Juvenile idiopathic arthritis (JIA) is a heterogeneous group of diseases characterized by synovial inflammation and is the most common rheumatic complaint in children. To facilitate research and treatment, JIA has been further classified on the basis of the number of joints involved, additional symptoms, family history, and serologic findings. Imaging in patients with JIA has historically relied on radiography, which allows the accurate assessment of chronic changes of JIA, including growth disturbances, periostitis, and joint malalignment. However, radiographic findings of active inflammation are nonspecific, and, in the past, clinical evaluation has taken precedence over imaging of acute disease. Recent advances in disease-modifying therapeutic agents that can help prevent long-term disability in patients with JIA have led to greater emphasis on the detection of early joint-centered inflammation that cannot be accurately assessed radiographically and may not be evident clinically. Both contrast material-enhanced magnetic resonance (MR) imaging and Doppler ultrasonography (US) are well suited for this application and are playing an increasingly important role in diagnosis, risk stratification, treatment monitoring, and problem solving. Contrast-enhanced MR imaging is the most sensitive technique for the detection of synovitis and is the only modality that can help detect bone marrow edema, both of which indicate active inflammation. US is more sensitive than radiography for the detection of synovial proliferation and effusions and is particularly useful in the evaluation of small peripheral joints. The complexity of the temporomandibular and sacroiliac joints limits the usefulness of radiographic or US evaluation, and contrast-enhanced MR imaging is the preferred modality for evaluation of these structures.

Diabetes mellitus is increasingly prevalent and results in various clinically important musculoskeletal disorders affecting the limbs, feet, and spine as well as in widely recognized end-organ complications such as neuropathy, nephropathy, and retinopathy. Diabetic muscle ischemia-a self-limited disorder-may be confused with infectious or inflammatory myositis, venous thrombosis, or compartment syndrome. The absence of fever and leukocytosis, combined with the presence of bilaterally distributed lesions in multiple and often noncontiguous muscles in the legs, including the thighs, is suggestive of ischemia; by contrast, the presence of well-defined intramuscular abscesses with rimlike enhancement favors a diagnosis of infectious pyomyositis. In the diabetic foot, an ulcer, sinus tract, or abscess with an adjacent region of abnormal signal intensity in bone marrow favors the diagnosis of pedal osteomyelitis over that of neuropathic arthropathy. Contrast material-enhanced magnetic resonance imaging is important when planning the treatment of foot infections in diabetic patients because it allows the differentiation of viable tissue from necrotic regions that require surgical débridement in addition to antibiotic therapy. Subtraction images are particularly useful for visualizing nonviable tissue. Dialysis-associated spondyloarthropathy characteristically occurs in diabetic patients with a long history of hemodialysis. Intervertebral disk space narrowing without T2 signal hyperintensity, extensive endplate erosions without endplate remodeling, and facet joint involvement are suggestive of spondyloarthropathy instead of infectious diskitis or degenerative disk disease. Although the clinical features of these conditions may overlap, knowledge of the patient's medical history, coupled with recognition of key imaging characteristics, allows the radiologist to make a prompt and correct diagnosis that leads to appropriate management.

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Hypophosphatasia (HPP) is the inborn error of metabolism that features low serum alkaline phosphatase (ALP) activity caused by lossof-function mutation(s) within the gene for the tissue nonspecific isoenzyme of ALP (TNSALP). In HPP, extracellular accumulation of inorganic pyrophosphate (PPi), a TNSALP substrate and inhibitor of mineralization, leads frequently to premature tooth loss and often to rickets or osteomalacia. In affected adults, the excess PPi sometimes also causes calcium pyrophosphate dihydrate (CPPD) deposition, PPi arthropathy, or pseudogout, or seemingly paradoxical deposition of hydroxyapatite crystals in ligaments or around joints when the condition is called calcific periarthritis (CP). We report three middle-aged sisters with CP as the only clinical manifestation of HPP. Each presented during early adult life with recurrent episodes of pain principally around the shoulders, elbows, wrists, hips, or Achilles tendon. Otherwise, they were in good health, including no history of unusual dental disease, fractures, or pseudofractures. Calcific deposits were identified in symptomatic areas principally by ultrasonographic assessment but also confirmed radiographically. All three sisters had low serum levels of total and bone-specific ALP, hyperphosphatemia, and increased serum concentrations of the TNSALP substrate pyridoxal 5 0 -phosphate together characteristic of HPP. Mutation analysis revealed that each carried a single unique 18-bp duplication within TNSALP (c.188_205dup18, p.Gly63_Thr68dup) as did two of their healthy sons and their mother, who was without signs of CPPD deposition or CP but had knee osteoarthritis. We find that CP can be the only complication of HPP in adults. Thus, multiple juxta-articular deposits of hydroxyapatite causing CP may be a useful sign of HPP, especially when the CP is familial.

The purpose of this article is to review both the pathophysiology and the computed tomography features of the hypoperfusion complex and shock viscera. The main findings include dilated fluid-filled loops of bowel with hyperenhancing mucosa, intensely enhancing kidneys and mesenteric vasculature, and small caliber, dense aorta and collapsed, slit-like inferior vena cava. Variable features include increased enhancement of the adrenals, decreased enhancement of the spleen, and altered enhancement of the pancreas with both hypo- and hyperenhancement described. This complex of findings indicates a tenuous hemodynamic status and has been associated with a poor prognosis. In addition, it is important to discern this collection of findings from direct injury to the viscera to aid in appropriate triage and management of the patients' injuries.

A case of a latissimus dorsi myotendinous junction strain in an avid CrossFit athlete is presented. The patient developed acute onset right axillary burning and swelling and subsequent palpable pop with weakness while performing a “muscle up.” Magnetic resonance imaging examination demonstrated a high-grade tear of the right latissimus dorsi myotendinous junction approximately 9 cm proximal to its intact humeral insertion. There were no other injuries to the adjacent shoulder girdle structures. Isolated strain of the latissimus dorsi myotendinous junction is a very rare injury with a scarcity of information available regarding its imaging appearance and preferred treatment. This patient was treated conservatively and was able to resume active CrossFit training within 3 months. At 6 months postinjury, he had only a mild residual functional deficit compared with his preinjury level.