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Hyperparathyroidism 2(HRPT2)

MedGen UID:
310065
Concept ID:
C1704981
Neoplastic Process
Synonyms: CDC73-Related Disorders; HRPT2; HYPERPARATHYROIDISM, FAMILIAL PRIMARY, WITH MULTIPLE OSSIFYING JAW FIBROMAS; Hyperparathyroidism-Jaw Tumor Syndrome; HYPERPARATHYROIDISM-JAW TUMOR SYNDROME, HEREDITARY
Modes of inheritance:
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM, Orphanet
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
Autosomal dominant inheritance (HPO, OMIM, Orphanet)
SNOMED CT: Hyperparathyroidism 2 (702378002); Hyperparathyroidism-jaw tumor syndrome (702378002); Familial primary hyperparathyroidism with multiple ossifying jaw fibromas (702378002); Familial cystic parathyroid adenomatosis (702378002)
 
OMIM®: 145001
Orphanet: ORPHA99880

Definition

The spectrum of CDC73-related disorders includes the following phenotypes: Hyperparathyroidism-jaw tumor syndrome (HPT-JT). Parathyroid carcinoma. Familial isolated hyperparathyroidism (FIHP). Primary hyperparathyroidism, the main finding of HPT-JT syndrome, occurs in more than 70% of affected individuals; onset is typically in late adolescence or early adulthood. HPT-JT-associated primary hyperparathyroidism is usually caused by a single parathyroid adenoma. In approximately 10%-15% of cases, primary hyperparathyroidism is caused by parathyroid carcinoma. Ossifying fibromas of the mandible or maxilla, also known as cementifying fibromas and cemento-ossifying fibromas, occur in 30%-40% of individuals with HPT-JT syndrome. Although benign, these tumors can be locally aggressive and may continue to enlarge if not treated. Approximately 20% of individuals with HPT-JT syndrome have kidney lesions, most commonly cysts; renal hamartomas and (more rarely) Wilms tumor have also been reported. Benign and malignant uterine tumors appear to be common in women with HPT-JT syndrome. [from GTR]

Additional descriptions

From GeneReviews
The spectrum of CDC73-related disorders includes the following phenotypes: Hyperparathyroidism-jaw tumor syndrome (HPT-JT). Parathyroid carcinoma. Familial isolated hyperparathyroidism (FIHP). Primary hyperparathyroidism, the main finding of HPT-JT syndrome, occurs in more than 70% of affected individuals; onset is typically in late adolescence or early adulthood. HPT-JT-associated primary hyperparathyroidism is usually caused by a single parathyroid adenoma. In approximately 10%-15% of cases, primary hyperparathyroidism is caused by parathyroid carcinoma. Ossifying fibromas of the mandible or maxilla, also known as cementifying fibromas and cemento-ossifying fibromas, occur in 30%-40% of individuals with HPT-JT syndrome. Although benign, these tumors can be locally aggressive and may continue to enlarge if not treated. Approximately 20% of individuals with HPT-JT syndrome have kidney lesions, most commonly cysts; renal hamartomas and (more rarely) Wilms tumor have also been reported. Benign and malignant uterine tumors appear to be common in women with HPT-JT syndrome.  https://www.ncbi.nlm.nih.gov/books/NBK3789
From OMIM
Hyperparathyroidism-jaw tumor syndrome is a rare autosomal dominant disorder characterized by synchronous or metachronous occurrence of primary hyperparathyroidism, ossifying fibroma of the maxilla and/or mandible, renal tumor, and uterine tumors. It is associated with increased risk of parathyroid cancer (summary by Shibata et al., 2015).  http://www.omim.org/entry/145001
From GHR
Hyperparathyroidism-jaw tumor syndrome is a condition characterized by overactivity of the parathyroid glands (hyperparathyroidism). The four parathyroid glands are located in the neck and secrete a hormone that regulates the body's use of calcium. Hyperparathyroidism disrupts the normal balance of calcium in the blood, which can lead to kidney stones, thinning of the bones (osteoporosis), nausea, vomiting, high blood pressure (hypertension), weakness, and fatigue.In people with hyperthyroidism-jaw tumor syndrome, hyperparathyroidism is caused by tumors that form in the parathyroid glands. Typically only one of the four parathyroid glands is affected, but in some people, tumors are found in more than one gland. The tumors are usually noncancerous (benign), in which case they are called adenomas. Approximately 15 percent of people with hyperparathyroidism-jaw tumor syndrome develop a cancerous tumor called parathyroid carcinoma. People with hyperparathyroidism-jaw tumor syndrome may also have a type of benign tumor called a fibroma in the jaw. Even though jaw tumors are specified in the name of this condition, it is estimated that only 25 to 50 percent of affected individuals have this symptom.Other tumors, both benign and cancerous, are often seen in hyperparathyroidism-jaw tumor syndrome. For example, tumors of the uterus occur in about 75 percent of women with this condition. The kidneys are affected in about 20 percent of people with hyperparathyroidism-jaw tumor syndrome. Benign kidney cysts are the most common kidney feature, but a rare tumor called Wilms tumor and other types of kidney tumor have also been found.  https://ghr.nlm.nih.gov/condition/hyperparathyroidism-jaw-tumor-syndrome

Clinical features

Hyperparathyroidism
MedGen UID:
6967
Concept ID:
C0020502
Disease or Syndrome
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
Parathyroid adenoma
MedGen UID:
75502
Concept ID:
C0262587
Neoplastic Process
A benign tumor arising from the parenchymal cells of the parathyroid glands. In the vast majority of cases, the tumor involves a single parathyroid gland. It is associated with the symptoms of primary hyperparathyroidism, resulting from the excessive production of parathyroid hormone. It is usually surrounded by a well-defined capsule. Capsular invasion, vascular invasion, and perineural invasion are absent.
Parathyroid carcinoma
MedGen UID:
146361
Concept ID:
C0687150
Neoplastic Process
The spectrum of CDC73-related disorders includes the following phenotypes: Hyperparathyroidism-jaw tumor syndrome (HPT-JT). Parathyroid carcinoma. Familial isolated hyperparathyroidism (FIHP). Primary hyperparathyroidism, the main finding of HPT-JT syndrome, occurs in more than 70% of affected individuals; onset is typically in late adolescence or early adulthood. HPT-JT-associated primary hyperparathyroidism is usually caused by a single parathyroid adenoma. In approximately 10%-15% of cases, primary hyperparathyroidism is caused by parathyroid carcinoma. Ossifying fibromas of the mandible or maxilla, also known as cementifying fibromas and cemento-ossifying fibromas, occur in 30%-40% of individuals with HPT-JT syndrome. Although benign, these tumors can be locally aggressive and may continue to enlarge if not treated. Approximately 20% of individuals with HPT-JT syndrome have kidney lesions, most commonly cysts; renal hamartomas and (more rarely) Wilms tumor have also been reported. Benign and malignant uterine tumors appear to be common in women with HPT-JT syndrome.
Hurthle cell thyroid adenoma
MedGen UID:
237009
Concept ID:
C1336750
Neoplastic Process
A kind of thyroid adenoma characterized by the presence of oxyphil cells.
Hamartoma
MedGen UID:
6713
Concept ID:
C0018552
Neoplastic Process
A benign and excessive tumor-like growth of mature cells and normal tissues which grow in a disorganized pattern.
Nephroblastoma
MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.
Parathyroid adenoma
MedGen UID:
75502
Concept ID:
C0262587
Neoplastic Process
A benign tumor arising from the parenchymal cells of the parathyroid glands. In the vast majority of cases, the tumor involves a single parathyroid gland. It is associated with the symptoms of primary hyperparathyroidism, resulting from the excessive production of parathyroid hormone. It is usually surrounded by a well-defined capsule. Capsular invasion, vascular invasion, and perineural invasion are absent.
Pancreatic adenocarcinoma
MedGen UID:
83800
Concept ID:
C0281361
Neoplastic Process
An adenocarcinoma which arises from the exocrine pancreas. Ductal adenocarcinoma and its variants are the most common types of pancreatic adenocarcinoma.
Renal cortical adenoma
MedGen UID:
577332
Concept ID:
C0346253
Neoplastic Process
The presence of an adenoma in the cortex of the kidney.
Parathyroid carcinoma
MedGen UID:
146361
Concept ID:
C0687150
Neoplastic Process
The spectrum of CDC73-related disorders includes the following phenotypes: Hyperparathyroidism-jaw tumor syndrome (HPT-JT). Parathyroid carcinoma. Familial isolated hyperparathyroidism (FIHP). Primary hyperparathyroidism, the main finding of HPT-JT syndrome, occurs in more than 70% of affected individuals; onset is typically in late adolescence or early adulthood. HPT-JT-associated primary hyperparathyroidism is usually caused by a single parathyroid adenoma. In approximately 10%-15% of cases, primary hyperparathyroidism is caused by parathyroid carcinoma. Ossifying fibromas of the mandible or maxilla, also known as cementifying fibromas and cemento-ossifying fibromas, occur in 30%-40% of individuals with HPT-JT syndrome. Although benign, these tumors can be locally aggressive and may continue to enlarge if not treated. Approximately 20% of individuals with HPT-JT syndrome have kidney lesions, most commonly cysts; renal hamartomas and (more rarely) Wilms tumor have also been reported. Benign and malignant uterine tumors appear to be common in women with HPT-JT syndrome.
Papillary renal cell carcinoma
MedGen UID:
266300
Concept ID:
C1306837
Neoplastic Process
Also known as chromophil carcinoma, it represents a minority of renal cell carcinomas. It can be hereditary or sporadic. The sporadic papillary renal cell carcinoma is characterized by trisomy of chromosomes 7, 16, and 17, and loss of chromosome Y. The peak incidence is in the sixth and seven decades. It is classified as type 1 or 2, based on the cytoplasmic volume and the thickness of the lining neoplastic cells. The prognosis is more favorable than for conventional (clear cell) renal cell carcinoma. -- 2003
Hurthle cell thyroid adenoma
MedGen UID:
237009
Concept ID:
C1336750
Neoplastic Process
A kind of thyroid adenoma characterized by the presence of oxyphil cells.
Polycystic kidney dysplasia
MedGen UID:
9639
Concept ID:
C0022680
Disease or Syndrome
A usually autosomal dominant and less frequently autosomal recessive genetic disorder characterized by the presence of numerous cysts in the kidneys leading to end-stage renal failure. The autosomal dominant trait is associated with abnormalities on the short arm of chromosome 16. Symptoms in patients with the autosomal dominant trait usually appear at middle age and include abdominal pain, hematuria, and high blood pressure. Patients may develop brain aneurysms and liver cysts. Patients with the autosomal recessive trait present with progressive renal failure early in life and symptoms resulting from hepatic fibrosis. The autosomal recessive trait is associated with abnormalities of chromosome 6. Polycystic kidney disease may also result as a side effect in patients on renal dialysis.
Nephroblastoma
MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.
Renal cortical adenoma
MedGen UID:
577332
Concept ID:
C0346253
Neoplastic Process
The presence of an adenoma in the cortex of the kidney.
Nephrolithiasis
MedGen UID:
98227
Concept ID:
C0392525
Disease or Syndrome
Formation of stones in the KIDNEY.
Papillary renal cell carcinoma
MedGen UID:
266300
Concept ID:
C1306837
Neoplastic Process
Also known as chromophil carcinoma, it represents a minority of renal cell carcinomas. It can be hereditary or sporadic. The sporadic papillary renal cell carcinoma is characterized by trisomy of chromosomes 7, 16, and 17, and loss of chromosome Y. The peak incidence is in the sixth and seven decades. It is classified as type 1 or 2, based on the cytoplasmic volume and the thickness of the lining neoplastic cells. The prognosis is more favorable than for conventional (clear cell) renal cell carcinoma. -- 2003
Chronic pancreatitis
MedGen UID:
101753
Concept ID:
C0149521
Disease or Syndrome
A chronic form of pancreatitis.
Pancreatic adenocarcinoma
MedGen UID:
83800
Concept ID:
C0281361
Neoplastic Process
An adenocarcinoma which arises from the exocrine pancreas. Ductal adenocarcinoma and its variants are the most common types of pancreatic adenocarcinoma.
Polycystic kidney dysplasia
MedGen UID:
9639
Concept ID:
C0022680
Disease or Syndrome
A usually autosomal dominant and less frequently autosomal recessive genetic disorder characterized by the presence of numerous cysts in the kidneys leading to end-stage renal failure. The autosomal dominant trait is associated with abnormalities on the short arm of chromosome 16. Symptoms in patients with the autosomal dominant trait usually appear at middle age and include abdominal pain, hematuria, and high blood pressure. Patients may develop brain aneurysms and liver cysts. Patients with the autosomal recessive trait present with progressive renal failure early in life and symptoms resulting from hepatic fibrosis. The autosomal recessive trait is associated with abnormalities of chromosome 6. Polycystic kidney disease may also result as a side effect in patients on renal dialysis.
Nephroblastoma
MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.
Renal cortical adenoma
MedGen UID:
577332
Concept ID:
C0346253
Neoplastic Process
The presence of an adenoma in the cortex of the kidney.
Nephrolithiasis
MedGen UID:
98227
Concept ID:
C0392525
Disease or Syndrome
Formation of stones in the KIDNEY.
Papillary renal cell carcinoma
MedGen UID:
266300
Concept ID:
C1306837
Neoplastic Process
Also known as chromophil carcinoma, it represents a minority of renal cell carcinomas. It can be hereditary or sporadic. The sporadic papillary renal cell carcinoma is characterized by trisomy of chromosomes 7, 16, and 17, and loss of chromosome Y. The peak incidence is in the sixth and seven decades. It is classified as type 1 or 2, based on the cytoplasmic volume and the thickness of the lining neoplastic cells. The prognosis is more favorable than for conventional (clear cell) renal cell carcinoma. -- 2003
Chronic pancreatitis
MedGen UID:
101753
Concept ID:
C0149521
Disease or Syndrome
A chronic form of pancreatitis.
Hypercalcemia
MedGen UID:
5686
Concept ID:
C0020437
Disease or Syndrome
Abnormally high concentration of calcium in the peripheral blood.
Abnormality of the head
MedGen UID:
867438
Concept ID:
C4021812
Anatomical Abnormality
An abnormality of the head.
Hyperparathyroidism
MedGen UID:
6967
Concept ID:
C0020502
Disease or Syndrome
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.
Parathyroid adenoma
MedGen UID:
75502
Concept ID:
C0262587
Neoplastic Process
A benign tumor arising from the parenchymal cells of the parathyroid glands. In the vast majority of cases, the tumor involves a single parathyroid gland. It is associated with the symptoms of primary hyperparathyroidism, resulting from the excessive production of parathyroid hormone. It is usually surrounded by a well-defined capsule. Capsular invasion, vascular invasion, and perineural invasion are absent.
Parathyroid carcinoma
MedGen UID:
146361
Concept ID:
C0687150
Neoplastic Process
The spectrum of CDC73-related disorders includes the following phenotypes: Hyperparathyroidism-jaw tumor syndrome (HPT-JT). Parathyroid carcinoma. Familial isolated hyperparathyroidism (FIHP). Primary hyperparathyroidism, the main finding of HPT-JT syndrome, occurs in more than 70% of affected individuals; onset is typically in late adolescence or early adulthood. HPT-JT-associated primary hyperparathyroidism is usually caused by a single parathyroid adenoma. In approximately 10%-15% of cases, primary hyperparathyroidism is caused by parathyroid carcinoma. Ossifying fibromas of the mandible or maxilla, also known as cementifying fibromas and cemento-ossifying fibromas, occur in 30%-40% of individuals with HPT-JT syndrome. Although benign, these tumors can be locally aggressive and may continue to enlarge if not treated. Approximately 20% of individuals with HPT-JT syndrome have kidney lesions, most commonly cysts; renal hamartomas and (more rarely) Wilms tumor have also been reported. Benign and malignant uterine tumors appear to be common in women with HPT-JT syndrome.
Hurthle cell thyroid adenoma
MedGen UID:
237009
Concept ID:
C1336750
Neoplastic Process
A kind of thyroid adenoma characterized by the presence of oxyphil cells.

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVHyperparathyroidism 2
Follow this link to review classifications for Hyperparathyroidism 2 in Orphanet.

Recent clinical studies

Etiology

Bellido V, Larrañaga I, Guimón M, Martinez-Conde R, Eguia A, Perez de Nanclares G, Castaño L, Gaztambide S
Endocr Pathol 2016 Jun;27(2):142-6. doi: 10.1007/s12022-016-9427-6. PMID: 26995009
Koberstein W, Fung C, Romaniuk K, Abele JT
Can Assoc Radiol J 2016 May;67(2):115-21. Epub 2015 Dec 11 doi: 10.1016/j.carj.2015.06.002. PMID: 26687323
Shibata Y, Yamazaki M, Takei M, Uchino S, Sakurai A, Komatsu M
Endocr J 2015;62(7):627-32. Epub 2015 May 8 doi: 10.1507/endocrj.EJ15-0057. PMID: 25959515
Kuczera P, Adamczak M, Wiecek A
Clin Endocrinol (Oxf) 2014 Apr;80(4):607-12. Epub 2013 Oct 10 doi: 10.1111/cen.12326. PMID: 24111496
Passeri E, Bugiardini E, Sansone VA, Valaperta R, Costa E, Ambrosi B, Meola G, Corbetta S
J Neurol Sci 2013 Aug 15;331(1-2):132-5. Epub 2013 Jun 25 doi: 10.1016/j.jns.2013.06.008. PMID: 23809192

Diagnosis

Bellido V, Larrañaga I, Guimón M, Martinez-Conde R, Eguia A, Perez de Nanclares G, Castaño L, Gaztambide S
Endocr Pathol 2016 Jun;27(2):142-6. doi: 10.1007/s12022-016-9427-6. PMID: 26995009
Koberstein W, Fung C, Romaniuk K, Abele JT
Can Assoc Radiol J 2016 May;67(2):115-21. Epub 2015 Dec 11 doi: 10.1016/j.carj.2015.06.002. PMID: 26687323
Passeri E, Bugiardini E, Sansone VA, Valaperta R, Costa E, Ambrosi B, Meola G, Corbetta S
J Neurol Sci 2013 Aug 15;331(1-2):132-5. Epub 2013 Jun 25 doi: 10.1016/j.jns.2013.06.008. PMID: 23809192
Tonelli F, Giudici F, Cavalli T, Brandi ML
Clinics (Sao Paulo) 2012;67 Suppl 1:155-60. PMID: 22584722Free PMC Article
Cetani F, Pardi E, Ambrogini E, Banti C, Viacava P, Borsari S, Bilezikian JP, Pinchera A, Marcocci C
J Endocrinol Invest 2008 Oct;31(10):900-4. doi: 10.1007/BF03346439. PMID: 19092296Free PMC Article

Therapy

Mathews JW, Winchester R, Alsaygh N, Bartlett AM, Luttrell L
Am J Med Sci 2016 Sep;352(3):302-5. Epub 2016 Jul 1 doi: 10.1016/j.amjms.2016.06.020. PMID: 27650236
Kuczera P, Adamczak M, Wiecek A
Clin Endocrinol (Oxf) 2014 Apr;80(4):607-12. Epub 2013 Oct 10 doi: 10.1111/cen.12326. PMID: 24111496
Wolff EF, Hill MJ, Simonds WF, Segars JH
Fertil Steril 2012 Dec;98(6):1616-9. Epub 2012 Sep 8 doi: 10.1016/j.fertnstert.2012.08.017. PMID: 22963808Free PMC Article
Schweitzer DH
Obes Surg 2007 Nov;17(11):1510-6. PMID: 18219780
Brown AJ
J Steroid Biochem Mol Biol 2007 Mar;103(3-5):578-83. Epub 2006 Dec 27 doi: 10.1016/j.jsbmb.2006.12.089. PMID: 17368185

Prognosis

Koberstein W, Fung C, Romaniuk K, Abele JT
Can Assoc Radiol J 2016 May;67(2):115-21. Epub 2015 Dec 11 doi: 10.1016/j.carj.2015.06.002. PMID: 26687323
Shen DF, Liu X, Yang XF, Fang L, Gao Y, Zhao S, Wu JC, Shi S, Li JJ, Zhao XX, Gou WF, Zheng HC
Tumour Biol 2016 Mar;37(3):2909-24. Epub 2015 Sep 26 doi: 10.1007/s13277-015-4103-x. PMID: 26409451
Parfitt J, Harris M, Wright JM, Kalamchi S
J Oral Maxillofac Surg 2015 Jan;73(1):194.e1-9. Epub 2014 Sep 28 doi: 10.1016/j.joms.2014.09.008. PMID: 25511968
Mehta A, Patel D, Rosenberg A, Boufraqech M, Ellis RJ, Nilubol N, Quezado MM, Marx SJ, Simonds WF, Kebebew E
Surgery 2014 Dec;156(6):1315-24; discussion 1324-5. Epub 2014 Oct 16 doi: 10.1016/j.surg.2014.08.004. PMID: 25444225Free PMC Article
Wang TT, Zhang R, Wang L, Chen Y, Dong Q, Li TJ
Diagn Pathol 2014 Mar 28;9:75. doi: 10.1186/1746-1596-9-75. PMID: 24678936Free PMC Article

Clinical prediction guides

Koberstein W, Fung C, Romaniuk K, Abele JT
Can Assoc Radiol J 2016 May;67(2):115-21. Epub 2015 Dec 11 doi: 10.1016/j.carj.2015.06.002. PMID: 26687323
Parfitt J, Harris M, Wright JM, Kalamchi S
J Oral Maxillofac Surg 2015 Jan;73(1):194.e1-9. Epub 2014 Sep 28 doi: 10.1016/j.joms.2014.09.008. PMID: 25511968
Wang TT, Zhang R, Wang L, Chen Y, Dong Q, Li TJ
Diagn Pathol 2014 Mar 28;9:75. doi: 10.1186/1746-1596-9-75. PMID: 24678936Free PMC Article
Tonelli F, Giudici F, Cavalli T, Brandi ML
Clinics (Sao Paulo) 2012;67 Suppl 1:155-60. PMID: 22584722Free PMC Article
Yajima I, Tanizawa T, Yamamoto N, Fukuda T, Higashi T, Tabata S, Yao R, Yamato H, Murayama H
Ther Apher Dial 2009 Feb;13(1):83-7. doi: 10.1111/j.1744-9987.2009.00605.x. PMID: 19379176

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