Case Report
Oxalosis and Livedo Reticularis
Oxalosis y livedo reticularis
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"apellidos" => "Borrero Martín" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Servicio de Dermatología Médico-Quirúrgica y Venereología, Hospital Juan Ramón Jiménez, Huelva, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Nefrología, Hospital Juan Ramón Jiménez, Huelva, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Servicio Anatomía Patológica, Hospital Juan Ramón Jiménez, Huelva, Spain" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Oxalosis y livedo reticularis" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 676 "Ancho" => 900 "Tamanyo" => 64246 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Red-violaceous, racemose, macular skin lesions on the inner thigh, consistent with livedo reticularis.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Oxalosis is defined as the systemic accumulation of calcium oxalate, an insoluble salt of oxalic acid, outside of the urinary tract. The pathologic processes responsible for systemic oxalosis include primary and secondary hyperoxalurias. Kidneys, bone, myocardium, blood vessels, and skin are the sites most susceptible to oxalate deposition and, therefore, to the appearance of clinical manifestations of oxalosis.</p><p id="par0010" class="elsevierStylePara elsevierViewall">The cutaneous findings associated with primary hyperoxaluria are usually caused by oxalate deposition in the blood vessel walls; this can cause livedo reticularis, acrocyanosis, ulceration, and peripheral gangrene. Skin changes caused by hyperoxaluria secondary to renal insufficiency, however, are rare. When such changes do occur, they are the result of extravascular calcium oxalate deposition, which leads to the appearance of calcified nodules and milium-like papules.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case Description</span><p id="par0015" class="elsevierStylePara elsevierViewall">The patient was a 60-year-old woman with terminal renal failure secondary to chronic lithiasic pyelonephritis who had been on hemodialysis followed by peritoneal dialysis for 3 years. She presented red-violaceous, racemose, macular skin lesions that had appeared suddenly on the lower limbs and were very tender to palpation (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Biopsy revealed the presence of deposits composed of a brownish material in the media of arterioles in the reticular dermis and hypodermis (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a> A) The deposits were intensely birefringent under polarized light (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a> B) and the classic spiculated crystals of oxalate salts were observed (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). Fat necrosis was also observed. On the basis of these histopathologic findings, a diagnosis of oxalate crystal–induced vascular disease was established.</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">A review of the patient's records revealed that she had had repeated episodes of nephrolithiasis in both kidneys since the age of 40 years. Previous tests had found a 24-hour urinary oxalate level of 101<span class="elsevierStyleHsp" style=""></span>mg/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span> (normal range, 4-44<span class="elsevierStyleHsp" style=""></span>mg/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>); at the time the patient was seen in our clinic, the level of oxalic acid in the blood was 11.3<span class="elsevierStyleHsp" style=""></span>mg/l (normal value, <<span class="elsevierStyleHsp" style=""></span>6<span class="elsevierStyleHsp" style=""></span>mg/l). The results of further tests to rule out the possibility of associated calciphylaxis (calcium levels, phosphorus levels, and arteriography) were normal. Electrocardiography and echocardiography showed no evidence of cardiac involvement and funduscopy revealed no retinal deposits.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The patient's clinical state gradually worsened. The livedo reticularis increased in intensity on all of the limbs and necrosis appeared on the left heel, the buttocks, and the tips of the second and third fingers of the right hand. She subsequently developed acute, intense abdominal pain, vomiting, and refractory hypotension that led to her death.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0035" class="elsevierStylePara elsevierViewall">In a patient with terminal renal failure and a history of lithiasis, the appearance of livedo reticularis should alert the clinician to consider a diagnosis of hyperoxaluria.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Hyperoxaluria is classified as primary or secondary (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). The primary hyperoxalurias, which have an autosomal recessive inheritance, are divided into various subtypes that are distinguished from one another on the basis of the enzyme deficiency in the hepatocytes. Type 1 primary hyperoxaluria is the most common. It is caused by a deficiency of the pyridoxine-dependent hepatic peroxisomal enzyme alanine:glyoxylate aminotransferase. The gene that encodes this protein consists of 11 exons located on chromosome 2q37.3. About 30 mutations of this gene have been described to date. Type 2 primary hyperoxaluria is caused by a deficiency of the cytosolic enzyme glyoxylate reductase/hydroxypyruvate reductase. Type 3 primary hyperoxaluria is linked to a mitochondrial-encoded enzyme. It is likely that other as-yet-unidentified alterations also exist.<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2,3</span></a> Secondary hyperoxaluria, which is caused by excessive oxalate intake, is seen in the context of other processes, including hemodialysis.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Because oxalate is excreted only via the kidneys, renal failure of any origin that requires hemodialysis can lead to the saturation of oxalate salt in the tissues, but always to a lesser extent than in the primary hyperoxalurias. The excess oxalate precipitates as calcium oxalate, first in the kidneys and later in other tissues. It has been suggested that the appearance of renal calculi caused by primary hyperoxalurias—smooth, whitish surface, unorganized section, and pure or virtually pure calcium oxalate monohydrate composition—is different from that of common calculi.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Cutaneous manifestations of hyperoxaluria are uncommon and very few cases have been reported in the literature.<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6–10</span></a> Most skin lesions of the primary hyperoxalurias are caused by vascular complications resulting from oxalate deposition in the arterial walls, which leads to the appearance of livedo, acrocyanosis, and gangrene. In secondary hyperoxaluria, mild cutaneous manifestations are caused by extravascular deposition, which leads to the appearance of acral or facial papules or nodules.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Our patient's advanced age at the time of diagnosis is noteworthy. Primary hyperoxalurias generally have an early onset, between the ages of 7 and 13 years; however, there have been cases, like that of our patient, in which the disease presents in the sixth decade of life. Because of their rarity, the primary hyperoxalurias are usually diagnosed between 24 and 33 years of age, by which time many patients have already developed terminal renal failure. Diagnosis of the primary hyperoxalurias is very challenging for clinicians.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Measurement of 24-hour urinary oxalate levels, L-glycerate levels, and the oxalate to creatinine ratio can be useful in the diagnostic process. However, once the patient has developed anuria these tests are no longer relevant. When a primary hyperoxaluria is suspected, the clinician can measure serum oxalate levels (which were very high in our patient) and, depending on the results, order liver biopsy and genetic testing (which our patient did not undergo, due to her rapid deterioration and death). We suspect that our patient died as a result of acute mesenteric ischemia, which has been described as a frequent cause of death in patients with primary hyperoxaluria.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The differential diagnosis should particularly include calciphylaxis. Calciphylaxis has clinical manifestations similar to those found in our patient, but it is usually seen in patients who are on long-term hemodialysis, have alterations of the calcium/phosphorus product or of parathyroid hormone levels, or who present radiologic and histopathologic findings of soft-tissue calcification with basophilic calcium deposits.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Treatment of hyperoxaluria depends on the cause. Patients who retain kidney function can be prescribed oral pyridoxine, which increases the activity of the deficient liver enzyme by acting as a cofactor. In patients who have developed renal failure, the only effective treatment is a combined liver and kidney transplant. Because the liver is the site of the enzyme problem, it must be transplanted at the same time as the kidney. Conventional dialysis is not suitable for patients with renal failure because it cannot eliminate the excess oxalate synthesized in the liver. Hemodialysis is more effective than peritoneal dialysis in eliminating oxalate.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Our patient's switch to peritoneal dialysis could explain the appearance of her cutaneous manifestations.</p><p id="par0065" class="elsevierStylePara elsevierViewall">In summary, we have presented the case of a 60-year-old woman with a history of recurrent nephrolithiasis and terminal renal failure who developed livedo reticularis and skin necrosis after starting a program of peritoneal dialysis. Histopathology revealed the existence of calcium oxalate deposits in the arterial walls, which supported a diagnosis of an underlying primary hyperoxaluria. The patient's condition then deteriorated rapidly and she died a few months later, before the type of primary hyperoxaluria could be confirmed by genetic testing or liver biopsy.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Ethical Disclosures</span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Protection of human and animal subjects</span><p id="par0070" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for the purpose of this study.</p></span></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Confidentiality of data.</span><p id="par0075" class="elsevierStylePara elsevierViewall">The authors declare that no patient data are disclosed in this article.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflicts of Interest</span><p id="par0080" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:2 [ "identificador" => "xres285033" "titulo" => "Abstract" ] 1 => array:2 [ "identificador" => "xpalclavsec268276" "titulo" => "Keywords" ] 2 => array:2 [ "identificador" => "xres285034" "titulo" => "Resumen" ] 3 => array:2 [ "identificador" => "xpalclavsec268275" "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:3 [ "identificador" => "sec0020" "titulo" => "Ethical Disclosures" "secciones" => array:1 [ 0 => array:2 [ "identificador" => "sec0025" "titulo" => "Protection of human and animal subjects" ] ] ] 8 => array:2 [ "identificador" => "sec0030" "titulo" => "Confidentiality of data." ] 9 => array:2 [ "identificador" => "sec0035" "titulo" => "Conflicts of Interest" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec268276" "palabras" => array:3 [ 0 => "Oxalosis" 1 => "Livedo reticularis" 2 => "Vasculopathy" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec268275" "palabras" => array:3 [ 0 => "Oxalosis" 1 => "Livedo reticularis" 2 => "Vasculopatía" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Oxalosis is a disease caused by the deposition of calcium oxalate in extrarenal tissues, most commonly bone, myocardium, retina, blood vessels, and skin, causing the clinical manifestations of the disease. Involvement of the blood vessels of the skin can give rise to livedo reticularis, acrocyanosis, ulcers, and gangrene. We present the case of a 60-year-old woman with a history of recurrent renal lithiasis that had led to terminal renal failure requiring hemodialysis and, subsequently, peritoneal dialysis. The patient developed tender red-violaceous skin discoloration of sudden onset, consistent with livedo reticularis; the lesions progressed to form ulcers. Skin biopsy revealed oxalate vasculopathy. In this article we describe the characteristics of this rare disorder, its differentiation from calciphylaxis, and the therapeutic options.</p>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La oxalosis es una enfermedad derivada del depósito de oxalato cálcico fuera del aparato urinario. Los lugares de depósito extrarrenales más frecuentes incluyen el hueso, el miocardio, la retina, los vasos sanguíneos y la piel, lo que da lugar a las manifestaciones clínicas de esta enfermedad.</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">En la piel las alteraciones pueden deberse a la afectación de los vasos sanguíneos, lo que da lugar a la aparición de cuadros de livedo reticularis, acrocianosis, úlceras y gangrena.</p><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Presentamos el caso de una mujer de 60 años con historia de litiasis renal recidivante, que le llevó a una insuficiencia renal terminal que requirió hemodiálisis y posteriormente diálisis peritoneal. La paciente desarrolló de forma súbita la aparición de elementos cutáneos de color rojo-violáceo, dolorosos a la palpación compatibles con livedo reticularis que evolucionaron a úlceras. La biopsia cutánea reveló una vasculopatía por oxalato.</p><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">En este artículo se describen las características de este raro proceso, su diagnóstico diferencial con la calcifilaxis y las alternativas terapéuticas.</p>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Jorquera-Barquero E, Súarez-Marrero MC, Fernández Girón F, Borrero Martín JJ. Oxalosis y livedo reticularis. Actas Dermosifiliogr. 2013;104:815–818.</p>" ] ] "multimedia" => array:4 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 676 "Ancho" => 900 "Tamanyo" => 64246 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Red-violaceous, racemose, macular skin lesions on the inner thigh, consistent with livedo reticularis.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 870 "Ancho" => 1301 "Tamanyo" => 262759 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">A, Deposits of amorphous material in the media of arterioles in the hypodermis (hematoxylin-eosin, original magnification × 37.5). B, Intense birefringence of the material located in the arteriolar walls (hematoxylin-eosin, original magnification × 37.5)</p>" ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 670 "Ancho" => 900 "Tamanyo" => 73183 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Birefringence of the characteristic spiculated crystals of calcium oxalate (polarized light, original magnification × 300).</p>" ] ] 3 => array:7 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:1 [ "tablaImagen" => array:1 [ 0 => array:4 [ "imagenFichero" => "fx1.jpeg" "imagenAlto" => 924 "imagenAncho" => 1667 "imagenTamanyo" => 112378 ] ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Types of Hyperoxaluria.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Livedo. De la physiopathologie au diagnostic" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "A. Duval" 1 => "J. Pouchot" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Rev Med Intern" "fecha" => "2008" "volumen" => "29" "paginaInicial" => "380" "paginaFinal" => "392" ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0010" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Primary hiperoxaluria" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "J. Harambat" 1 => "S. Fargue" 2 => "J. Bacchetta" 3 => "C. Acquaviva" 4 => "P. Cochat" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.4061/2011/864580" "Revista" => array:5 [ "tituloSerie" => "Int J Nephrol" "fecha" => "2011" "volumen" => "2011" "paginaInicial" => "864580" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/21748001" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0015" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The primary hiperoxalurias" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "E. Leumann" 1 => "B. 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| 2018 Junio | 0 | 8 | 8 |
| 2018 Mayo | 0 | 4 | 4 |
| 2018 Abril | 0 | 4 | 4 |
| 2018 Marzo | 6 | 5 | 11 |
| 2018 Febrero | 42 | 6 | 48 |
| 2018 Enero | 57 | 12 | 69 |
| 2017 Diciembre | 48 | 10 | 58 |
| 2017 Noviembre | 50 | 7 | 57 |
| 2017 Octubre | 33 | 16 | 49 |
| 2017 Septiembre | 30 | 11 | 41 |
| 2017 Agosto | 59 | 13 | 72 |
| 2017 Julio | 30 | 17 | 47 |
| 2017 Junio | 52 | 30 | 82 |
| 2017 Mayo | 46 | 21 | 67 |
| 2017 Abril | 37 | 11 | 48 |
| 2017 Marzo | 44 | 24 | 68 |
| 2017 Febrero | 73 | 19 | 92 |
| 2017 Enero | 39 | 25 | 64 |
| 2016 Diciembre | 49 | 15 | 64 |
| 2016 Noviembre | 70 | 38 | 108 |
| 2016 Octubre | 109 | 31 | 140 |
| 2016 Septiembre | 182 | 17 | 199 |
| 2016 Agosto | 192 | 12 | 204 |
| 2016 Julio | 40 | 19 | 59 |
| 2016 Junio | 7 | 14 | 21 |
| 2016 Mayo | 6 | 13 | 19 |
| 2016 Abril | 2 | 3 | 5 |
| 2016 Marzo | 3 | 13 | 16 |
| 2016 Febrero | 9 | 14 | 23 |
| 2016 Enero | 14 | 15 | 29 |
| 2015 Diciembre | 5 | 2 | 7 |
| 2015 Noviembre | 9 | 17 | 26 |
| 2015 Octubre | 4 | 15 | 19 |
| 2015 Septiembre | 2 | 14 | 16 |
| 2015 Agosto | 3 | 3 | 6 |
| 2015 Julio | 81 | 2 | 83 |
| 2015 Junio | 55 | 10 | 65 |
| 2015 Mayo | 52 | 8 | 60 |
| 2015 Abril | 39 | 5 | 44 |
| 2015 Marzo | 50 | 13 | 63 |
| 2015 Febrero | 40 | 4 | 44 |
| 2015 Enero | 32 | 5 | 37 |
| 2014 Diciembre | 41 | 13 | 54 |
| 2014 Noviembre | 28 | 9 | 37 |
| 2014 Octubre | 49 | 12 | 61 |
| 2014 Septiembre | 36 | 14 | 50 |
| 2014 Agosto | 45 | 4 | 49 |
| 2014 Julio | 40 | 11 | 51 |
| 2014 Junio | 44 | 5 | 49 |
| 2014 Mayo | 32 | 10 | 42 |
| 2014 Abril | 35 | 5 | 40 |
| 2014 Marzo | 34 | 3 | 37 |
| 2014 Febrero | 34 | 9 | 43 |
| 2014 Enero | 38 | 2 | 40 |
| 2013 Diciembre | 20 | 7 | 27 |
| 2013 Noviembre | 20 | 5 | 25 |
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