Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/12/10 22:57:02」(JST)

wiki en

Hyperplasia (from ancient Greek ὑπέρ huper, "over" + πλάσις plasis, "formation"), or hypergenesis, means an increase in the number of cells or a proliferation of cells. It may result in the gross enlargement of an organ and the term is sometimes confused with benign neoplasia or benign tumor.

Hyperplasia is a common preneoplastic response to stimulus. Microscopically, cells resemble normal cells but are increased in numbers. Sometimes cells may also be increased in size (hypertrophy).^[1] Hyperplasia is different from hypertrophy in that the adaptive cell change in hypertrophy is an increase in the size of cells, whereas hyperplasia involves an increase in the number of cells.

Simple illustration to show the difference between hyperplasia and hypertrophy

Difference from neoplasia

Hyperplasia is considered to be a physiological (normal) response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.^[2]

As seen in examples below, such physiological proliferation of cells may in fact be secondarily due to a pathological cause. Still, the proliferation itself is a normal response to another abnormal condition, in contrast to neoplasia, where the proliferation in itself is abnormal.

Causes

Hyperplasia may be due to any number of causes, including increased demand (for example, proliferation of basal layer of epidermis to compensate skin loss), chronic inflammatory response, hormonal dysfunctions, or compensation for damage or disease elsewhere. Hyperplasia may be harmless and occur on a particular tissue. An example of a normal hyperplastic response would be the growth and multiplication of milk-secreting glandular cells in the breast as a response to pregnancy, thus preparing for future breast feeding.

Hyperplasia may also be induced artificially by injecting hormones such as IGF-1 and human growth hormone. Perhaps the most interesting and potent effect IGF has on the human body is its ability to cause hyperplasia, which is an actual splitting of cells.^{[original research?]} By contrast, hypertrophy is what occurs, for example, to skeletal muscle cells during weight training and steroid use and is simply an increase in the size of the cells. With IGF use, one is able to cause hyperplasia which actually increases the number of muscle cells present in the tissue. Weight training with or without anabolic steroid use enables these new cells to mature in size and strength. In addition, animal tests have shown that stretching a muscle can trigger hyperplasia, though this phenomenon has yet to be confirmed in humans. It is theorized that hyperplasia may also be induced through specific power output training for athletic performance, thus increasing the number of muscle fibers instead of increasing the size of a single fiber. This mechanism has thus far only been observed in birds.^[3]

Hyperplasia may also occur abnormally, and is associated with a variety of clinical diseases.

Examples in human biology and disease

Patient with hemihyperplasia involving the upper and lower left extremities. The leg length discrepancy can be noted by the pelvic tilt.

Some of the more commonly known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:

Benign prostatic hyperplasia, also known as prostate enlargement.
Cushing's disease – Physiopathology of hyperplasia of adrenal cortex due to increased circulating level of ACTH (adrenocorticotropic hormone).
Congenital adrenal hyperplasia
Endometrial hyperplasia – Hyperproliferation of the endometrium, usually in response to unopposed estrogen stimulation in the setting of polycystic ovary syndrome or exogenous administration of hormones. Atypical endometrial hyperplasia may represent an early neoplastic process which can lead to endometrial adenocarcinoma.
Hemihyperplasia when only half (or one side) of the body is affected, sometimes generating limbs of different lengths.
Hyperplasia of the breast – "Hyperplastic" lesions of the breast include usual ductal hyperplasia, a focal expansion of the number of cells in a terminal breast duct, and atypical ductal hyperplasia, in which a more abnormal pattern of growth is seen, and which is associated with an increased risk of developing breast cancer. The biology of these lesions is the subject of dispute, with some authorities arguing that both of these lesions are the result of neoplasia, and that the application of the term "hyperplasia" in this instance is "inaccurate."^[4]
Intimal hyperplasia – The thickening of the Tunica intima of a blood vessel as a complication of a reconstruction procedure or endarterectomy. Intimal hyperplasia is the universal response of a vessel to injury and is an important reason of late bypass graft failure, particularly in vein and synthetic vascular grafts.
Focal epithelial hyperplasia (also known as Heck's disease) – This is a wart-like growth in the mucous tissues of the mouth or, rarely, throat that is caused by certain sub-types of the human papillomavirus (HPV). Heck's disease has not been known to cause cancer.
Sebaceous hyperplasia – In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.
Compensatory liver hyperplasia – The liver undergoes cellular division after acute injury, resulting in new cells that restore liver function back to baseline. Approximately 75% of the liver can be acutely damaged or resected with seemingly full regeneration through hepatocyte division, i.e., hyperplasia. This is what makes living-donor liver transplants possible.

References

^ M. Donald McGavin, James F. Zachary (2007). Pathologic Basis of Veterinary Disease, Fourth Edition. Mosby Elsevier.
^ Ramzi Cotran et al (1999). Robbins pathologic basis of disease (6th ed.). W.B. Saunders. ISBN 0-7216-7335-X. OCLC 222671811.
^ Antonio J, Gonyea WJ (Aug 1994). "Muscle fiber splitting in stretch-enlarged avian muscle". Med Sci Sports Exerc. 26 (8): 973–977. PMID 7968431.
^ Tavassoli FA (2005). "Breast pathology: rationale for adopting the ductal intraepithelial neoplasia (DIN) classification". Nature Clinical Practice Oncology 2 (3): 116–117. doi:10.1038/ncponc0109. PMID 16264885.

External links

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. ベックウィズ・ヴィーデマン症候群 beckwith wiedemann syndrome
2. ウィルムス腫瘍の症状、診断、および病期分類 presentation diagnosis and staging of wilms tumor
3. Klippel-Trenaunay syndrome: Clinical manifestations, diagnosis, and management
4. 限局性結節性過形成 focal nodular hyperplasia
5. 低身長の原因 causes of short stature

English Journal

High frequency of copy number variations (CNVs) in the chromosome 11p15 region in patients with Beckwith-Wiedemann syndrome.

Baskin B, Choufani S, Chen YA, Shuman C, Parkinson N, Lemyre E, Micheil Innes A, Stavropoulos DJ, Ray PN, Weksberg R.Author information The Rudbeck Laboratory, Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.AbstractBeckwith-Wiedemann syndrome (BWS), an overgrowth and tumor predisposition syndrome is clinically heterogeneous. Its variable presentation makes molecular diagnosis particularly important for appropriate counseling of patients with respect to embyronal tumor risk and recurrence risk. BWS is characterized by macrosomia, omphalocele, and macroglossia. Additional clinical features can include hemihyperplasia, embryonal tumors, umbilical hernia, and ear anomalies. BWS is etiologically heterogeneous arising from dysregulation of one or both of the chromosome 11p15.5 imprinting centers (IC) and/or imprinted growth regulatory genes on chromosome 11p15.5. Most BWS cases are sporadic and result from loss of maternal methylation at imprinting center 2 (IC2), gain of maternal methylation at imprinting center 1 (IC1) or paternal uniparental disomy (UPD). Heritable forms of BWS (15 %) have been attributed mainly to mutations in the growth suppressor gene CDKN1C, but have also infrequently been identified in patients with copy number variations (CNVs) in the chromosome 11p15.5 region. Four hundred and thirty-four unrelated BWS patients referred to the molecular diagnostic laboratory were tested by methylation-specific multiplex ligation-dependent probe amplification. Molecular alterations were detected in 167 patients, where 103 (62 %) showed loss of methylation at IC2, 23 (14 %) had gain of methylation at IC1, and 41 (25 %) showed changes at both ICs usually associated with paternal UPD. In each of the three groups, we identified patients in whom the abnormalities in the chromosome 11p15.5 region were due to CNVs. Surprisingly, 14 patients (9 %) demonstrated either deletions or duplications of the BWS critical region that were confirmed using comparative genomic hybridization array analysis. The majority of these CNVs were associated with a methylation change at IC1. Our results suggest that CNVs in the 11p15.5 region contribute significantly to the etiology of BWS. We highlight the importance of performing deletion/duplication testing in addition to methylation analysis in the molecular investigation of BWS to improve our understanding of the molecular basis of this disorder, and to provide accurate genetic counseling.
Human genetics.Hum Genet.2013 Oct 24. [Epub ahead of print]
Beckwith-Wiedemann syndrome (BWS), an overgrowth and tumor predisposition syndrome is clinically heterogeneous. Its variable presentation makes molecular diagnosis particularly important for appropriate counseling of patients with respect to embyronal tumor risk and recurrence risk. BWS is character
PMID 24154661

Diffuse capillary malformation with overgrowth: a clinical subtype of vascular anomalies with hypertrophy.

Lee MS, Liang MG, Mulliken JB.Author information Dermatology Program, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: margaret.lee@childrens.harvard.edu.AbstractBACKGROUND: Categorization of vascular anomalies with overgrowth is evolving rapidly with the aid of massively parallel genomic sequencing; however, accurate clinical diagnosis is still essential. We identified a group of patients with an extensive, diffuse, reticulate capillary malformation (CM) and variable hypertrophy without major complications.
Journal of the American Academy of Dermatology.J Am Acad Dermatol.2013 Oct;69(4):589-94. doi: 10.1016/j.jaad.2013.05.030. Epub 2013 Jul 29.
BACKGROUND: Categorization of vascular anomalies with overgrowth is evolving rapidly with the aid of massively parallel genomic sequencing; however, accurate clinical diagnosis is still essential. We identified a group of patients with an extensive, diffuse, reticulate capillary malformation (CM) an
PMID 23906555

Clinical features of three girls with mosaic genome-wide paternal uniparental isodisomy.

Kalish JM, Conlin LK, Bhatti TR, Dubbs HA, Harris MC, Izumi K, Mostoufi-Moab S, Mulchandani S, Saitta S, States LJ, Swarr DT, Wilkens AB, Zackai EH, Zelley K, Bartolomei MS, Nichols KE, Palladino AA, Spinner NB, Deardorff MA.Author information The Division of Genetics, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.AbstractHere we describe three subjects with mosaic genome-wide paternal uniparental isodisomy (GWpUPD) each of whom presented initially with overgrowth, hemihyperplasia (HH), and hyperinsulinism (HI). Due to the severity of findings and the presence of additional features, SNP array testing was performed, which demonstrated mosaic GWpUPD. Comparing these individuals to 10 other live-born subjects reported in the literature, the predominant phenotype is that of pUPD11 and notable for a very high incidence of tumor development. Our subjects developed non-metastatic tumors of the adrenal gland, kidney, and/or liver. All three subjects had pancreatic hyperplasia resulting in HI. Notably, our subjects to date display minimal features of other diseases associated with paternal UPD loci. Both children who survived the neonatal period have displayed near-normal cognitive development, likely due to a favorable tissue distribution of the mosaicism. To understand the range of UPD mosaicism levels, we studied multiple tissues using SNP array analysis and detected levels of 5-95%, roughly correlating with the extent of tissue involvement. Given the rapidity of tumor growth and the difficulty distinguishing malignant and benign tumors in these GWpUPD subjects, we have utilized increased frequency of ultrasound (US) and alpha-fetoprotein (AFP) screening in the first years of life. Because of a later age of onset of additional tumors, continued tumor surveillance into adolescence may need to be considered in these rare patients.
American journal of medical genetics. Part A.Am J Med Genet A.2013 Aug;161A(8):1929-39. doi: 10.1002/ajmg.a.36045. Epub 2013 Jun 26.
Here we describe three subjects with mosaic genome-wide paternal uniparental isodisomy (GWpUPD) each of whom presented initially with overgrowth, hemihyperplasia (HH), and hyperinsulinism (HI). Due to the severity of findings and the presence of additional features, SNP array testing was performed,
PMID 23804593

Japanese Journal

半側(片側)肥大症の1例

村山高章,森崎市治郎
障害者歯科 = JOURNAL OF THE JAPANESE SOIETY FOR DISABILITY AND ORAL HEALTH 25(2), 161-167, 2004-06-30
NAID 10013298260

多発奇形を合併した胸部腎の 2 例

細川友佳子,水田祥代,野口伸一,田口智章,増本幸二
日本小児外科学会雑誌 37(2), 292-298, 2001-04-20
胸部腎は非常にまれな病態である.われわれは多発奇形を合併した胸部腎を2例経験したので, 文献的考察を加え報告する.症例1は0生日, 女児で, Body Stalk Anomaryの精査にて体部CTを行った際, 左胸部腎を指摘された.その他左横隔膜弛緩症, 右足趾低形成を合併していた.症例2は10カ月, 男児.肺炎を罹患した時の胸写にて右胸部腎を偶然発見されている.外性器奇形(両側停留睾丸, 尿道下 …
NAID 110002112328

片側過形成症の歯科矯正学的観察

坂本朝,野口規久男,黒田敬之
日本矯正歯科学会雑誌 56(4), 234-244, 1997-08
片側過形成症はまれな疾患であり, 胎生期における発育異常が原因と考えられている.歯科矯正学的には上下顎骨や歯の成長発育に左右非対称が生じ, それに起因したさまざまな不正咬合を生じる.今回, 著者らは2例の片側過形成症をそれぞれ数年間にわたって観察したので報告する.症例1 : 病変が右側顔面に限局した顔面片側過形成症患者で初診時年齢の男子.症例2 : 病変が右側全身に現れている片側過形成症患者で初 …
NAID 110004018175

Related Pictures

Bring my sons from afar: BWS - Hemihypertrophy/Hemihyperplasia Hemihypertrophy & Hemihyperplasia – DrGreene.com Beckwith – Wiedemann syndrome (Genetics) Hemihyperplasia Informative Speech - YouTube Hemihyperplasia | Children's Hospital of Philadelphia facial hemihypertrophy Hemihypertrophy | definition of hemihypertrophy by Medical dictionary

★リンクテーブル★

リンク元

「片側肥大症候群」

Hyperplas
	Classification and external resources
MedlinePlus	003441
MeSH	D006965

　　[★]

英: hemihyperplasia syndrome HHS hemihyperplasia
関: 過成長症候群

[McGavin-1] M. Donald McGavin, James F. Zachary (2007). Pathologic Basis of Veterinary Disease, Fourth Edition. Mosby Elsevier.

[robbins-2] Ramzi Cotran et al (1999). Robbins pathologic basis of disease (6th ed.). W.B. Saunders. ISBN 0-7216-7335-X. OCLC 222671811.

[3] Antonio J, Gonyea WJ (Aug 1994). "Muscle fiber splitting in stretch-enlarged avian muscle". Med Sci Sports Exerc. 26 (8): 973–977. PMID 7968431.

[4] Tavassoli FA (2005). "Breast pathology: rationale for adopting the ductal intraepithelial neoplasia (DIN) classification". Nature Clinical Practice Oncology 2 (3): 116–117. doi:10.1038/ncponc0109. PMID 16264885.

匿名

検索

案内

案内

hemihyperplasia