Case Report
Large Joint Destructive Arthropathy and Tumoral Calcinosis Associated to Primary Oxalosis: Case Report and Literature Review
Artropatía destructiva de grandes articulaciones y calcinosis tumoral asociada a oxalosis primaria: reporte de un caso y revisión de la literatura
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Superior and inferior vertebral plate osteosclerosis (rugby jersey spine) and vertebral collapse of dorsal vertebrae 5 and 6. Bulbous growth on the ends of the ribs and clavicles. Osteosclerosis of clavicles and rib fracture sequelae. Fracture of the right humerus.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Oxalate crystal deposition disease is a rare condition seen primarily in patients with primary hyperoxaluria (PHO) and oxalate nephropathy and forms of secondary oxalosis in patients with ESRD on chronic dialysis, oxalate supplementation, thiamine deficiency and pyridoxine or oxalate formation due to Aspergillus niger. Musculoskeletal manifestations of calcium oxalate deposition disease are similar to those presented in calcium pyrophosphate crystals arthropathies. We report the case of a patient with arthropathy and tumoral calcinosis and associated deposits of calcium oxalate.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case Description</span><p id="par0010" class="elsevierStylePara elsevierViewall">The case is a 22-year-old Latin American Mestizo O positive male, with no toxic habits. The patient had no family history of kidney stones. He was diagnosed with short stature at age 6. At age 8 he presented repeated episodes of kidney stones and at 10 was diagnosed with primary hyperoxaluria, with progression to ESRD. At 12 he underwent renal replacement therapy with peritoneal dialysis and at 13 underwent living donor transplantation with graft loss after 5 months, so hemodialysis was started at a rate of 3 sessions a week and has remained so since then. 2 years after starting hemodialysis he presented bone pain and carpal, metacarpophalangeal and bilateral knee symmetrical and additive arthritis. At 16 he had a pathological fracture of the right femur, which required open reduction and internal fixation. The bone pain and polyarthritis followed a progressive course, with no response to treatment with non steroidal anti-inflammatory drugs (NSAID), and the patient noted the development of tumors located in soft tissue, which prevented gait at age 19. The symptoms persisted despite infiltration with glucocorticoids, low-dose oral steroids, opioid analgesics and NSAID. During the patients latest assessment we found that the patient had low height, pectus carinatum, short limbs, wrist and ankle subluxation and periarticular tumors located on shoulders, hips and knees, at the expense of soft tissue.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Laboratory studies showed: Vitamin A 7.1<span class="elsevierStyleHsp" style=""></span>ng/ml (low <10), ferritin 1342<span class="elsevierStyleHsp" style=""></span>ng/ml (30–400), cortisol 7.87<span class="elsevierStyleHsp" style=""></span>mg/dl (5–25) parathyroid hormone (PTH) 4.08<span class="elsevierStyleHsp" style=""></span>pg/ml (10–65), iron saturation percentage of 101% (15–55), iron binding capacity without saturating 63<span class="elsevierStyleHsp" style=""></span>g/dl (250–450), iron 64<span class="elsevierStyleHsp" style=""></span>mg/dl (50–170<span class="elsevierStyleHsp" style=""></span>mg/dl), creatinine 3.4<span class="elsevierStyleHsp" style=""></span>mg/dl (0.4–1.2), BUN 36.45<span class="elsevierStyleHsp" style=""></span>mg/dl (5–23), glucose 83<span class="elsevierStyleHsp" style=""></span>mg/dl, calcium 9.7<span class="elsevierStyleHsp" style=""></span>mg/dl (8.4–10.2), phosphorous 5.1<span class="elsevierStyleHsp" style=""></span>mg/dl (2.7–4.5), magnesium 2.4<span class="elsevierStyleHsp" style=""></span>mg/dl (1.6–2.6), alkaline phosphatase, 296<span class="elsevierStyleHsp" style=""></span>U/l (40–129) LDH 507<span class="elsevierStyleHsp" style=""></span>U/l (240–480), gamma glutamyl transferase 640<span class="elsevierStyleHsp" style=""></span>U/l (10–71), alanine aminotransferase 23<span class="elsevierStyleHsp" style=""></span>U/l (2–41), aspartate transaminase 50<span class="elsevierStyleHsp" style=""></span>U/l (2–38), albumin 2.3<span class="elsevierStyleHsp" style=""></span>g/dl (3.4–4.8) and uric acid 6.5<span class="elsevierStyleHsp" style=""></span>mg/dl (2.4–7).</p><p id="par0020" class="elsevierStylePara elsevierViewall">An abdominal ultrasound showed both kidneys to be hypoplastic with increased echogenicity and renal calcifications, with hepatic and spleen enlargement and a normal pancreas. An abdominopelvic computed tomography showed nephrocalcinosis, hepatomegaly, splenomegaly, arteriosclerosis and, osteosclerosis of vertebral and pelvic bones.</p><p id="par0025" class="elsevierStylePara elsevierViewall">A transthoracic echocardiogram showed a systolic pressure of 61<span class="elsevierStyleHsp" style=""></span>mmHg in the pulmonary artery, normal left ventricular diameter, a thickened wall, normal mobility, mild dilated right chambers, valvular sclerosis, mild mitral regurgitation and moderate tricuspid regurgitation.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The chest X-ray (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>) demonstrated nodular periarticular calcification in the shoulders, dorsal vertebral osteosclerosis and vertebral collapse of thoracic vertebrae 5 and 6, with sequelae of rib fractures and a fracture of the right humerus. An abdominal X-ray (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>) showed bilateral nephrocalcinosis, vertebral osteosclerosis which also affected pelvic bones, bilateral nodular calcifications and a subtrochanteric fracture.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0035" class="elsevierStylePara elsevierViewall">PHO is an autosomal recessive inborn error of metabolism leading to an enzyme deficiency of alanine-glyoxylate aminotransferase in hepatic peroxisomes. The enzyme deficiency causes an overproduction of oxalate which is eliminated by the kidneys and precipitates forming crystals that are deposited in various tissues. PHO diagnosis is performed before the age of 5 in 65% of cases. The main cause of death is uremia, which in 80% of cases occurs before age 20.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Since oxalate is eliminated through the kidney, this is the first and primary target organ, leading to the appearance of repeated stone formation in the first decades of life, nephrocalcinosis and early renal failure.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> When terminal renal failure occurs and oxalic acid cannot be excreted, rapidly evolving tissue deposits develop particularly in the kidneys and skeleton.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a> Bones are one of the main affected organs, with unusually serious lesions having been described, especially in patients with chronic renal failure on dialysis.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Oxalate deposits and the surrounding granulomatous reaction induce lesions similar to secondary hiperparatiroidism which are particularly serious.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The pattern of joint involvement is more commonly acute or chronic symmetrical polyarthritis or oligoarthritis, with involvement of the metacarpophalangeal and proximal interphalangeal joints, with or without tenosynovitis, along with miliary or cottony skin and finger arterial calcifications<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5,6</span></a> (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>), but can occur in other joints, such as knees, elbows, ankles and the first metatarsophalangeal joint. In autopsy studies, calcium oxalate deposits in joint tissue and bone oxalosis occur in approximately 90% of patients with renal insufficiency undergoing chronic hemodialysis.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">El Hage et al. conducted a review of 12 consecutive patients with type 1 PHO, all with renal involvement, 4 with ESRD undergoing dyalisis.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> The main symptom was bone pain and was present in only 4 of the severely involved patients and appeared in the second year of dialysis. The 2 most severely affected patients had evidence of pathologic fractures.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Kidney damage is usually the result of a combination of nephrolithiasis, secondary nephrocalcinosis and interstitial fibrosis. Renal failure is associated with the rapid deposit of the crystals in the kidney, myocardium, skin, blood vessels and bones; when the glomerular filtration rate decreases below 30–40<span class="elsevierStyleHsp" style=""></span>ml/min/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>, oxalate cannot be efficiently excreted by the kidneys and reaches saturation levels.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Oxalate saturation depends on serum levels and these are inversely related to the glomerular filtration rate.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> This saturation, which occurs almost universally in the serum of patients with terminal uremic PHO, causes the systemic oxalosis affecting patients on dialysis.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In the work of Worcester et al. the saturation threshold for serum oxalate was found to be 40–50<span class="elsevierStyleHsp" style=""></span>μUmol/l, and a threshold was reached with serum creatinine levels of about 9<span class="elsevierStyleHsp" style=""></span>mg/dl<span class="elsevierStyleSup">2</span>. Other studies and follow up of patients with renal oxalosis and renal failure have reported that patients with predialysis renal failure have no clinical or radiological manifestations of bone disease.</p><p id="par0060" class="elsevierStylePara elsevierViewall">Typical locations of crystal deposits in the skeleton are the segments of the metaphysis of tubular bones.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> The distribution of crystals in bone at sites of endochondral or intramembranous ossification suggests precipitation in vascularized areas when levels are high. Bone oxalosis may be due to the combination of hyperparathyroidism, renal osteodystrophy and the inflammatory response induced by calcium oxalate crystals.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">11,12</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">As regular dialysis treatment can prolong survival of patients, a new syndrome, characterized by intense and continuous deposition of calcium oxalate crystals in the soft tissues and bones can develop.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> The appearance of bone problems in dialysis patients demonstrates that dialysis is less effective in removing oxalate than the healthy kidney. Likewise, cases of oxalosis secondary to dialysis have been reported and chronic renal failure may lead to serum oxalate levels 4–8 times higher than normal, resulting in inefficient removal of oxalate by hemodialysis and peritoneal dialysis.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> The type of dialysis also affects the rate of deposition of crystals: an oxalic acid clearance of 80<span class="elsevierStyleHsp" style=""></span>ml/min by hemodialysis has been reported, but is only 6<span class="elsevierStyleHsp" style=""></span>ml/min in the case of peritoneal dialysis.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> Marangella et al. studied oxalate balance in PHO patients undergoing hemodialysis and the daily generation rate in the study was 360–630<span class="elsevierStyleHsp" style=""></span>mg and removal during dialysis did not reach 30% of the amount generated, resulting in a daily calcium oxalate deposits of 180–360<span class="elsevierStyleHsp" style=""></span>mg; to achieve balance in dialysis oxalate, sessions should last from 13 to 15<span class="elsevierStyleHsp" style=""></span>h, resulting impracticable.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,15</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Imaging examination may reveal small kidneys, with parenchymal calcifications. The spectrum of radiologic abnormalities in the skeleton is the result of changes caused by the deposition of oxalate in bone and renal osteodystrophy in patients with chronic renal insufficiency.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Radiological signs can be divided into those with greater specificity and those with less specificity. More specific imaging signs of oxalosis are found mainly in severely affected patients and include irregular sclerotic transverse bands in the metaphyseal segments of tubular bones (femur, humerus, tibia, fibula, metacarpals, metatarsals and phalanges), radiolucent metaphyseal bands and osteosclerosis of vertebral bodies which involve first the upper and then the lower vertebral endplates, creating the appearance of a rugby jersey before spreading to the rest of the vertebral body and the appearance of the “bone in bone” typical image.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Metaphyseal bands and sclerotic areas of the vertebral bodies are not specific for oxalosis and differential diagnosis includes, among others, lead poisoning, leukemia and thalassemia.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Other, less specific findings include clubbing of the metacarpal bones, sclerosis of the clavicles, a radiolucent or radiodense rim around the epiphyses, carpal and tarsal bones, cystic bone changes, epiphyseal invagination, bulbous growth of the ends of the ribs and clavicles, osteosclerosis in patches (Paget-like), subperiosteal resorption and pathological fractures. Day et al. found that bone radiographic abnormalities depend on the patient's age at the time of occurrence of renal failure and the degree of renal transplant success; the most characteristic skeletal changes occurred in 6 of 7 patients who developed renal disease before age 7.</p><p id="par0080" class="elsevierStylePara elsevierViewall">Soft tissue calcifications are a frequent complication in patients with chronic renal failure. The term tumoral calcinosis refers to massive deposit of calcium salts that form multiloculated tumors around joints. The pathogenesis of the skeletal and soft tissue alterations associated with chronic renal failure is multifactorial and, although not entirely clear, there are two main factors that work together in its development: secondary hyperparathyroidism and an altered metabolism of vitamin D.</p><p id="par0085" class="elsevierStylePara elsevierViewall">Soft tissue calcification may be seen in up to 79% of patients on dialysis. Chronic renal insufficiency leads to secondary hyperparathyroidism which causes release of calcium from bones and inhibition of the tubular phosphate reabsorption area. When the product of calcium<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>phosphorus is high, in the order of 65–70 (usually 40), subcutaneous deposition of calcium phosphate occurs.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Idiopathic tumoral calcinosis is characterized by the development of large amorphous calcium phosphate deposits around large joints, elevated levels of normal serum phosphorus and PTH levels. The most likely cause is an increase in the tubular reabsorption of phosphate.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> These lesions are usually asymptomatic and may rarely produce symptoms of compression of adjacent structures.</p><p id="par0095" class="elsevierStylePara elsevierViewall">Tumoral calcinosis associated with uremia is a rare complication seen in patients on long term dialysis and has a multifactorial etiology; it is characterized by deposits of calcium salts in periarticular areas, sometimes in mass. The most important etiopathogenic factor is the deterioration of the product of serum calcium x phosphorus; hyperparathyroidism and periarticular tumors frequently coexist without joint involvement or invasive process.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">18,19</span></a> Clinically, patients present periarticular painless firm masses which show progressive growth. This growth is expansive, and there is no visceral, muscle or bone invasion. Predisposing factors are severe hyperparathyroidism and a calcium<span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span>phosphorus product greater than 70.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> In the absence of secondary hyperparathyroidism, the elevation of the calcium–phosphorus product is originated by iatrogenic hypercalcemia and/or multifactorial hyperphosphatemia: excessive and prolonged administration of calcium carbonate and calcitriol, inadequate intake of phosphate binders and insufficient dialysis.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Chronic ingestion of high doses of vitamin D can cause hypervitaminosis D; its symptoms and signs are due to hypercalcemia and include weakness, headache, nausea, polyuria and nephrolithiasis.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">In our case we ruled out the above-described factors as inducers of calcifications. Vitamin D levels were below the reference range, which rules out hypervitaminosis D. We did not document secondary hyperparathyroidism; by contrast, PTH levels were found suppressed, and we did not find elevated levels of calcium–phosphorous (about 50) to justify tumoral calcinosis. In addition, the most common skeletal manifestation of hypoparathyroidism is osteosclerosis, with radio opaque bands in the metaphyses of long bones and, although subcutaneous calcifications may be seen especially in the hips and shoulders, these are asymptomatic; likewise the patient did not present hypocalcemia or neuromuscular signs to support the diagnosis of hypoparathyroidism. For technical reasons at baseline and due to the subsequent loss of patient follow-up, it was not possible to perform bone biopsies and the study of crystals in synovial fluid, which would have helped clarify the pathogenesis of the disease.</p><p id="par0110" class="elsevierStylePara elsevierViewall">Our patient was clinically compatible with primary hyperoxaluria and presenting recurrent nephrolithiasis, nephrocalcinosis with childhood onset progressing to ESRD; the key was the diagnosis of hyperoxaluria, but this data are only useful in the absence of renal failure, which was not determined. The absence of musculoskeletal symptoms before dialysis is consistent with reports that patients with PHO in a predialysis stage are asymptomatic, without radiographic bone oxalosis, and in a period of 1–2 years after dialysis, most evolved with progressive bone pain, which can produce severe bone disease with skeletal deformities, spontaneous fractures and disability.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The longer survival of our patient due to renal replacement therapy, with increased exposure time and precipitation of oxalate crystals at the osteoarticular level, is considered the main factor for late changes in bone oxalosis, the presence of pathological fractures and tumoral calcinosis. In a series of more than 200 patients on dialysis and serum PTH levels above those of our patient, vertebral or pelvic osteosclerosis is not usually found, whereby this pattern is readily attributable solely to renal osteodystrophy.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Lab data found moderately elevated alkaline phosphatase, which has been described in the course of patients with oxalosis mainly in those undergoing hemodialysis.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">Brancaccio et al. reported that the deposition of oxalate and hyperparathyroidism is involved in the genesis of bone lesions, but the former is much more important, in patients with PHO and hyperparathyroidism who undergo parathyroidectomy, bone lesions progress despite normal serum PTH levels and threshold serum calcium levels, indicative of bone resorption independent of PTH.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">As a result, oxalosis secondary to hemodialysis combined with primary hyperoxaluria could have aggravated the skeletal changes in our patient. Furthermore, most of the changes in the patient's bones could be the result of the combined effects of oxalate crystal deposition and progressive development of renal osteodystrophy. However, skeletal changes are more likely to be related to oxalosis. It seems logical to consider oxalate deposits as the main cause of severe bone lesions and the tumoral calcinosis observed in this patient.</p><p id="par0125" class="elsevierStylePara elsevierViewall">The aim of this article was to describe the radiographic spectrum of bone oxalosis in the major joints. To our knowledge, no other article mentions a destructive arthropathy disease associated with this complex, which can be due to the increased survival of patients on hemodialysis. A comprehensive literature search was unable to retrieve any items that describe a relationship between oxalosis and destructive arthropathy of the shoulders, hips and knees.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusion</span><p id="par0130" class="elsevierStylePara elsevierViewall">The spectrum of radiographic bone changes in primary hyperoxaluria and oxalosis are due to many factors that influence bone metabolism in this complex disease, including high levels of calcium oxalate, secondary hyperparathyroidism and renal osteodystrophy. We described the case of a patient with destructive arthropathy of the large joints, in whom we reasonably ruled out hyperparathyroidism, hypoparathyroidism and related phosphocalcic disorders, suggesting deposition of oxalate as the cause of his arthropathy.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Ethical Responsibilities</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Protection of People and Animals</span><p id="par0135" class="elsevierStylePara elsevierViewall">The authors state that no experiments were performed on humans or animals.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Data Confidentiality</span><p id="par0140" class="elsevierStylePara elsevierViewall">The authors state that no patient data appear in this article.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Right to Privacy and Informed Consent</span><p id="par0145" class="elsevierStylePara elsevierViewall">The authors have obtained informed consent from patients and/or subjects referred to in the article. This document is in the possession of the author of correspondence.</p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Conflict of Interest</span><p id="par0150" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:2 [ "identificador" => "xres243416" "titulo" => "Abstract" ] 1 => array:2 [ "identificador" => "xpalclavsec229995" "titulo" => "Keywords" ] 2 => array:2 [ "identificador" => "xres243415" "titulo" => "Resumen" ] 3 => array:2 [ "identificador" => "xpalclavsec229996" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Case Description" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Discussion" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Conclusion" ] 8 => array:3 [ "identificador" => "sec0025" "titulo" => "Ethical Responsibilities" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0030" "titulo" => "Protection of People and Animals" ] 1 => array:2 [ "identificador" => "sec0035" "titulo" => "Data Confidentiality" ] 2 => array:2 [ "identificador" => "sec0040" "titulo" => "Right to Privacy and Informed Consent" ] ] ] 9 => array:2 [ "identificador" => "sec0045" "titulo" => "Conflict of Interest" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2012-02-21" "fechaAceptado" => "2012-09-19" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec229995" "palabras" => array:4 [ 0 => "Tumoral calcinosis" 1 => "Arthropathy" 2 => "Primary hyperoxaluria" 3 => "Bone oxalosis" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec229996" "palabras" => array:4 [ 0 => "Calcinosis tumoral" 1 => "Artropatía" 2 => "Hiperoxaluria primaria" 3 => "Oxalosis ósea" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A case of destructive arthropathy of hips and shoulders with tumoral calcinosis associated with calcium oxalate deposits in a patient with primary oxalosis and end stage renal disease on hemodialysis.</p>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Se presenta el caso de artropatía destructiva de caderas y hombros con calcinosis tumoral asociada a depósitos de oxalato de calcio en un paciente con oxalosis primaria e insuficiencia renal terminal en hemodiálisis.</p>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Horta-Baas G, et al. Artropatía destructiva de grandes articulaciones y calcinosis tumoral asociada a oxalosis primaria: reporte de un caso y revisión de la literatura. Reumatol Clin. 2013;9:181–5.</p>" ] ] "multimedia" => array:3 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 741 "Ancho" => 900 "Tamanyo" => 84209 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Nodular calcifications of the shoulders. Superior and inferior vertebral plate osteosclerosis (rugby jersey spine) and vertebral collapse of dorsal vertebrae 5 and 6. Bulbous growth on the ends of the ribs and clavicles. Osteosclerosis of clavicles and rib fracture sequelae. Fracture of the right humerus.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 893 "Ancho" => 900 "Tamanyo" => 94794 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Bilateral nephrocalcinosis, vertebral osteoscleorosis (rugby jersey spine), osteosclerosis in Paget-like pelvic bones. Osteomalacia. Nodular calcifications. Bilateral subtrochanteric fracture. Surgical material at the proximal end of the right femur.</p>" ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1194 "Ancho" => 1600 "Tamanyo" => 174368 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">(A) X-ray of hands with periarticular calcinosis on interphalangeal, metacarpophalangeal and wrist joints, decreased bone density, resorption of the distal epiphysis of the radius and ulna. (B) X-ray showing periarticular calcinosis on interphalangeal and metatarsophalangeal tibiotalar joints, osteosclerosis of the phalanges and metatarsal tibiotalar joints dislocation and bone resorption of the distal epiphysis of the tibia and fibula. (C) X-ray of the knees with periarticular tumoral calcinosis, bilateral supracondylar fracture with medial deviation of the femoral shaft. (D) X-ray of shoulder with periarticular tumoral calcinosis, resorption of the humeral head and neck, clavicle bone resorption.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:19 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Radiological findings in primary hyperoxaluria" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "A. Martijn" 1 => "C.J.P. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 10 | 18 | 28 |
| 2024 October | 68 | 58 | 126 |
| 2024 September | 84 | 33 | 117 |
| 2024 August | 95 | 44 | 139 |
| 2024 July | 100 | 34 | 134 |
| 2024 June | 96 | 42 | 138 |
| 2024 May | 91 | 42 | 133 |
| 2024 April | 62 | 30 | 92 |
| 2024 March | 84 | 29 | 113 |
| 2024 February | 76 | 30 | 106 |
| 2024 January | 90 | 40 | 130 |
| 2023 December | 51 | 38 | 89 |
| 2023 November | 67 | 30 | 97 |
| 2023 October | 75 | 33 | 108 |
| 2023 September | 105 | 47 | 152 |
| 2023 August | 70 | 21 | 91 |
| 2023 July | 71 | 29 | 100 |
| 2023 June | 70 | 22 | 92 |
| 2023 May | 73 | 26 | 99 |
| 2023 April | 41 | 9 | 50 |
| 2023 March | 128 | 35 | 163 |
| 2023 February | 73 | 32 | 105 |
| 2023 January | 99 | 32 | 131 |
| 2022 December | 97 | 50 | 147 |
| 2022 November | 107 | 45 | 152 |
| 2022 October | 87 | 48 | 135 |
| 2022 September | 64 | 46 | 110 |
| 2022 August | 99 | 46 | 145 |
| 2022 July | 77 | 56 | 133 |
| 2022 June | 105 | 40 | 145 |
| 2022 May | 105 | 40 | 145 |
| 2022 April | 139 | 43 | 182 |
| 2022 March | 84 | 57 | 141 |
| 2022 February | 94 | 43 | 137 |
| 2022 January | 109 | 48 | 157 |
| 2021 December | 62 | 36 | 98 |
| 2021 November | 91 | 49 | 140 |
| 2021 October | 82 | 50 | 132 |
| 2021 September | 72 | 57 | 129 |
| 2021 August | 68 | 58 | 126 |
| 2021 July | 38 | 43 | 81 |
| 2021 June | 64 | 59 | 123 |
| 2021 May | 86 | 52 | 138 |
| 2021 April | 136 | 119 | 255 |
| 2021 March | 79 | 25 | 104 |
| 2021 February | 53 | 33 | 86 |
| 2021 January | 32 | 26 | 58 |
| 2020 December | 61 | 20 | 81 |
| 2020 November | 47 | 25 | 72 |
| 2020 October | 24 | 14 | 38 |
| 2020 September | 43 | 27 | 70 |
| 2020 August | 23 | 14 | 37 |
| 2020 July | 26 | 9 | 35 |
| 2020 June | 40 | 26 | 66 |
| 2020 May | 42 | 14 | 56 |
| 2020 April | 42 | 18 | 60 |
| 2020 March | 14 | 13 | 27 |
| 2020 February | 2 | 0 | 2 |
| 2020 January | 4 | 0 | 4 |
| 2019 September | 4 | 0 | 4 |
| 2019 June | 1 | 0 | 1 |
| 2019 March | 1 | 0 | 1 |
| 2019 January | 1 | 0 | 1 |
| 2018 May | 6 | 1 | 7 |
| 2018 April | 80 | 7 | 87 |
| 2018 March | 123 | 6 | 129 |
| 2018 February | 109 | 11 | 120 |
| 2018 January | 104 | 7 | 111 |
| 2017 December | 125 | 5 | 130 |
| 2017 November | 111 | 6 | 117 |
| 2017 October | 134 | 3 | 137 |
| 2017 September | 78 | 8 | 86 |
| 2017 August | 112 | 16 | 128 |
| 2017 July | 75 | 8 | 83 |
| 2017 June | 97 | 12 | 109 |
| 2017 May | 122 | 16 | 138 |
| 2017 April | 98 | 8 | 106 |
| 2017 March | 108 | 22 | 130 |
| 2017 February | 85 | 19 | 104 |
| 2017 January | 83 | 6 | 89 |
| 2016 December | 155 | 23 | 178 |
| 2016 November | 168 | 4 | 172 |
| 2016 October | 217 | 26 | 243 |
| 2016 September | 416 | 8 | 424 |
| 2016 August | 338 | 13 | 351 |
| 2016 July | 95 | 7 | 102 |
| 2016 June | 2 | 0 | 2 |
| 2016 April | 1 | 0 | 1 |
| 2016 March | 0 | 18 | 18 |
| 2016 February | 2 | 0 | 2 |
| 2016 January | 1 | 0 | 1 |
| 2015 December | 5 | 0 | 5 |
| 2015 November | 0 | 18 | 18 |
| 2015 October | 1 | 0 | 1 |
| 2015 September | 3 | 0 | 3 |
| 2015 August | 1 | 0 | 1 |
| 2015 July | 105 | 7 | 112 |
| 2015 June | 176 | 11 | 187 |
| 2015 May | 195 | 10 | 205 |
| 2015 April | 177 | 22 | 199 |
| 2015 March | 229 | 11 | 240 |
| 2015 February | 237 | 21 | 258 |
| 2015 January | 182 | 15 | 197 |
| 2014 December | 185 | 16 | 201 |
| 2014 November | 167 | 10 | 177 |
| 2014 October | 221 | 17 | 238 |
| 2014 September | 176 | 19 | 195 |
| 2014 August | 168 | 11 | 179 |
| 2014 July | 185 | 17 | 202 |
| 2014 June | 180 | 19 | 199 |
| 2014 May | 185 | 18 | 203 |
| 2014 April | 180 | 16 | 196 |
| 2014 March | 216 | 20 | 236 |
| 2014 February | 160 | 20 | 180 |
| 2014 January | 187 | 21 | 208 |
| 2013 December | 141 | 12 | 153 |
| 2013 November | 189 | 11 | 200 |
| 2013 October | 148 | 15 | 163 |
| 2013 September | 152 | 15 | 167 |
| 2013 August | 144 | 28 | 172 |
| 2013 July | 102 | 15 | 117 |
| 2013 June | 109 | 33 | 142 |
| 2013 May | 14 | 9 | 23 |
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