Case Reports in Endocrinology最新文献

{"title":"Adrenal Tuberculosis Presenting as Adrenal Crisis: A Rare Presentation of Common Disease.","authors":"Berhanu Kelemework Fenta, Akberet Semere Yihdego, Bereket Kusse Kurtaile, Worku Ketema","doi":"10.1155/crie/9086526","DOIUrl":"10.1155/crie/9086526","url":null,"abstract":"<p><p>We report a case of a 45-year-old man presenting with hypotension, hyponatremia, hyperkalemia, hypoglycemia and diffuse hyperpigmentation. Monitoring serum cortisol was 0.5 μg/dL, and the computerized tomography (CT) scan showed bilateral adrenal enlargement, consistent with primarily adrenal insufficiency (AI) likely due to adrenal tuberculosis (TB). There was no active pulmonary TB. This case underscores the diagnostic delay and management challenges of TB-related AI in resource-limited settings. Even today, clinicians should remain aware of AI due to TB in resource-limited settings.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"9086526"},"PeriodicalIF":0.8,"publicationDate":"2026-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13311310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148350911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-Autoimmune Hyperthyroidism Associated With a Novel Germline Mutation (D633N) in the TSH Receptor.","authors":"Sayuri Mori, Yoshinori Osaki, Hiroshi Fukazawa, Takaaki Matsuda, Yuki Murayama, Yoko Sugano, Hitoshi Iwasaki, Bryan J Mathis, Motohiro Sekiya, Hitoshi Shimano","doi":"10.1155/crie/3274433","DOIUrl":"10.1155/crie/3274433","url":null,"abstract":"<p><p>Nonautoimmune hyperthyroidism resulting from an activating germline thyroid-stimulating hormone receptor (TSHR) gene mutation is a rare condition that often presents a diagnostic challenge. We report the case of a 75-year-old woman with a 20-year history of goiter and subclinical hyperthyroidism who presented with overt thyrotoxicosis. Laboratory tests confirmed hyperthyroidism with suppressed TSH, whereas thyrotropin receptor antibody (TRAb) and thyroid-stimulating antibody (TSAb) were negative, making it difficult to distinguish from toxic multinodular goiter. Initial management with potassium iodide was ineffective. Subsequent radioactive iodine (RI) therapy was complicated by severe destructive thyroiditis with worsening thyrotoxicosis and heart failure. Following hormonal control with methimazole (MMI) and dexamethasone, a total thyroidectomy was performed for definitive management, successfully normalizing thyroid function. Histopathology revealed an adenomatous goiter. Postoperative genetic analysis using peripheral blood DNA, prompted by the atypical clinical course, identified a novel heterozygous germline mutation in the TSHR gene: c.1897G > A (p.D633N). This case expands the spectrum of activating TSHR mutations causing nonautoimmune hyperthyroidism. Functional analysis demonstrated modest constitutive activity of the variant, which may explain the unusually late clinical onset. This report underscores the importance of considering nonautoimmune hyperthyroidism, including nonautoimmune hyperthyroidism, in patients with antibody-negative hyperthyroidism, even in elderly individuals without a known family history.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"3274433"},"PeriodicalIF":0.8,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13306117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe Osteoporosis in a Young Woman With Type 1 Diabetes and Pancreatic Exocrine Insufficiency.","authors":"Jeremy A Knott, Terrence H Diamond","doi":"10.1155/crie/3988709","DOIUrl":"10.1155/crie/3988709","url":null,"abstract":"<p><p>Patients with type 1 diabetes mellitus (T1DM) are at increased risk of osteoporosis; however, contributing secondary factors may be under-recognised. We report a case of a 29-year-old woman with a 10-year history of suboptimally controlled T1DM (HbA1c 10.1%-14.7%) who presented with an atraumatic tibial fracture and vertebral compression fractures. She had a history of significant weight loss (nadir 37 kg) and chronic malabsorption. Investigations demonstrated severe pancreatic exocrine insufficiency (PEI; faecal elastase 42 μg/g), vitamin D deficiency (25 nmol/L), and secondary hyperparathyroidism (PTH 10.8 pmol/L). Dual-energy X-ray absorptiometry revealed reduced bone mineral density at the total hip (<i>Z</i>-score -3.4) and lumbar spine (<i>Z</i>-score -2.1). Management included pancreatic enzyme replacement, vitamin D and calcium repletion, and optimisation of glycaemic control. At the 12-month follow-up, biochemical parameters improved (vitamin D 112 nmol/L), and no further fractures occurred. This case highlights the importance of identifying secondary contributors to bone fragility in young patients with T1DM, particularly malabsorption due to PEI.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"3988709"},"PeriodicalIF":0.8,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13273022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alternating Therapy With Osilodrostat and Etomidate in Severe Ectopic Cushing's Syndrome Complicated by Silent Bowel Perforation.","authors":"Hery Mejia, Carmen Villabona, Renato Savian, Susana Barreiro Sacco, Alejandra Razzeto, Tanira Ferreira, Virginia Kondas, Sixto Arias, Elio Donna, Violet Lagari","doi":"10.1155/crie/4689206","DOIUrl":"10.1155/crie/4689206","url":null,"abstract":"<p><p>Ectopic adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome (CS), ectopic ACTH secretion (EAS) is a rare condition caused by ACTH-secreting neuroendocrine tumors (NETs), such as bronchial carcinoids. We report a 65-year-old woman with severe EAS complicated by bowel perforation. She presented with hypokalemia (K⁺ 2.3 mmol/L), metabolic alkalosis, resistant hypertension (180/110 mmHg), worsening diabetes (HbA1c 6.7%-9.1%), proximal muscle weakness, and 14 kg weight gain over 3 months. A silent sigmoid colon perforation required emergency resection and colostomy. Biochemical tests confirmed hypercortisolism (urine free cortisol [UFC], 1256 µg/24 h, plasma ACTH 175 pg/mL, and cortisol >40 µg/dL post-dexamethasone). Imaging identified a 2.3 cm pulmonary nodule with mild uptake on Ga-68 DOTATATE PET/CT. Bronchoscopic biopsy confirmed an ACTH-positive low-grade bronchial carcinoid tumor. Initial treatment with osilodrostat was interrupted due to acute illness and oral medication intolerance. Intravenous etomidate was employed in the ICU for rapid cortisol suppression, followed by resumption of osilodrostat after stabilization. Thoracoscopic lobectomy confirmed a low-grade carcinoid tumor (Ki-67 < 2%). Postoperatively, cortisol normalized, electrolytes stabilized, and HbA1c improved to 6.5%. This case highlights bowel perforation as a severe complication of EAS and underscores the importance of dynamic, alternating therapy with osilodrostat and etomidate, along with individualized surgical and medical management strategies.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"4689206"},"PeriodicalIF":0.8,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13248108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Rare Case of Bartter Syndrome Type 3 Diagnosed in Elderly Age.","authors":"Tsuyoshi Okura, Kenji Fukaya, Tetsuya Okazaki, Kaori Adachi, Yoshiharu Kinugasa, Masaru Kato","doi":"10.1155/crie/9463565","DOIUrl":"10.1155/crie/9463565","url":null,"abstract":"<p><p>Bartter syndrome (BS) type 3 typically presents in childhood and is caused by defects in NaCl transporters of the thick ascending limb of the loop of Henle. We report a 66-year-old woman with asymptomatic but severe hypokalemia (2.0 mmol/L), metabolic alkalosis, and hyperreninemic hyperaldosteronism. Initial clinic blood pressure was 157/88 mmHg, but repeated office and home measurements were ~120/70 mmHg, consistent with white-coat hypertension. Imaging excluded renovascular disease. Sequential diuretic testing supported BS physiology: a thiazide loading test increased fractional excretion of chloride (FECl) from 0.46% to 3.88% (ΔFECl 3.4%), exceeding the 2.3% cutoff that argues against Gitelman syndrome; a furosemide test showed chloride reabsorption of 10.1%, indicating a profound loop-segment defect, even lower than values commonly reported in BS3. Targeted next-generation sequencing identified a homozygous CLCNKB stop-gain variant (c.1830G >A; p.Trp610Ter), confirming BS type 3. High-dose potassium chloride (9.9 g/day) failed to correct hypokalemia, whereas low-dose enalapril plus spironolactone normalized serum potassium (4.0 mmol/L) without persistent hypotension. The urine calcium/creatinine ratio was borderline-normal (0.65 mmol/mmol), rather than hypocalciuric. This case suggests that BS3 should remain in the differential diagnosis of refractory hypokalemia in older adults and highlights the diagnostic value of physiology-guided diuretic testing combined with genetic analysis, as well as the potential efficacy of low-dose ACE inhibitor plus mineralocorticoid receptor antagonist therapy when potassium supplementation alone is insufficient.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"9463565"},"PeriodicalIF":0.8,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13248106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"21-Hydroxylase Deficient Congenital Adrenal Hyperplasia Due to Maternal Uniparental Isodisomy.","authors":"Michelle L Kluge, Lynn Schema, Katy Schroepfer, Emily K Thoreson, Kyriakie Sarafoglou, Ross A Rowsey, Cherisse A Marcou, Ann M Moyer, Matthew J Schultz","doi":"10.1155/crie/3596318","DOIUrl":"10.1155/crie/3596318","url":null,"abstract":"<p><p>Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency (21-OHD CAH) is an autosomal recessive genetic condition that results from pathogenic variants in the <i>CYP21A2</i> gene. Noncarrier parents are found in a small percentage of cases, typically due to de novo variants. However, uniparental disomy (UPD) should also be considered. UPD is generally suspected when an individual with an autosomal recessive condition is found to be homozygous for a rare pathogenic variant and consanguinity has been ruled out. However, UPD in <i>CYP21A2</i> may be hard to recognize because homozygous genotypes are not uncommon. We present the case of a 19-month-old male born preterm who presented to pediatric endocrinology after a positive newborn screen for CAH. He was small for gestational age, with a history of adrenal crisis and elevated 17-hydroxyprogesterone (17-OHP). Genetic testing revealed homozygosity for two common pathogenic <i>CYP21A2</i> variants: c.293-13C >G and c.1360C >T (p.Pro454Ser), both variants were found in the heterozygous state in the mother while the father's <i>CYP21A2</i> molecular testing was negative. UPD testing was pursued and the results were consistent with the patient having maternal isodisomy of chromosome 6. In cases of patients with CAH due to homozygous <i>CYP21A2</i> variants, suspicion for UPD may be increased if the child also presents with intrauterine growth restriction (IUGR), or transient neonatal diabetes (TNDM) mellitus, associated with maternal and paternal UPD of chromosome 6, respectively.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"3596318"},"PeriodicalIF":0.8,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Risk Pregnancy Associated With Maternal Hypoparathyroidism and Medium-Chain Acyl-CoA Dehydrogenase Deficiency.","authors":"Isabel Huguet, Cristina Sevillano Collantes, Laura Pérez-Olivares Martín, Guillermo Martínez Díaz-Guerra","doi":"10.1155/crie/9924065","DOIUrl":"10.1155/crie/9924065","url":null,"abstract":"<p><strong>Purpose: </strong>Fatty acid oxidation disorders are inherited metabolic errors that result in deficient energy production during prolonged fasting and catabolic stress. Few cases of hypoparathyroidism (HypoPT) related to medium-chain acyl-CoA dehydrogenase (MCAD) deficiency have been reported. We present the perinatal management of a female patient previously diagnosed with MCAD deficiency due to a homozygous G985A mutation and HypoPT.</p><p><strong>Case presentation: </strong>A 24-year-old woman with MCAD deficiency and HypoPT presented with stage IV intrauterine growth restriction (IUGR) and preeclampsia at 28 weeks of gestation, requiring an emergency cesarean section. The fetus had been diagnosed with aortic arch hypoplasia and ventricular septal defect. Despite multidisciplinary management, the infant died at 8 months, with the underlying cardiopathy considered the most likely cause. This case highlights the challenges of managing coexisting metabolic and endocrine disorders during pregnancy.</p><p><strong>Conclusions: </strong>In this case, although MCAD deficiency may have contributed, HypoPT and its renal complications likely played a major role in adverse maternal and fetal outcomes. To the best of our knowledge, this is the first published case describing the coexistence of MCAD deficiency and HypoPT during pregnancy.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"9924065"},"PeriodicalIF":0.8,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"A Decade With Sheehan's Syndrome: A Case Report and Personal Experience\".","authors":"","doi":"10.1155/crie/9876731","DOIUrl":"https://doi.org/10.1155/crie/9876731","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/crie/6010326.].</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"9876731"},"PeriodicalIF":0.9,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Timing of Denosumab Therapy in Relation to Parathyroidectomy in the Setting of Primary Hyperparathyroidism: Case Report.","authors":"Ryan S MacLeod, Adriana Ramirez, Barbara Gulanski, Sachin K Majumdar","doi":"10.1155/crie/8562872","DOIUrl":"10.1155/crie/8562872","url":null,"abstract":"<p><p>The optimal timing of denosumab therapy in relation to parathyroid surgery to avoid hypocalcemia and rebound bone resorption is not well described. Herein we report the case of a 62-year-old woman with steroid-induced osteoporosis who received denosumab for several years prior to undergoing parathyroidectomy. She had a history of lupus and required 20-60 mg of daily prednisone. Prior to her presentation at our institution, she was initially treated with alendronate and calcium/vitamin D supplementation. A dual-energy X-ray absorptiometry (DXA) scan 4 years after starting prednisone showed stable osteopenia in the lumbar spine and total hip but osteoporosis in the femoral neck with a significant reduction of bone mineral density (BMD) by 15.4% since baseline. Denosumab was initiated by her local endocrinologist for antiresorptive therapy due to declining bone density while on alendronate. She remained on prednisone for three additional years while on denosumab. 3 years of denosumab therapy resulted in stable bone density. Vitamin D levels were appropriate but elevations in PTH and calcium were noted. What was initially thought to be secondary hyperparathyroidism was at this point consistent with primary hyperparathyroidism (PHPT). A 4-dimensional computed tomography (4D CT) scan of the neck identified a parathyroid adenoma, and she was referred to our institution for parathyroidectomy. The timing of parathyroidectomy in relationship to the next denosumab injection was a concern due to the rebound bone resorption phenomenon and increased risk of vertebral fractures if denosumab is delayed or missed. Conversely, if denosumab is given in the periprocedural period, severe postsurgical hypocalcemia can result if denosumab prevents liberation of calcium from bone. Considering this, parathyroidectomy was performed 6 months after the last denosumab dose, and it was resumed 8 weeks after surgery. 1 month after surgery, calcium was normal, and PTH had recovered to mid-normal range. Her postoperative course was uncomplicated, and she was able to resume denosumab.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"8562872"},"PeriodicalIF":0.8,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coexisting ADAR and TSHB Mutations in an Infant With Retinal Detachment and Transient Cardiomyopathy.","authors":"Tamer Draidi, Mohammad Khalil, Abed Kabaha, Rafat Zuriqi, Mohammad Masu'd","doi":"10.1155/crie/5534847","DOIUrl":"10.1155/crie/5534847","url":null,"abstract":"<p><strong>Background: </strong>Central congenital hypothyroidism (C-CH) due to thyroid-stimulating hormone beta (TSHB) variants is rare and often missed by thyroid-stimulating hormone (TSH)-based neonatal screening. Adenosine deaminase acting on RNA (ADAR)-related Aicardi-Goutières syndrome type 6 (AGS6) is an interferonopathy with early-onset encephalopathy.</p><p><strong>Case summary: </strong>A term small-for-gestational-age male infant of consanguineous parents presented at 3 months with failure to thrive, generalized edema, transient hyperinsulinemic hypoglycemia and biventricular hypertrophy on echocardiography. Biochemistry showed profoundly low free thyroxine (FT4) and free triiodothyronine with inappropriately low TSH, consistent with central hypothyroidism, together with hypoalbuminemia and elevated liver enzymes. L-thyroxine replacement and nutritional rehabilitation corrected hypoglycemia and were followed by complete normalization of cardiac structure and function on repeat echocardiography. Persistent global developmental delay, hypotonia and abnormal eye movements prompted neuro-ophthalmological assessment, which demonstrated bilaterally small globes with peripheral retinal/choroidal detachment. Whole-exome sequencing identified a homozygous pathogenic ADAR frameshift variant (NM_001111.5:c.2433_2434del) and a homozygous likely pathogenic TSHB variant (NM_000549.5:c.313T >C; p.Cys105Arg), confirming combined ADAR-related encephalopathy and isolated C-CH. At 8 months the child remained growth-restricted with marked developmental delay but stable cardiorespiratory status.</p><p><strong>Conclusion: </strong>This case underscores the value of early genetic evaluation in infants with central hypothyroidism and syndromic features and of systematic cardiac surveillance in severe neonatal hypoglycemia to detect potentially reversible cardiomyopathy. To our knowledge, this is the first reported case of coexisting TSHB-related C-CH and ADAR-related AGS6 in the same infant.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2026 ","pages":"5534847"},"PeriodicalIF":0.8,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}