Hypothyroidism (= "Myxedema") The most common form
of hypothyroidism likely is due to a burnt out Hashimoto's thyroiditis, a common
autoimmune disease where autoantibodies lead to a chronic inflammation and eventual
fibrotic transformation of the thyroid gland. This may be associated with a
goiter, but most often shows no change in size of the thyroid gland. There
are two types of hypothyroidism,
primary and secondary. The symptoms are identical, but with primary
hypothyroidism the reason for low thyroid production is at the level of the thyroid
gland itself. With secondary hypothyroidism there is a lack of either thyrotropin-releasing
hormone(TRH) from the hypothalamus or low thyroid stimulating hormone (low TSH)
from the pituitary gland, which leads to a lack of stimulation of the thyroid
gland. It is important to carefully investigate the patient and for the physician
to do appropriate testing before therapy is instituted. Hypothyroidism
symptoms: The symptoms of hypothyroidism
can be very difficult to notice in the beginning. There is a lack of energy. The
patient develops a hoarse voice and slow speech. The facial appearance changes
due to eye puffiness and around the mouth (lip swelling) from abnormal mucopolysaccharide
deposits in these tissues. Brittle dry hair, coarse hair and general
hair loss are common. Often there is thinning
and a loss of the temporal aspect of the eyebrows on both sides with the
inside of the eyebrows being more preserved. Skin dryness and skin thickening
develop and weight gain occurs from fluid retention and a slowing of the metabolism.
Depression and hypothyroidism are commonly linked, but depression is one of the
symptoms that is often overlooked in hypothyroidism. The danger is to consider
this symptom in isolation and to start antidepressants, which will not help as
the real reason behind this symptom is the hypothyroidism, which requires thyroid
hormone replacement, not antidepressants. With severe hypothyroidism there can
be a psychotic state, which is called "myxedema madness". Again it is
a challenge for the physician and psychiatrist to recognize that these symptoms
are only part of the whole symptom complex of hypothyroidism. One cause
of low body temperature can be hypothyroidism and other symptoms are a swollen
tongue and discoloration of hands (yellow palms) and the soles of the feet. Hypothyroidism
is one of the causes of bradycardia (slow heart beat) and heart enlargement (fluid
accumulation around the heart) can also be caused by it. Fluid can also accumulate
in the chest cavities (pleural effusions) or in the abdominal cavity (ascites
fluid). This is due to protein leakage, which is characteristic for severe hypothyroidism.
Swelling inside the carpal tunnel space of both wrists and in the tarsal tunnel
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around
both ankles leads to a loss of feeling (=paresthesias) of both hands and feet.
There is a slowing of the reflexes and this causes carpal tunnel syndrome symptoms
and symptoms of tarsal tunnel syndrome. In women of childbearing age there is
a prolongation of the menstrual periods (one of the causes of menorrhagia), which
can result in pronounced anemia. However, generally speaking with hypothyroidism
anemia the hemoglobin is in the range of about 9 to 10 g/dL. It takes often 7
to 9 months after correction of hypothyroidism with thyroid replacement before
this anemia normalizes. Slow thinking is another symptom separate from depression.
Patients with hypothyroidism complain that the room temperature would be too cold,
even in a normal environment. A life threatening complication of hypothyroidism
is the "myxedema
coma". This can occur in patients who have been hypothyroid
for a long time. They may slip into a coma, either on their own or precipitated
by an infection, by a central nervous system suppressant drug or by exposure to
cold temperatures. This coma is characterized by an extremely low body temperature
of 25 to 32°C (=76 to 90°F), missing reflexes, depressed breathing activity
and seizures. There is a high mortality rate associated with this condition and
an endocrinologist should attend to this endocrinological emergency. Tests
for hypothyroidism: The most important blood test for
hypothyroidism is the TSH level. This is the hormone, which is secreted
from the pituitary gland and is elevated in the case of primary hypothyroidism.
However, if it is low, then this points to a secondary cause (either pituitary
gland or hypothalamus related). These patients need an urgent referral to an endocrinologist
who will do further testing.
In
the past the endocrinologist may have occasionally ordered a TRH
stimulation test, where synthetic TRH is injected. If this leads
to a response of TSH, the patient has a deficiency of the hypothalamus. If there
is no response, there would be a lesion at the pituitary gland (usually an adenoma).
Further clarification can be obtained from an MRI scan of the hypothalamus and
pituitary gland. In more rare cases, there can be a genetic defect of some of
the thyroid hormone synthetic steps within the thyroid gland or a defect of thyroxin-binding
globulin capacity. With primary hypothyroidism there is often a high cholesterol
level. T4 levels are usually low, but T3 levels are mostly normal. Only in severe
hypothyroidism is there both a low T3 and T4 level.
Hypothyroidism
treatment: Treatment of hypothyroidism
is by administering regular thyroid hormone replacement. This is best given once
per day at a certain time of the day (first thing in the morning or last thing
before bedtime) so that a routine is followed and the medication is not forgotten.
There are various thyroid medications such as purified T4 hormone, called levothyroxine
(brand names: Eltroxin, Levotec, Synthroid). Thyroid hormone can also be given
as desiccated thyroid ( brand name: thyroid hormone Parke-Davis), which contains
both T4 and T3 hormones. For patients with a genetic enzyme defect an endocrinologist
needs to be consulted to provide a specific hormone replacement schedule.
Myxedema coma should also be in the hands of an endocrinologist,
who will initially use fairly high thyroid hormone replacement doses, which are
then gradually tapered to a maintenance program. In the initial stages intubation
and artificial breathing with a respirator may be required for a period of time.
At the other end of the extremes is subclinical thyroid dysfunction,
which is characterized in the lab tests by an elevated TSH and normal T3 and T4
hormones. This is particularly common in elderly women, particularly if there
has been a history of Hashimoto thyroiditis in the past. Thyroid peroxidase antibodies
are measured in these patients to confirm Hashimoto's autoimmune thyroiditis.
These patients need replacement with thyroid hormone on an ongoing basis. Other
patients with this condition must be watched closely to see whether their hormone
levels stay normal or drop, at which time they need hormone replacement. The sad
story in the past was, before these sensitive TSH monitoring tests were available,
that the patients entered into a deep depression due to hypothyroidism and died
from suicide as a result of the intractable depression or else suddenly died of
a myxedema coma. Even today there is the occasional patient who is living in denial
and refuses to see a doctor.
Today the problem is not how to
diagnose hypothyroidism, but to convince the patients that they have a condition,
which will require lifelong hormone replacement. The challenge is to overcome
noncompliance and persuade the patient to take the thyroid medication on a regular
basis! |
Subclinical
hypothyroidism: There is a group of patients who have no classical
signs of hypothyroidism, but who are perhaps chronically tired and who have a
TSH test that is borderline elevated. This constellation happens in about 15%
of elderly women who have or had underlying Hashimoto's thyroiditis (Dr. Hashimoto
described this syndrome first). They have subclinical hypothyroidism, which would
turn into full blown hypothyroidism in later years. Special tests (=peroxidase
antibody titers) are often positive and these patients should be given replacement
L-thyroxine therapy (Ref. 3, p. 96). Many of these women when they present in
the child bearing age have a history of pregnancy
loss as is discussed in this reference. Careful thyroid replacement
will allow these women to have normal pregnancies. Hyperthryoidism
can also cause pregancy loss. Anti-aging and hypothyroidism: With
the anti-aging movement well on its way due to Suzanne Somers' books (like Ref.
16 and 17) and others, I like to point out that hypothyroidism can often be the
first sign of the "change of life" in women (menopause). In males this
typically is not as sudden as in women and often occurs 5 to 10 years later in
life. Other factors also play a role such as stress (move, divorce, debts, death
of a loved one etc.) where cortisol levels are increased and the thyroid simply
"burns out" (there is normally a balance between the thyroid hormone
gland and the adrenal gland where cortisol is manufactured). So, in the age group
above 30 it is wise to do blood tests (a whole battery of hormones and DHEA-S)
to determine what else is low other than the thyroid hormones. A common occurrence
is the presence of high fasting insulin levels and low cortisol levels. The physician
should address this head-on, and if uncomfortable, refer to one of the anti-aging
physicians in this setting. See more on anti-aging
with this link. |