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     Acromegaly and Gigantism

Acromegaly (from Greek akros "extreme" or "extremities" and megas "large" - extremities enlargement) is a hormonal disorder that results when the pituitary gland produces excess growth hormone (hGH). Most commonly it is a benign hGH producing tumor derived from a distinct type of cells (somatotrophs) and called pituitary adenoma.

Acromegaly most commonly affects middle-aged adults and can result in serious illness and premature death. Because of its insidious pathogenesis and slow progression, the disease is hard to diagnose in the early stages and is frequently missed for many years.

Symptoms Features that result from high level of hGH or expanding tumor include: * Soft tissue swelling of the hands and feet * Brow and lower jaw protrusion * Enlarging hands * Enlarging feet * Arthritis and carpal tunnel syndrome * Teeth spacing increase * Macroglossia [enlarged tongue] * Heart failure * Compression of the optic chiasm leading to loss of vision in the outer visual fields (typically bitemporal hemianopia) * Headache * Diabetes mellitus * Hypertension * Increased palmar sweating and sebum production over the face (seborrhea) are clinical indicators of active growth hormone (GH) producing pituitary tumours. These symptoms can also be used to monitor the activity of the tumour after surgery although biochemical monitoring is confirmatory. [edit] Causes [edit] Pituitary adenoma In over 90 percent of acromegaly patients, the overproduction of GH is caused by a benign tumor of the pituitary gland, called an adenoma. These tumors produce excess GH and, as they expand, compress surrounding brain tissues, such as the optic nerves. This expansion causes the headaches and visual disturbances that are often symptoms of acromegaly. In addition, compression of the surrounding normal pituitary tissue can alter production of other hormones, leading to changes in menstruation and breast discharge in women and impotence in men because of reduced testosterone production. There is a marked variation in rates of GH production and the aggressiveness of the tumor. Some adenomas grow slowly and symptoms of GH excess are often not noticed for many years. Other adenomas grow rapidly and invade surrounding brain areas or the sinuses, which are located near the pituitary. In general, younger patients tend to have more aggressive tumors. Most pituitary tumors arise spontaneously and are not genetically inherited. Many pituitary tumors arise from a genetic alteration in a single pituitary cell which leads to increased cell division and tumor formation. This genetic change, or mutation, is not present at birth, but is acquired during life. The mutation occurs in a gene that regulates the transmission of chemical signals within pituitary cells; it permanently switches on the signal that tells the cell to divide and secrete GH. The events within the cell that cause disordered pituitary cell growth and GH oversecretion currently are the subject of intensive research. [edit] Other tumors In a few patients, acromegaly is caused not by pituitary tumors but by tumors of the pancreas, lungs, and adrenal glands. These tumors also lead to an excess of GH, either because they produce GH themselves or, more frequently, because they produce GHRH, the hormone that stimulates the pituitary to make GH. In these patients, the excess GHRH can be measured in the blood and establishes that the cause of the acromegaly is not due to a pituitary defect. When these non-pituitary tumors are surgically removed, GH levels fall and the symptoms of acromegaly improve. In patients with GHRH-producing, non-pituitary tumors, the pituitary still may be enlarged and may be mistaken for a tumor. Therefore, it is important that physicians carefully analyze all "pituitary tumors" removed from patients with acromegaly in order not to overlook the possibility that a tumor elsewhere in the body is causing the disorder. [edit] Diagnosis If acromegaly is suspected, medical imaging and medical laboratory investigations are generally used together to confirm or rule out the presence of this condition. [edit] Hormonal IGF1 provides the most sensitive and useful lab test for the diagnosis of acromegaly. A single value of the Growth hormone (GH) is not useful in view of its pulsatality (levels in the blood vary greatly even in healthy individuals). GH levels taken 2 hours after a 75 gram glucose tolerance test are helpful in the diagnosis: GH levels are suppressed below 1 ?g/L in normal people, and levels higher than this cutoff are confirmatory of acromegaly. Other pituitary hormones have to be assessed to address the secretory effects of the tumour as well as the mass effect of the tumor on the normal pituitary gland. They include TSH (thyroid stimulating hormone), gonadotropic hormones (FSH,LH), ACTH (adrenocorticotropic hormone), prolactin. [edit] Radiological An MRI of the brain focussing on the sella turcica after gadolinium administration allows for clear delineation of the pituitary and the hypothalamus and the location of the tumour. [edit] Treatment The goals of treatment are to reduce GH production to normal levels, to relieve the pressure that the growing pituitary tumor exerts on the surrounding brain areas, to preserve normal pituitary function, and to reverse or ameliorate the symptoms of acromegaly. Currently, treatment options include surgical removal of the tumor, drug therapy, and radiation therapy of the pituitary. [edit] Surgery Surgery is a rapid and effective treatment, of which there are two alternative methods. The first method, a procedure known as transsphenoidal surgery, involves the surgeon reaching the pituitary through an incision in the nose and, with special tools, removing the tumor tissue. The second method is the removal of the tumor via a craniotomy, during which a bone flap is removed from the patient's skull to allow access to the tumor from the front and side. Once the tumor has been removed, the section of bone is replaced. Transsphenoidal surgery is a less invasive procedure with a shorter recovery time than a craniotomy, yet the likelihood of successfully removing the entire tumor is lower. Consequently, transsphenoidal surgery is often used as a first option, with craniotomy and other treatments being used to remove any remaining tumor. These procedures promptly relieve the pressure on the surrounding brain regions and lead to a lowering of GH levels. If the surgery is successful, facial appearance and soft tissue swelling improve within a few days. Surgery is most successful in patients with blood GH levels below 40 ng/ml before the operation and with pituitary tumors no larger than 10 mm in diameter. Success depends on the skill and experience of the surgeon. The success rate also depends on what level of GH is defined as a cure. The best measure of surgical success is normalization of GH and IGF-1 levels. Ideally, GH should be less than 2 ng/ml after an oral glucose load. A review of GH levels in 1,360 patients worldwide immediately after surgery revealed that 60 percent had random GH levels below 5 ng/ml. Complications of surgery may include cerebrospinal fluid leaks, meningitis, or damage to the surrounding normal pituitary tissue, requiring lifelong pituitary hormone replacement. Even when surgery is successful and hormone levels return to normal, patients must be carefully monitored for years for possible recurrence. More commonly, hormone levels may improve, but not return completely to normal. These patients may then require additional treatment, usually with medications. [edit] Drug therapy Two medications currently are used to treat acromegaly. These drugs reduce both GH secretion and tumor size. Medical therapy is sometimes used to shrink large tumors before surgery. Bromocriptine (Parlodel) in divided doses of about 20 mg daily reduces GH secretion from some pituitary tumors. Side effects include gastrointestinal upset, nausea, vomiting, light-headedness when standing, and nasal congestion. These side effects can be reduced or eliminated if medication is started at a very low dose at bedtime, taken with food, and gradually increased to the full therapeutic dose. Because bromocriptine can be taken orally, it is an attractive choice as primary drug or in combination with other treatments. However, bromocriptine lowers GH and IGF-1 levels and reduces tumor size in less than half of patients with acromegaly. Some patients report improvement in their symptoms although their GH and IGF-1 levels still are elevated. The second medication used to treat acromegaly is octreotide (Sandostatin) and lanreotide (Somatulin). Both are synthetic forms of a brain hormone, somatostatin, that stops GH production. The long-acting forms of these drugs must be injected every 2 to 4 weeks for effective treatment. Most patients with acromegaly respond to this medication. In many patients, GH levels fall within one hour and headaches improve within minutes after the injection. Several studies have shown that octreotide and lanreotide are effective for long-term treatment. Octreotide and lanreotide have also been used successfully to treat patients with acromegaly caused by non-pituitary tumors. Because octreotide inhibits gastrointestinal and pancreatic function, long-term use causes digestive problems such as loose stools, nausea, and gas in one third of patients. In addition, approximately 25 percent of patients develop gallstones, which are usually asymptomatic. In rare cases, octreotide treatment can cause diabetes. On the other hand, scientists have found that in some acromegaly patients who already have diabetes, octreotide can reduce the need for insulin and improve blood sugar control. The latest development in the medical treatment of acromegaly is the use of growth hormone receptor antagonists. The only available member of this family is pegvisomant (Somavert). By blocking the action of the endogenous growth hormone molecules, this compound is able to control disease activity of acromegaly in virtually all patients. Pegvisomant has to be administered subcutaneously by daily injections. Combinations of long-acting somatostatin analogues and weekly injections of pegvisomant seem to be equally effective as daily injections of pegvisomant. [edit] Radiation therapy Radiation therapy has been used both as a primary treatment and combined with surgery or drugs. It is usually reserved for patients who have tumor remaining after surgery. These patients often also receive medication to lower GH levels. Radiation therapy is given in divided doses over four to six weeks. This treatment lowers GH levels by about 50 percent over 2 to 5 years. Patients monitored for more than 5 years show significant further improvement. Radiation therapy causes a gradual loss of production of other pituitary hormones with time. Loss of vision and brain injury, which have been reported, are very rare complications of radiation treatments. No single treatment is effective for all patients. Treatment should be individualized depending on patient characteristics, such as age and tumor size. If the tumor has not yet invaded surrounding brain tissues, removal of the pituitary adenoma by an experienced neurosurgeon is usually the first choice. After surgery, a patient must be monitored for a long time for increasing GH levels. If surgery does not normalize hormone levels or a relapse occurs, a doctor will usually begin additional drug therapy. The first choice should be bromocriptine because it is easy to administer; octreotide is the second alternative. With both medications, long-term therapy is necessary because their withdrawal can lead to rising GH levels and tumor re-expansion. Radiation therapy is generally used for patients whose tumors are not completely removed by surgery; for patients who are not good candidates for surgery because of other health problems; and for patients who do not respond adequately to surgery and medication. [edit] Pituitary gigantism in children This condition of growth hormone excess is rare in children and is referred to as pituitary gigantism, because the excessive growth hormone produces excessive growth of bones and the child can achieve excessive height. As an affected child becomes an adult, many of the adult problems can gradually develop. The distinction between gigantism (occurring in children) and acromegaly (occurring in adults) can be made by the occurrence of the adenoma in relation to the closure of the epiphyses. If elevated growth hormone levels occur before the closure of the epiphyses (i.e. in prepubertal children), then gigantism ensues. If it occurs after the closure of the epiphyses (i.e., in adults) then acromegaly ensues. [edit] Notable sufferers Famous patients, all standing in excess of 2.00 metres: * Actor Richard Kiel ('Jaws' in the James Bond movies), 7'2" tall * Actor Carel Struycken (known e.g as Lurch in the Addams Family -movies, and for his other giant roles), 7' tall * Actor Matthew McGrory (listed in the Guinness Book of World Records for having the largest feet - size 29 1/2), 7'6" tall (died at the age of 32) * Actor Rondo Hatton * Wrestler and actor André the Giant, 6'9" tall after he had a back surgery that made him a couple inches shorter than he originially was, which was closer to 7 feet tall. He died at the age of 46, when most sufferers weren't expected to live past the age of 40. (chose not to be treated and died from disease) * Wrestler Paul Wight (The Big Show), had surgery on his pituitary gland in the 1990s to fix the condition, his height peaking at 6'11 1/2" tall * Wrestler Maurice Tillet ( 1903?- August 4, 1954 ) * Former NBA player Gheorghe Muresan (star of My Giant), 7'7" tall * Aspiring basketball player Sun Ming Ming, 7'9" tall * Makeup artist Kevyn Aucoin It has been suggested that the character 'Punch' from Punch and Judy was originally a caricature of an Acromegaly sufferer.[1] The actor Paul Benedict had an arrested case of acromegaly. After his performance in a stage production, a member of the audience came backstage and introduced himself as an endocrinologist; he had diagnosed Benedict's condition during the performance and was ultimately able to cure him before the disease reached its later stages.

Greek gigas, gigantas "giant") is a condition characterized by excessive height growth. As a medical term, gigantism is rarely used except to refer to the rare condition of pituitary gigantism due to prepubertal growth hormone excess. There is no precise definition of the degree of height that qualifies a person to be termed a "giant." The term has been typically applied to those whose height is not just in the upper 1% of the population but several standard deviations above mean for persons of the same sex, age, and ethnic ancestry. Typical adult heights of Americans and Europeans to whom the term might be applied are 225 - 240 cm (7'6 - 8 feet). The term is rarely applied to those whose heights appear to be the healthy result of normal genetics and nutrition.

[edit] Pituitary gigantism Pituitary gigantism due to growth hormone excess is the single condition that accounts for nearly all cases of pathologic extreme height. The excess growth hormone usually results from oversecretion by a group of somatotrope cells of the anterior pituitary gland (termed a "somatotrope adenoma"). These cells do not respond to normal controls of growth or function. They grow very slowly, so that for many years the only effects of such an adenoma are the secretion of excessive growth hormone. Over decades, such an adenoma may reach a large enough size (2 cm or more in diameter) to cause headaches, impair vision, or damage other pituitary functions. Many years of growth hormone excess can cause other problems as well. The primary effect of growth hormone excess in childhood is excessive growth, but the extreme height is accompanied by a characteristic physique recognizable to an endocrinologist. The typical physique involves heavy, thick bones, with large hands and feet and a heavy jaw. Once puberty is complete and adult height is achieved, continued thickening of the skin and growth of the jaw results in a combination of features referred to as acromegaly. If a physician suspects pituitary gigantism or acromegaly, the simplest diagnostic screening test is measurement of insulin-like growth factor 1 in the blood. This is usually quite elevated but levels must be interpreted in relation to age and pubertal status. Additional confirmatory testing may include magnetic resonance imaging (MRI) of the pituitary to look for a visible adenoma, and suppressibility of growth hormone levels by glucose. Treatment depends on the size of the adenoma and may involve removal by a neurosurgeon, drugs such as octreotide or bromocriptine, or radiation. Treatment is discussed in more detail in the acromegaly article. Childhood pituitary gigantism is a rare condition, and those affected are often unusual enough to attain a degree of celebrity status (for example, André the Giant). Acromegaly is the term used for the condition of growth hormone excess when it occurs in adults. Acromegaly is a far more common disease in adults than pituitary gigantism is in children. [edit] Other conditions of overgrowth or excessive tallness in childhood Children who are excessively tall are often referred to as Giantigionists. The majority of children who seem excessively tall or large to their parents usually have a combination of simple familial tallness and childhood obesity. Early onset of obesity results in above-average growth in mid-childhood, such that over half of overweight children have heights in the 70 - 99 percentile range at around 10 years of age. The adult heights achieved by these children are what would be expected from their families because the excess mid-childhood growth is offset by attenuation of the pubertal growth spurt. Precocious puberty and a variety of conditions associated with excessive amounts of testosterone or estrogen in childhood will result in tallness by mid-childhood. However, the acceleration of bone maturation by the early rise of estradiol results in early completion of growth, and adult heights for these children may actually be below average for genetic potential. Extra sex chromosomes (beyond the normal two) with therefore extra copies of the SHOX gene (beyond the normal two) usually results in enhancement of height growth. The most common of these karyotypes are 47,XXY (Klinefelter syndrome), 47,XYY, and 47,XXX. The added height increment is usually modest. Hypogonadism is the condition of deficiency of sex hormones due to reduced function of the testes or ovaries at adolescence. When secretion of testosterone or estradiol remains below average throughout the teenage years, a taller adult height will be gradually achieved by extra growth of the arms and legs. This long-limbed tallness is termed "eunuchoid" tallness, but rarely adds more than 2.5 - 7.5 cm (1-3 inches) to adult height. The extra growth is prevented if the child is given appropriate replacement of testosterone or estrogen from early adolescence. A very rare but more extreme version of "eunuochoid" tallness occurs when a mutation of the estrogen receptor reduces the response of the bones to estradiol. Estradiol is a byproduct of testosterone in both males and females, and is the most potent accelerator of bone maturation and closure known. If a person fails to respond to estrogen, growth can continue until late-20s or longer, and the affected person can reach 8 feet or more in height. Estrogen resistance is the only other endocrine condition that can rival growth hormone excess in producing gigantism. In contrast, the tallness associated with the more common androgen insensitivity syndrome averages only a few inches, as estradiol is not produced directly but rather through conversion from androgens by aromatase. Marfan syndrome is an uncommon genetic disease due to an inherited defect of connective tissue. In addition to moderate tallness, persons with this condition usually have a slender body build with unusually long fingers (arachnodactyly). Many can also develop a dislocaton of the lens of the eye or, more seriously, a progressive deterioration of the walls of the aorta which can result in sudden death in adulthood. It is usually inherited as an autosomal dominant trait. Sotos syndrome resembles acromegaly in its mild distortion of facial growth. In addition to tallness, the chief characteristics are large head size, slow development, and autosomal-dominant inheritance. There are about 50 even rarer genetic syndromes in which childhood growth is above average. These conditions are often associated with developmental delay or other more serious problems, and adult height may or may not be mildly increased. [edit] Etymology and terminology Other names somewhat obsolete for this pathology are hypersomy (Greek: hyper over the normal level; soma body), macrogenesis (Greek: makros great, large, long; genesis production, generation) and somatomegaly (Greek; soma body, object pronoun somatos of the body; megas, megalos great).


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