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Chronic Care Programme
Treatment guidelines
Hypothyroidism
Chronic condition
Consultations protocols
Preferred treating provider
Notes
 preferred as indicated by option
 referral protocols apply
Option/plan
Provider
GMHPP
Gold Options
G1000, G500 and
G200.
Blue Options
B300 and B200.
GMISHPP
General Practitioner
Pulmonologist
Physician
Gastroenterologist
Neurologist
Cardiologist
Paediatrician
Cardiology Paediatrician
Surgeon
Thoracic Surgeon
Maximum consultations per annum
 Initial consultation
 Follow-up consultation
Tariff codes
New Patient
All severity
levels
Existing Patient
Mild / Stable
Moderate to Severe /
Unstable
1
0
3
1
0183; 0142; 0187; 0108
1
1
Investigations protocols
Type
Provider
Tariff
code
Thyrotropin (TSH) /Free Thyroxin
(FT4). (This item includes items
4507 & 4482)
ICD 10 coding
Pathologist
Maximum investigations per annum
New patient
Existing patient
All severity
Mild /
Moderate to
levels
Stable
Severe /
Unstable
4484
or
4507
4
1
2
E01-E03.
General
Hypothyroidism is the disease state in humans and animals caused by insufficient production
of thyroid hormone by the thyroid gland. Cretinism is a form of hypothyroidism found in
infants
Signs and symptoms
The ability of hypothyroidism to mimic a number of medical conditions originates in the vast
functions of the thyroid hormones, which are reduced or absent in this case. The functions of
thyroid hormones include modulation of carbohydrate, protein and fat metabolism, vitamin
utilization, mitochondrial function, digestive process, muscle and nerve activity, blood flow,
oxygen utilization, hormone secretion and sexual and reproductive health[7] to mention a few.
Thus, when the thyroid hormone content gets out of balance, systems covering the whole body
are affected. This is why hypothyroidism can look like other diseases. Conversely, sometimes
other conditions can be mistaken for hypothyroidism.
Adults
In adults, hypothyroidism is associated with the following symptoms:[5][8]
Early symptoms

Poor muscle tone (muscle hypotonia)

Fatigue

Cold intolerance, increased sensitivity to cold

Depression

Constipation

Muscle cramps and joint pain

Arthritis

Goiter

Thin, brittle fingernails

Thin, brittle hair

Paleness

Dry, itchy skin

Weight gain

Bradycardia (low HR <60 BPM)
Late symptoms

Slowed speech and a hoarse, breaking voice. Deepening of the voice can also be noticed.

Dry puffy skin, especially on the face

Thinning of the outer third of the eyebrows

Abnormal menstrual cycles

Low basal body temperature
Less common symptoms

Heat intolerance, increased sensitivity to heat

Impaired memory

Impaired cognitive function (brain fog) and inattentiveness

Urticaria (hives)

Migraine headache

A slow heart rate with ECG changes including low voltage signals. Diminished cardiac
output and decreased contractility.

Reactive (or post-prandial) hypoglycemia[9]

Pericardial effusions may occur.

Sluggish reflexes

Hair loss

Anemia caused by impaired hemoglobin synthesis (decreased EPO levels), impaired
intestinal iron and folate absorption or B12 deficiency from pernicious anemia

Anxiety/panic attacks

Difficulty swallowing

Shortness of breath with a shallow and slow respiratory pattern.

Impaired ventilatory responses to hypercapnia and hypoxia.

Increased need for sleep

Osteopenia or Osteoporosis

Irritability and mood instability

Yellowing of the skin due to impaired conversion of beta-carotene to vitamin A

Impaired renal function with decreased GFR.

Thin, fragile or absent cuticles

Elevated serum cholesterol

Acute psychosis (myxedema madness) is a rare presentation of hypothyroidism

Decreased libido

Decreased sense of taste and smell (late, less common symptoms)

Puffy face, hands and feet (late, less common symptoms)

Depression
Pediatric
Hypothyroidism in pediatric patients can cause the following additional symptoms:

short stature

mental retardation if present at birth, and untreated.

Previously called Cretinism
Severity
The severity of hypothyroidism varies widely. Some have few overt symptoms, others with
moderate symptoms can be mistaken for having other diseases and states. Advanced
hypothyroidism may cause severe complications including cardiovasular and psychiatric
myxedema.
Diagnosis
To diagnose primary hypothyroidism, many doctors simply measure the amount of Thyroidstimulating hormone (TSH) being produced by the pituitary gland. High levels of TSH indicate
that the thyroid is not producing sufficient levels of Thyroid hormone (mainly as thyroxine (T4)
and smaller amounts of triiodothyronine (fT3)). However, measuring just TSH fails to diagnose
secondary and tertiary forms of hypothyroidism, thus leading to the following suggested blood
testing if the TSH is normal and hypothyroidism is still suspected:

free triiodothyronine (fT3)

free levothyroxine (fT4)

total T3

total T4
Additionally, the following measurements may be needed:

24 hour urine free T3 [10]

antithyroid antibodies - for evidence of autoimmune diseases that may be damaging the
thyroid gland

serum cholesterol - which may be elevated in hypothyroidism

prolactin - as a widely available test of pituitary function
 testing for anemia, including ferritin
Causes
About three percent of the general population is hypothyroid.[1] Factors such as iodine deficiency
or exposure to I-131 can increase that risk. There are a number of causes for overt
hypothyroidism. Historically, and still in many developing countries, iodine deficiency is the
most common cause of hypothyroidism worldwide. In iodine-replete individuals, hypothyroidism
is mostly caused by Hashimoto's thyroiditis, or by a lack of the thyroid gland or a deficiency of
hormones from either the hypothalamus or the pituitary.
Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all
women within a year after giving birth. The first phase is typically hyperthyroidism. Then, the
thyroid either returns to normal or a woman develops hypothyroidism. Of those women who
experience hypothyroidism associated with postpartum thyroiditis, one in five will develop
permanent hypothyroidism requiring life-long treatment.
Hypothyroidism can also result from sporadic inheritance, sometimes autosomal recessive.
Hypothyroidism is also a relatively common hormone disease in domestic dogs, with some
specific breeds having a definite predisposition.[2]
Temporary hypothyroidism can be due to the Wolff-Chaikoff effect. A very high intake of iodine
can be used to temporarily treat hyperthyroidism, especially in an emergency situation. Although
iodine is substrate for thyroid hormones, high levels prompt the thyroid gland to take in less of
the iodine that is eaten, reducing hormone production.
Hypothyroidism is often classified by the organ of origin:[3][4]
Type
Origin
Description
thyroid
gland
The most common forms include Hashimoto's
thyroiditis (an autoimmune disease) and
radioiodine therapy for hyperthyroidism.
Secondary
pituitary
gland
Occurs if the pituitary gland does not create
enough thyroid stimulating hormone (TSH) to
induce the thyroid gland to produce enough
thyroxine and triiodothyronine. Although not
every case of secondary hypothyroidism has a
clear-cut cause, it is usually caused by
damage to the pituitary gland, as by a tumor,
radiation, or surgery.[5]
Tertiary
Results when the hypothalamus fails to
produce sufficient thyrotropin-releasing
hypothalam hormone (TRH). TRH prompts the pituitary
us
gland to produce thyrotropin (TSH). Hence
may also be termed hypothalamic-pituitaryaxis hypothyroidism.
Primary
General psychological associations
Hypothyroidism can be caused by lithium-based mood stabilizers, usually used to treat bipolar
disorder (previously known as manic depression).
In addition, patients with hypothyroidism and psychiatric symptoms may be diagnosed with:[6]

atypical depression (which may present as dysthymia)

bipolar spectrum syndrome (including bipolar I or bipolar II disorder, cyclothymia, or
premenstrual syndrome)

borderline personality disorder[citation needed]

a psychotic disorder (typically, paranoid schizophrenia)

inattentive ADHD or sluggish cognitive tempo
Treatment
Hypothyroidism is treated with the levorotatory forms of thyroxine (L-T4) and triiodothyronine
(L-T3). Both synthetic and animal-derived thyroid tablets are available and can be prescribed for
patients in need of additional thyroid hormone. Thyroid hormone is taken daily, and doctors can
monitor blood levels to help assure proper dosing. There are several different treatment protocols
in thyroid replacement therapy:
T4 Only
This treatment protocol involves supplementation of levothyroxine alone, in a synthetic form. It is
currently the standard treatment in mainstream medicine.[11]
T4 and T3 in Combination
This treatment protocol involves administering both synthetic L-T4 and L-T3 simultaneously in
combination. [12]
Desiccated Thyroid Extract
Desiccated thyroid extract is an animal based thyroid extract, most commonly from a porcine
source. It is also a combination therapy, containing natural forms of L-T4 and L-T3. [13]
Treatment Controversy
Though the current standard treatment in thyroid therapy is levothyroxine only, there exists some
controversy about which treatment protocol is most effective. The American Association of
Clinical Endocrinologists (AACE) states that desiccated thyroid hormone, combinations of
thyroid hormone, or triiodothyronine should not generally be used for replacement therapy.[14]
However, the medical journal Thyroid Science claims that, "today's conventional thyroid
hormone therapy, T4-replacement, has been documented to be ineffective and harmful to many
patients". [15] Other recent publications have also challenged the status quo, showing that
combination therapies can be more effective.[16][17]
Subclinical hypothyroidism
Subclinical hypothyroidism occurs when thyrotropin (TSH) levels are elevated but thyroxine (T4)
and triiodothyronine (T3) levels are normal.[18] In primary hypothyroidism, TSH levels are high
and T4 and T3 levels are low. Endocrinologists are puzzled because TSH usually increases when
T4 and T3 levels drop. TSH prompts the thyroid gland to make more hormone. Endocrinologists
are unsure how subclinical hypothyroidism affects cellular metabolic rates (and ultimately the
body's organs) because the levels of the active hormones are adequate. Some have proposed
treating subclinical hypothyroidism with levothyroxine, the typical treatment for overt
hypothyroidism, but the benefits and the risks are unclear. Reference ranges have been debated as
well. The American Association of Clinical Endocrinologists (ACEE) supports a narrower TSH
range, especially when the person has clinical signs of thyroid disease. This reference range may
reduce the risks of goiter, thyroid nodules, thyroid cancer, and overt hypothyroidism, but remains
controversial.[19] There is always the risk of overtreatment and hyperthyroidism. Some studies
have suggested that subclinical hypothyroidism does not need to be treated. A meta-analysis by
the Cochrane Collaboration found no benefit of thyroid hormone replacement except "some
parameters of lipid profiles and left ventricular function".[20]
Medicine formularies
Plan or option
GMHPP
Gold Options
G1000, G500 and
G200
Blue Options
B300 and B200
[Link to appropriate Mediscor formulary]
[Core]
GMISHPP
Blue Option B100
n/a
References
1. Jack DeRuiter (2002). Thyroid Pathology (PDF), 30.
2. Brooks W (01/06/2008). Hypothyroidism in Dogs. The Pet Health Library.
VetinaryPartner.com. Retrieved on 2008-02-28.
3. Simon H (4/19/2006). Hypothyroidism. University of Maryland Medical Center.
Retrieved on 2008-02-28.
4. Department of Pathology (June 13, 2005). Pituitary Gland -- Diseases/Syndromes.
Virginia Commonwealth University (VCU). Retrieved on 2008-02-28.
5.
ab
American Thyroid Association (ATA) (2003). Hypothyroidism Booklet (PDF), 6.
6. Heinrich TW, Grahm G (2003). "Hypothyroidism Presenting as Psychosis: Myxedema
Madness Revisited" 5 (6): 260-266. PMID 15213796.
7. Comprehensive Thyroid Assessment. Geneva Diagnostics. Retrieved on 2007-05-21.
8. MedlinePlus Encyclopedia Hypothyroidism - primary - see list of Symptoms
9. Hofeldt FD, Dippe S, Forsham PH (1972). "Diagnosis and classification of reactive
hypoglycemia based on hormonal changes in response to oral and intravenous glucose
administration" (PDF). Am. J. Clin. Nutr. 25 (11): 1193–201. PMID 5086042.
10. Baisier W. Hertoghe J. Eeckhaut W. Thyroid insufficiency. Is TSH the only diagnostic
tool? J Nutr Environ ed. 2000;10:105-113. "Thyroid insufficiency. Is TSH the only
diagnostic tool?"
11. American Association of Clinical Endocrinologists (November/Decemcer 2002). "Medical
Guidelines For Clinical Practice For The Evaluation And Treatment Of Hyperthyroidism
And Hypothyroidism" (PDF). Endocrine Practice 8 (6): 457-469.
12. Bunevicious et. al (February 1999). "Effects of Thyroxine as Compared to Thyroxine plus
Triiodothyronine in Patients with Hypothyroidism" (html). New England Journal of
Medicine 340 (6): 424-429.
13. Baisier, W.V.; Hertoghe, J.; Eeckhaut, W. (September 2001). "Thyroid Insufficiency. Is
Thyroxine the Only Valuable Drug?" (html). Journal of Nutritional and Environmental
Medicine 11 (3): 159-166.
14. American Association of Clinical Endocrinologists (November/Decemcer 2002). "Medical
Guidelines For Clinical Practice For The Evaluation And Treatment Of Hyperthyroidism
And Hypothyroidism" (PDF). Endocrine Practice 8 (6): 457-469.
15. Thyroid Science journal guidelines
16. Bunevicious et. al (February 1999). "Effects of Thyroxine as Compared to Thyroxine plus
Triiodothyronine in Patients with Hypothyroidism" (html). New England Journal of
Medicine 340 (6): 424-429.
17. Baisier, W.V.; Hertoghe, J.; Eeckhaut, W. (September 2001). "Thyroid Insufficiency. Is
Thyroxine the Only Valuable Drug?" (html). Journal of Nutritional and Environmental
Medicine 11 (3): 159-166.
18. Jack DeRuiter (2002). Thyroid Pathology (PDF), 30.
19. "Subclinical Thyroid Disease" The American Association of Clinical Endocrinologists
20. Villar H, Saconato H, Valente O, Atallah A (2007). "Thyroid hormone replacement for
subclinical hypothyroidism". Cochrane database of systematic reviews (Online) (3):
CD003419. doi:10.1002/14651858.CD003419.pub2. PMID 17636722