idiopathic Arthritis







Modified from Cassidy JT, Petty RE: Textbook of pediatric rheumatology, ed 5, Philadelphia, 2005, WB Saunders.




Differential Diagnosis


Because JIA is a clinical diagnosis, strict clinical criteria have been established to make the diagnosis. Most authors suggest the presence of objective joint findings (arthritis) for a minimum of 6 consecutive weeks coupled with the exclusion of other causes of arthritis in children (Table 7-6).


Table 7-6 Differential Diagnosis of Juvenile Idiopathic Arthritis















Systemic Onset

Polyarticular Onset

Oligoarticular Onset


Because of its destructive nature, pyogenic arthritis (e.g., staphylococci, streptococci, Haemophilus influenzae) must be ruled out in any child with active joint disease, especially monoarthritis. The intensely red and tender joint should raise suspicion of a bacterial pathogen. This combined with systemic symptoms of infection (fever, chills, malaise, rigors) should prompt the clinician to perform an arthrocentesis early in the course of the illness.


Lyme arthritis can mimic oligoarticular JIA. This spirochetal form of arthritis is tick-borne and usually affects the knee, elbow, or wrist in a monoarthritic pattern with spontaneous exacerbations and remissions. Malaise, fever, myalgia, lymphadenopathy, headache, meningismus, and weakness also may occur in the first phase of the illness. The distinctive rash, known as erythema migrans (Fig. 7-26), begins as an erythematous macule or papule. After this clears, the borders of the lesion expand to form an erythematous circular lesion that can be as large as 30 cm in diameter. These lesions can initially occur singly but can progress to multiple lesions over the legs, arms, and trunk. Other manifestations of Lyme disease include neurologic complications such as seventh nerve palsy, meningitis, radiculoneuritis, and the cardiac manifestations of heart block and myopericarditis. Bilateral Bell’s palsy or seventh nerve paralysis even more strongly suggests the diagnosis of Lyme disease.



Other infections cause a reactive arthritis that dissipates in less than 6 weeks. Salmonella, Shigella, Yersinia, and Campylobacter organisms should also be considered. A multitude of viruses cause arthritis. These include rubella; hepatitis B; adenovirus; and herpesviruses including Epstein-Barr virus, cytomegalovirus, varicella zoster, and herpes simplex. Parvoviruses, mumps, and enteroviruses including echovirus and coxsackievirus are associated with acute polyarthritis and occasionally have been recovered from joints. Other viruses result in reactive arthritis and may not infect the joint directly.


Poststreptococcal phenomena include acute rheumatic fever (ARF) and poststreptococcal reactive arthritis. In ARF, Jones criteria are met. The child must be monitored for cardiac sequelae such as valvulitis and congestive heart failure. In poststreptococcal reactive arthritis, Jones criteria are not met. Arthritis will resolve but arthralgia can last for 6 months. The joint pain may be axial and affect the spine. In both cases, children are given prophylactic antibiotics to try and prevent future streptococcal infections.


Malignancies such as neuroblastoma and leukemia may present with musculoskeletal pain. More careful evaluation generally reveals bone pain. Sickle cell disease, particularly in the form of dactylitis, can have prominent digital involvement. Hemophilia, tuberculosis, and gonorrhea infection must be considered in the patient with arthritis. Differential diagnoses of JIA are proposed in Table 7-6.



Systemic Lupus Erythematosus


Systemic lupus erythematosus (SLE) is a multisystem auto-immune disease with a myriad of clinical presentations. SLE may present in an insidious fashion and hence escape early diagnosis, or it may present acutely and progress rapidly, leading to the patient’s demise. Frequently, children will present with nonspecific constitutional symptoms, such as fever, diffuse alopecia, weight loss, fatigue, and evidence of diffuse body inflammation with lymphadenopathy and hepatosplenomegaly. All organ systems have the potential to become involved, but the most common are skin, musculoskeletal, and renal systems in pediatric SLE (pSLE). As with other collagen vascular diseases, the etiology of SLE is unknown. Because of the large number of serologic markers known to occur in SLE, it is considered by many to be the prototype of autoimmune diseases. To increase diagnostic accuracy, the American College of Rheumatology (ACR) revised its classification criteria of lupus (Table 7-7). This classification, which combines clinical and serologic markers, is highly sensitive and specific for the diagnosis of this disease, reaching almost 100% sensitivity and specificity when 4 of the 11 criteria are present; however, the criteria are not meant for the clinical application of diagnosis and should be used as a study guide rather than applied to the clinical arena.


Table 7-7 Criteria for the Classification of Systemic Lupus Erythematosus*







* Four of 11 criteria provide a sensitivity of 96% and a specificity of 96%.


Any one item satisfies this criterion.


Modified from Hochberg MC: Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus, Arthritis Rheum 40:1725, 1997.


The word lupus, which means wolf, alludes to the erosive nature of the rash of SLE (“wolf bite”) (Fig. 7-27). This feature of the disease was critical to the diagnosis of SLE until the discovery of the lupus erythematosus (LE) cell in 1948. The LE cell represents a healthy neutrophil that has phagocytosed the nuclear debris of a nonliving cell that has been coated with antibody. The antibody is directed against deoxyribonucleoprotein (DNP), which is made up of both DNA and histones. The presence of this serologic marker for lupus greatly expanded the recognized clinical entity of SLE. Although the LE preparation has proved to be of historical interest, time has shown that it is a nonspecific immunologic phenomenon and has no specificity with respect to the diagnosis of SLE; hence, although it was included in the ACR 1982 criteria, it was not included in the ACR 1997 criteria.



SLE accounts for 10% of patients with rheumatic diseases and for less than 5% of children seen in pediatric rheumatology practices. The incidence is estimated at 0.5 per 100,000 children per year. From prevalence data, it has been inferred that there are between 5000 and 10,000 children with SLE in the United States. The disease is rare in children younger than the age of 5 years. Before menarche, the boy-to-girl ratio is equal. After menarche, the ratio of affected girls to boys approaches 8 : 1. African Americans and Asians are more commonly affected than the white population.


The incidence of other connective tissue diseases is higher among family members of patients with SLE. Hematologic malignancies and immunodeficiencies are also reported in increased frequency among the relatives of patients with SLE. These well-described phenomena may reflect a genetic alteration of immunity or, as some researchers suggest, the effects of a transmissible agent. The high incidence of the disease in girls supports the role of hormonal factors as contributing or modulating agents in the pathogenesis of SLE. Other investigators suggest the influence of viruses, sunlight, and emotional stress on those developing lupus.


Although immunologic markers contribute to making the diagnosis of SLE, a high index of suspicion is necessary to obtain these studies. The early symptoms are often nonspecific and sometimes go unrecognized as harbingers of serious disease. Fever, fatigue, malaise, anorexia, and weight loss may be the only symptoms. In the adolescent population these symptoms may be all the more difficult to interpret. Conversely, this multisystem disease may present with a plethora of physical findings and the presentation may be so dramatic that the diagnosis is readily apparent. The most common organ manifestations at disease presentation in pSLE are musculoskeletal, cutaneous, renal, and hematologic.


Cutaneous manifestations of SLE occur at some time during the course of the disease in 80% of affected individuals. There are a variety of cutaneous findings including a malar rash, photosensitive rash, palmar erythema (Fig. 7-28), annular erythema, vasculitic skin lesions with nodules or ulcerations, Raynaud phenomenon and associated ulceration, alopecia, and discoid lupus. Isolated discoid lupus is rarely seen in children, but when it occurs is usually without systemic manifestations. The same holds true for subacute cutaneous lupus, which is uncommon, presenting as a serpiginous-like photosensitive erythematous rash associated with positive SS-A (anti-Ro) antibody. The most frequent skin manifestations of SLE are malar rash and photosensitive rash. The classic malar or butterfly rash is a maculopapular rash distributed over the cheeks (malar eminences) and extending over the bridge of the nose, while sparing the nasolabial folds (see Fig. 7-27). The malar rash is photosensitive in 30% of the patients. In general, sun exposure may not only exacerbate the skin disease but also cause a systemic flare of disease, theoretically through large exposure of the immune system to intracellular proteins through massive apoptosis of damaged skin cells. Therefore, appropriate sun protection and avoidance is strongly encouraged. An annular photosensitive rash is frequently associated with the “Sjögren syndrome antibodies” anti-Ro (SS-A) and anti-La (SS-B). The typical morphology of the rash of lupus is defined as reddish purple and raised with a whitish scale (Fig. 7-29). When the scale is removed, the underlying skin often shows “carpet tack–like” fingers on the unexposed side of the scale itself. Carpet tacking is caused by the contouring of the scale into the skin follicles. These finger-like projections on a scale strongly suggest the diagnosis of lupus. Vasculitic rashes are more violaceous and may be associated with nodules, ulceration, and palpable purpura (Fig. 7-30). These lesions are commonly found in an acral distribution, and typically result in postinflammatory hyperpigmentation. Discoid lupus, although uncommon (5% to 10% of patients with pSLE), leaves the most damage with follicular plugging and scarring. Mucosal erosions and ulcers of the oral cavity and nasal mucosa are part of lupus as well, with the most well-recognized manifestation being the “silent” large violaceous ulceration of the hard palate (Fig. 7-31). Alopecia occurs in 20% of patients and may present as broken hair shafts or patchy, red, scaling areas on the scalp, which may eventually scar and cause permanent hair loss (Fig. 7-32). Other reported mucocutaneous findings are livedo reticularis (lacy, fishnet appearance of the skin), urticaria, atrophy, and telangiectasia. The presence of livedo reticularis may be the clinician’s only clue to an associated hypercoagulable state manifested by anti-phospholipid antibodies. This tendency can be diagnosed by obtaining a lupus anticoagulant panel, a functional assay that includes a partial thromboplastin time (PTT), anti-cardiolipin antibodies, and anti–β2-glycoprotein antibodies. Although anti-phospholipid antibody syndrome (APS) can occur as an entity alone, it is commonly associated with SLE. APS is defined as a hypercoagulable state characterized by both positive laboratory findings of anti-phospholipid antibodies and clinical findings of a variety of venous and arterial thromboses and recurrent fetal loss.







The heart is often significantly involved in patients with lupus. Although the pericardium is involved most commonly, the myocardium and the endocardium may also be of clinical importance. Pericarditis with associated pericardial effusion can be painless and may present only as cardiomegaly on a chest radiograph (Fig. 7-33) or as pericardial effusion on an echocardiogram. However, chest pain may be noted, especially on deep inspiration and when lying down. Auscultation of a friction rub signifies pericarditis. Although pericarditis is usually mild, it can progress to life-threatening cardiac tamponade. If the myocardium is affected, life-threatening complications including dysrhythmias, heart failure, and infarction can result. Libman-Sacks endocarditis is the term given to the verrucous projections of fibrinoid necrosis in the endocardium. These lesions rarely cause clinical symptoms, although the presence of a murmur raises suspicion of endocardial disease. The mitral valve is most commonly involved, although aortic and tricuspid valves may be similarly affected. The presence of Libman-Sacks endocarditis should also alert the clinician to the possibility of an underlying anti-phospholipid antibody syndrome. The major cardiac morbidity associated with SLE, which is gaining more recognition in the adolescent pediatric SLE population, is premature atherosclerosis. Several factors contribute to the risk of atherosclerosis, including chronic inflammatory processes, altered endothelial function, lipid abnormalities, nephritis, and proteinuria. Monitoring and controlling classic Framingham risk factors in addition to factors attributable to lupus are critical for long-term morbidity.


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Jul 11, 2016 | Posted by in PEDIATRICS | Comments Off on Rheumatology

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