atrophy

a wasting away of an organ or part, or a failure to grow to normal size as the result of disease, faulty nutrition, etc.

Collins Discovery Encyclopedia, 1st edition © HarperCollins Publishers 2005

atrophy

[′a·trə·fē]

(medicine)

Diminution in the size of a cell, tissue, or organ that was once fully developed and of normal size.

The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.

Atrophy

the decrease in the size of an organ or tissue of the living organism of animals and man, accompanied by a disorder or cessation of functions. Atrophy is the result of a predominance of dissimilation over the processes of assimilation.

Atrophy can be physiological and pathological, systemic and local. Physiological atrophy is a function of the growth changes of an organism (atrophy of the thymus during puberty, atrophy of the sex glands, skin, and bones in old people, and so on). General pathological atrophy (emaciation, cachexia) appears in cases of insufficient nutrition, chronic infection or intoxication, or disorders of the endocrine glands or of the central nervous system. Local pathological atrophy arises from various causes—from a disorder in the regulation of the trophic nerves (for example, atrophy of the skeletal muscles during poliomyelitis), from insufficient supply of blood (for example, atrophy of the brain cortex during atherosclerosis of the blood vessels of the brain); dysfunctional atrophy (for example, atrophy of the optic nerve after removal of an eye), as a result of pressure (for example, atrophy of the kidney in cases of embolism of the urether and accumulation of urine in the renal pelvis), from lack of use (for example, atrophy of the muscles in the extremities after long immobilization), or from the effects of physiological and chemical factors (for example, atrophy of the lymphoid tissue from the effects of solar energy, atrophy of the thyroid gland upon application of iodine preparations).

When an organ atrophies it diminishes in size but subsequently sometimes appears larger as a result of the expansion of fat tissue which replaces the atrophied cellular elements. Pathological atrophy is, up to a certain stage, a reversible process. Treatment consists of the elimination of the causes producing atrophy.

REFERENCES

Strukov, A. I. Patologicheskaia anatomiia. Moscow, 1967.
Cameron, G. R. Pathology of the Cell. Edinburgh, 1952.

L. D. LIOZNER

Mentioned in

References in periodicals archive

Sample profile: An individual over 18 years of age previously diagnosed with Charcot-Marie-Tooth disease and now suffering with mechanical neck and arm pain.

The Bournemouth questionnaire as an outcome measure in the rehabilitation of a person suffering with mechanical neck and arm pain and concurrent Charcot-Marie-Tooth disease: a case report

Ganglioside-induced differentiation-associated protein-1 is mutant in Charcot-Marie-Tooth disease type 4A/8q21.

Genetics of hereditary motor and sensory neuropathy and the Costa Rican contribution

Charcot-Marie-Tooth disease. Eur J Hum Genet 2009; 17: 703-10.

Charcot-Marie-Tooth type 1A disease from patient to laboratory

Flexor digitorum superficialis opposition tendon transfer improves hand function in children with Charcot-Marie-Tooth disease: Case series.

Nine-hole Peg Test and Ten-meter Walk Test for Evaluating Functional Loss in Chinese Charcot-Marie-Tooth Disease

The peripheral myelin PMP-22/GAS-3 is duplicated in Charcot-Marie-Tooth disease type 1A.

Polymorphic short tandem repeats for diagnosis of the Charcot-Marie-Tooth IA duplication

- The United States Food and Drug Administration has granted Fast Track designation to ACE-083, US-based biopharmaceutical company Acceleron Pharma Inc.'s (NASDAQ: XLRN) locally-acting "Myostatin+" muscle agent, for the treatment of patients with Charcot-Marie-Tooth disease.

Acceleron Receives FDA Fast Track Designation for ACE-083 in Charcot-Marie-Tooth Disease

Charcot-Marie-Tooth disease (CMT), also termed hereditary motor and sensory neuropathy (HNSN), is the most common inherited neuromuscular disorders with an incidence of one in 2500 individuals.[sup][1] It is clinically characterized by progressive distal muscle weakness, muscle atrophy, areflexia, sensory deficit, and skeletal deformities.

A Novel Missense Mutation in Peripheral Myelin Protein-22 Causes Charcot-Marie-Tooth Disease

Charcot-Marie-Tooth disease (CMT, [4] MIM 118220) is a common Mendelian disorder with a frequency of 1 in 2500 (1).

New polymorphic short tandem repeats for PCR-based Charcot-Marie-Tooth disease type 1A duplication diagnosis

- US-based biopharmaceutical company Regenacy Pharmaceuticals, LLC has forged a collaboration with the Charcot-Marie-Tooth Association, a registered non-profit organization serving the hereditary neuropathy patient community, to validate the role of HDAC6 in multiple forms of Charcot-Marie-Tooth disease and evaluate the efficacy of ricolinostat, a selective HDAC6 inhibitor, in animal models, the company said.

Regenacy Pharmaceuticals Teams with the Charcot-Marie-Tooth Association to Advance Ricolinostat for the Treatment of Hereditary Neuropathy

Transient white matter lesions in X-linked Charcot-Marie-Tooth disease type 1 with novel I20T mutation of gap junction protein beta 1 gene (in Chinese).

Clinical and Genetic Features of Chinese X-linked Charcot-Marie-Tooth Type 1 Disease

Two examples of diseases caused by alterations in gene dosage are the autosomal dominant demyelinating peripheral neuropathy Charcot-Marie-Tooth disease type 1A (CMT1A) [1] and hereditary neuropathy with liability to pressure palsies (HNPP).

Rapid real-time fluorescent PCR gene dosage test for the diagnosis of DNA duplications and deletions