The management of Hypothyroidism

February 22, 2012

Am going to look at this paper as the key points all look good.... Wonder when

we'll find these two docs before the GMC ?

x

>

> http://www.onmedica.com/ClinicalArticleView.aspx?id=e5c5b5fb-516b-4f4d-9e1f-

> 5b9a3d44ffde

>

> The management of hypothyroidism

>

> Tillmann i, general practitioner, York. Reviewed by Luke Koupparis,

> general practitioner, Bristol.

>

February 22, 2012

From: thyroid treatment

[mailto:thyroid treatment ] On Behalf Of Galathea

Sent: 22 February 2012 22:21

thyroid treatment

Subject: The management of Hypothyroidism

Am going to look at this paper as the key

points all look good.... Wonder when we'll find these two docs before the GMC ?

x

>

> http://www.onmedica.com/ClinicalArticleView.aspx?id=e5c5b5fb-516b-4f4d-9e1f-5b9a3d44ffde

>

> The management of hypothyroidism

>

> Tillmann i, general practitioner, York. Reviewed by Luke Koupparis,

> general practitioner, Bristol.

>

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February 22, 2012

Here it is in full , because you have to sign in to be

able to read it.

http://www.onmedica.com/ClinicalArticleView.aspx?id=e5c5b5fb-516b-4f4d-9e1f-5b9a3d44ffde

The

management of hypothyroidism

Tillmann i, general practitioner, York. Reviewed by Luke

Koupparis, general practitioner, Bristol.

Tuesday, 21 February 2012

Key learning points

The development of hypothyroidism

can be complex and subtle.

A proportion of patients with

hypothyroidism in the UK may not be identified or treated adequately.

Measuring only TSH for diagnosis

can miss the rarer secondary or tertiary forms of hypothyroidism.

The development of a goitre is an

unreliable sign for hypothyroidism.

Some patients may not respond to

straightforward treatment with L-Thyroxine (T4) for physiological reasons

and therefore may need additional treatment.

The diagnosis and management of

subclinical hypothyroidism remains partially inconsistent or even

controversial, despite international expert advice.

Background

Hypothyroidism describes a deficient production of thyroid

hormones with subsequent systemic effects. The two main thyroid hormones are

thyroxine (T4) and triiodothyronine (T3).

Hypothyroidism may remain subclinical for some time but can, in

some rare cases, lead to acutely life threatening complications.

There is some controversy regarding its detection and management

in the UK. For example, a 2011 study concluded that up to 8% of the UK

population may be hypothyroid and a substantial proportion of patients could

benefit from treatment, which they are currently not receiving.1 Other

sources state a UK prevalence of spontaneous hypothyroidism between 1% and 2%

and the overall prevalence between 0.5% and 6.3%.2

Thyroid problems (hypo- and hyperthyroidism) are 10 times more

common in women than men.

Classification and causes

Primary hypothyroidism describes thyroid

hyposecretion due to thyroid gland disease at the organ level. This deficiency

leads to an increased secretion of thyroid stimulating hormone (TSH) and

elevation of serum TSH concentrations. Commonly cited causes include

auto-immune thyroiditis, ablative thyroid surgery, iodine deficiency or excess,

certain medications (amiodarone, lithium, interferons and others).

Secondary hypothyroidism develops through insufficient

TSH stimulation of the thyroid gland because of a dysfunction of the pituitary

gland. This can be due to tumours, trauma, infection or vascular issues. Also,

congenital hypoplasia may occur. In some cases the pituitary gland is actually

intact, but there are defects in the TSH biosynthesis or its release.

Tertiary hypothyroidism is due to a problem another

level above, when there is a lack of hypothalamic thyroid releasing hormone

(TRH) release. This consequently affects the function of the pituitary gland

and there therefore leads to reduced TSH.

Autoimmune hypothyroidism mostly affects patients

with a positive family history, type 1 diabetes, ’s or Down’s

syndrome or after postpartum thyroiditis.3 TSH levels correlate

positively with physiological stress and emotional stress may lead to temporary

or permanent hypothyroidism over time, probably as a result of a disturbance of

the immune system.

Worldwide, the most common cause for hypothyroidism is iodine

deficiency. Thyroid function is particularly crucial in early childhood.

Congenital hypothyroidism (1 in 4,000 live births in the UK) is likely to

result, if undetected, in so-called cretinism, a severe metabolic disability

with subsequent irreversible neurological problems and poor growth. Contrary to

this, young children who lose their normal thyroid function will develop

problems with hypothyroidism, which, however are reversible with treatment. All

babies in the UK are routinely screened at birth via a pinprick test, which is

also analysed for phenylketonuria, cystic fibrosis and sickle cell disease.

Symptoms

Typical symptoms voiced by patients with high TSH are often

non-specific, but they are significant if considered in combination: fatigue

and low mood, weight gain, cold intolerance, constipation, bradycardia, dry and

fragile skin, hair and nails, muscle cramps or hypotonia, declining memory

function, period or fertility disorders, and others.

Complications

The most extreme acute complication of hypothyroidism is called

myxoedema coma, which typically features hypothermia, seizures, confusion,

hypoventilation, blood pressure changes.

It is rare and affects mostly patients of 60 years or above and

occurs more often in winter time. The mortality overall is high due to

overwhelming and sometimes rapid multi-organ failure. Many patients are

actually not initially “comatose”, therefore the most crucial

element of diagnosis is the consideration (or knowledge) that the patient may

have a crisis related to the underlying thyroid problem.

Pregnant women with subclinical hypothyroidism are at increased

risk of becoming symptomatic with a higher chance of pre-eclampsia and raised

overall perinatal mortality.

Diagnosis

The primary diagnostic test for hypothyroidism is the

measurement of TSH and free thyroxine (T4). Both can be affected by

non-thyroidal illnesses, and therefore need to be repeated if there are any

doubts in the given clinical situation.

There is some international debate regarding the exact

biochemical reference ranges to indicate need for active treatment and that

appropriate treatment levels have been achieved. Therefore there can be some

variation between countries and even within countries regarding this.

Overt hypothyroidism can be diagnosed when a

symptomatic patient has TSH levels > 10mU/L; combined with T4 levels below

the local reference range.

Subclinical or mild hypothyroidism will have TSH levels of <

10mU/L, but above the normal reference range with T4 levels within the

reference range.3

Pituitary or hypothalamic disease will

result in a normal or decreased TSH with decreased free T4. This means that

measuring only TSH and nothing else can miss the diagnosis of the rarer

secondary or tertiary forms of hypothyroidism.

The detection of anti-thyroid antibodies suggests autoimmune

disease.

In all patients, a thorough physical examination should

be performed, including:

cardiovascular parameters:

weight, blood pressure, pulse

a general neuromuscular

assessment

thyroid palpation and

auscultation

eye and dermatologic examination

Goitre means an abnormal enlargement of the thyroid gland. This

can occur in under or over-activity of the gland and is therefore not specific

for hypothyroidism. Autoimmune hypothyroidism may be present with a goitre (Hashimoto's disease) or

without a goitre (atrophic thyroiditis).

Figure 1: A female patient with a goitre that is

clearly visible.

Treatment

Hypothyroidism is treated with the replacement of T3 and/or T4,

typically with the synthetic levorotatory forms. Most patients with

hypothyroidism in the UK receive synthetic T4 only and are titrated to TSH level.

Some may get treatment with T3 or a combination of T4 and T3, and very few may

have (unlicensed) treatment with porcine desiccated thyroid extract, which

contains natural forms of T4 and T3. Both the combination treatment and

desiccated thyroid extract are currently not manufactured in the UK.

The evidence for or against combination therapy with T3 and T4

as a standard treatment for all hypothyroid patients is, so far, inconclusive.4,5

There are significant cost implications to this debate: T3

treatment (for example liothyronine sodium) is very expensive in comparison

with T4. Also, patients on thyroid treatment will receive free prescriptions on

the NHS for the duration of their treatment (often regarded to be life-long),

which may have impact on NHS medication budgets.

There can be significant variation between patients regarding

the treatment dose they need to relieve symptoms: for some patients 50mcg of T4

daily may be sufficient, whereas others may need 200mcg or more. The required

dose can change in the individual patient as well throughout their lifetime,

depending on their circumstances and with age; therefore it will need regular

monitoring and adjusting if needed.

The careful treatment of the following two patient groups is

particularly important:

1.

Pregnant women, who

are already on T4, will usually need an overall dose increase of 25-50

micrograms by 4-6 weeks gestation. After delivery they can usually go back to

their pre-pregnancy dose.

2.

Elderly patients with a history of ischaemic heart disease and a

new diagnosis of hypothyroidism should start on a very low dose, for example

12.5mcg, and only gradually increased every 2-3 months. It may even be worth to

consider a resting electro-cardiogram (ECG) before starting therapy.6

All new hypothyroid patients on medication would ideally have a

TSH check every three months in the beginning or after a change in dose, until

they are stable, with the aim to eventually reach and stay in

the lower half of the respective reference range. In

many areas this will mean between about 0.4-2.5mL/L.7

Patients may state that they experience differences of

efficiency between various brands or generics. Although a doctor will rarely

choose to prescribe a branded T3 or T4 product, it may be important to support

the patient to communicate effectively with their supplying pharmacy to receive

consistent generic treatment.

Overall it is important to treat the patient and not the TSH

level. If a patient feels well, even if the TSH appears elevated or high

normal, then the dose doesn’t necessarily need to be increased. A long

standing complete suppression of TSH may bear an increased risk for developing

heart disease or osteoporosis.

Management of subclinical hypothyroidism

The term subclinical hypothyroidism (TSH is above the reference

range, for example > 4.0mU/L but < 10mU/L) is often misleading, since

many patients appear to be symptomatic with it. Therefore, in a clinical

setting it may sound reasonable to start treatment, although the guidance

regarding the management is more complicated.

Evidence suggests that 20% of patients with subclinically

abnormal TSH will experience a spontaneous normalisation of TSH without any

treatment.7 In other words the statistical conversion rate to overt

hypothyroidism is less than 3% per year, whereas for a TSH > 10mU/L it is

more than 5% (possibly up to 20%) a year and therefore significant enough to

suggest treatment at detection.

The main risk of active treatment for subclinical hypothyroidism

might therefore merely be the possible development of (subclinical)

hyperthyroidism.8

For a GP, this advice may mean that a symptomatic patient with

biochemically subclinical hypothyroidism can be actively treated. This is

provided that the condition is reviewed regularly, to establish if the patient

may have actually reverted back to normal function.

Treatment of subclinical hypothyroidism in order to decrease

cardiovascular morbidity is not supported by the evidence, unless the TSH is rising,

a patient is pregnant or is developing a goitre.3

Patient involvement

Information

services for patients and carers can be useful and relevant for

compliance.

T4 is best taken 30-60 minutes before breakfast. Some foods can

affect the absorption of it: compared to water, coffee reduces absorption of T4

by about 30 percent. Also, several medications such as anticonvulsants,

antibiotics (ciprofloxacin), iron or calcium supplements, raloxifene and

orlistat have been reported to affect the absorption of levothyroxine.

Some patients with significant lactose intolerance may require a

lactose-free version on T4.

It is worth advising the patient at diagnosis that it can take

several weeks of initial treatment before they may experience any benefit.

Referral-criteria

A patient should be referred in suspected cases of secondary

hypothyroidism, suspected thyroiditis, continuing symptoms despite T4 treatment

or any apparent complications.3 However, the history given by the

patient can be more significant and relevant in any case rather than seemingly

satisfactory laboratory results at the time.

References

1.

Abu-Helalah M, Law MR, Bestwick JP et al.: A randomized

double-blind crossover trial to investigate the efficacy of screening for adult

hypothyroidism J Med Screen December 2010; 17:164—169

2.

British Thyroid Association (BTA). UK guidelines

for the use of thyroid function tests. Sheffield: BTA; 2006.

3.

Clinical Knowledge Summaries (CKS). Hypothyroidism. Newcastle

upon Tyne: CKS; 2009.Cited in Map

of Medicine.

4.

Baisier, W. V.; Hertoghe, J. et al.: Thyroid Insufficiency. Thyroid

Insufficiency. Is Thyroxine the Only Valuable Drug?. Journal of Nutritional and

Environmental Medicine September 2001; 11 (3): 159–66.

5.

Escobar-Morreale, H. F., Botella-Carretero, JI et al.: Treatment of

Hypothyroidism with Combinations of Levothyroxine plus Liothyronine. Journal of Clinical Endocrinology

& Metabolism 2005;

90 (8): 4946–54.

6.

The Endocrine Society. Management of

thyroid dysfunction during pregnancy and postpartum. J Clin Endocrinol Metab

2007; 92: S1-47.

7.

Map of Medicine (MoM) Clinical Editorial team and Fellows.

London: MoM; 2011.

8.

Hueston WJ; Treatment of hypothyroidism.;

Am Fam Physician. 2001; Nov 15;64(10):1717-24.

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