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$Unique_ID{BRK03622}
$Pretitle{}
$Title{Conn Syndrome}
$Subject{Conn Syndrome Aldosteronism, Primary Hyperaldosteronism, Primary
Aldosteronism, Secondary Bartter Syndrome }
$Volume{}
$Log{}
Copyright (C) 1989 National Organization for Rare Disorders, Inc.
628:
Conn Syndrome
** IMPORTANT **
It is possible that the main title of this article (Conn Syndrome) is not
the name you expected. Please check the SYNONYM list to find the alternate
names and disorder subdivisions covered by this article.
Synonyms
Aldosteronism, Primary
Hyperaldosteronism, Primary
Information on the following disorders can be found in the Related
Disorders section of this report:
Aldosteronism, Secondary
Bartter Syndrome
General Discussion
** REMINDER **
The information contained in the Rare Disease Database is provided for
educational purposes only. It should not be used for diagnostic or treatment
purposes. If you wish to obtain more information about this disorder, please
contact your physician and/or the agencies listed in the "Resources" section
of this report.
Conn Syndrome is characterized by an increased level of the hormone
aldosterone in the blood causing increased sodium levels in the blood. An
increase in blood volume (hypervolemia), and a low potassium level
(hypokalemic alkalosis) also occur. This disorder is characterized by
periods of weakness, unusual sensations such as tingling and warmness, a
transient paralysis, and muscle cramps. An increase in blood pressure
(hypertension), excessive urination (polyuria), and excessive thirst
(polydipsia) can also occur.
Symptoms
Conn Syndrome (Primary Hyperaldosteronism) is a rare metabolic endocrine
disorder characterized by oversecretion of the hormone aldosterone. This
hormone is produced by the adrenal glands. The disorder is caused by an
abnormal growth (adenoma) in the cortex of the adrenal glands. Aldosterone
causes salt (sodium or Na) retention and potassium (K) loss. In the kidneys,
salivary and sweat glands, and in the cells of the mucous membranes in the
intestines, aldosterone causes transfer of sodium in exchange for potassium
and hydrogen. Aldosterone secretion is regulated by the renin-angiotensin
mechanism in the kidneys and liver, and to a lesser extent by
adrenocorticotropin hormone (ACTH). The sodium and water retention resulting
from increased aldosterone secretion increases the blood volume and reduces
renin secretion.
Increased blood levels of sodium (hypernatremia), an increase in blood
volume (hypervolemia), and low potassium (hypokalemic alkalosis), can cause
periods of weakness, unusual sensations such as tingling and warmness, a
transient paralysis, and muscle spasms. An increase in blood pressure
(hypertension), kidney disease with excessive urination (polyuria), and
excessive thirst (polydipsia) can also occur.
With removal of the abnormal adrenal growth, remission usually occurs.
Causes
Conn Syndrome is caused by an abnormal growth or tumor (adenoma) in the
adrenal glands. The exact cause of this growth is unknown.
Related Disorders
Symptoms of the following disorders can resemble those of Conn Syndrome.
Comparisons may be useful for a differential diagnosis:
Bartter Syndrome (Aldosteronism with Normal Blood Pressure) is a rare
metabolic disorder which may involve the kidneys. It is characterized by an
overproduction of the adrenal hormone aldosterone. Major symptoms may
include mental retardation, slowed growth, weakness, dwarfism, excessive
thirst and excessive urination. Vomiting, diarrhea, and weight loss may also
occur. (For more information, choose "Bartter" as your search term in the
Rare Disease Database.)
Secondary Aldosteronism is a metabolic endocrine disorder characterized
by increased production of aldosterone by the cortex of the adrenal glands
caused by stimuli originating outside the adrenal glands. It is similar to
Conn Syndrome and related to high blood pressure (hypertension) and disorders
with fluid retention and/or swelling (edema) such as heart failure and
cirrhosis of the liver with fluid in the abdomen (kidney syndrome). It is
believed to be caused by excessive secretion of the enzyme renin, secondary
to constriction of the blood vessels in the kidney. This syndrome also
occurs as a symptom of other kidney disorders. Conn Syndrome is not marked
by the decreased salt (sodium) levels and increased plasma-renin activity as
is Secondary Aldosteronism.
Therapies: Standard
Treatment of Conn Syndrome consists in surgical removal of the adrenal tumor
that causes the symptoms. Additional therapy with the adrenocorticolytic
drug, mitotane, may be helpful. Treatment with the aldosterone antagonist
drug, spironolactone, and the diuretic antihypertensive drug,
hydrochlorothiazide, may also be recommended.
Therapies: Investigational
This disease entry is based upon medical information available through April
1989. Since NORD's resources are limited, it is not possible to keep every
entry in the Rare Disease Database completely current and accurate. Please
check with the agencies listed in the Resources section for the most current
information about this disorder.
Resources
For more information on Conn Syndrome, please contact:
National Organization for Rare Disorders (NORD)
P.O. Box 8923
New Fairfield, CT 06812-1783
(203) 746-6518
The National Adrenal Diseases Foundation, Inc.
505 Northern Blvd., Suite 200
Great Neck, NY 11021
(516) 487-4992
National Digestive Diseases Information Clearinghouse
Box NDDIC
Bethesda, MD 20892
(301) 468-6344
NIH/National Heart, Lung, and Blood Institute (NHLBI)
9000 Rockville Pike
Bethesda, MD 20892
(302) 496-4236
References
CLINICAL IMPLICATIONS OF PRIMARY ALDOSTERONISM WITH RESISTANT HYPERTENSION:
E.L. Bravo, et al.; Hypertension (February 1988: issue 11(2 Pt 2). Pp.
1207-1211.
PURE PRIMARY HYPERALDOSTERONISM DUE TO ADRENAL CORTICAL CARCINOMA: D.J.
Greathouse, et al.; Amer Journal Med (June 1984: issue 76(6)). Pp. 1132-
1136.
AGING AND ALDOSTERONE: R. Hegstad, et al.; Amer Journal Med (March
1983: issue 74(3)). Pp. 442-448.
ISOLATED CLINICAL SYNDROME OF PRIMARY ALDOSTERONISM IN FOUR PATIENTS WITH
ADRENOCORTICAL CARCINOMA: D. Farge, et al.; Amer Journal Med (October 1987:
issue 83(4)). Pp. 635-640.