FROM THE HISTORY1
Goiter was first described in China in 2700 BC. Da Vinci described thyroid as a thing that is designed to fill empty spaces in the neck. According to Parry – thyroid works as a buffer to protect the brain from surges in blood flow. Roman physicians have reported thyroid enlargement as a sign of puberty. In 500 AD Abdul Kasan Kelebis Abis performed the first goiter excision in Baghdad, the procedure remained unknown. In 1200s AD advancements in goiter procedures included applying hot irons through the skin and slowly withdrawing them at right angles. The remaining mass or pedicled tissue was excised. Patients were tied to the table and held down to prevent unwanted movement, but most died from haemorrhage or sepsis. In 1646 AD Wilhelm Fabricus performed a thyroidectomy with standard surgical scalpels, for which he was imprisoned. In 1656 thyroid was first identified by the anatomist Thomas Wharton. In 1808 AD Guillaume Dupuytren performed a total thyroidectomy, but the patient died postoperatively of “shock”. In 1820 AD Johann Straub and Francois Coindet found that use of seaweed (iodine) reduced goiter size and vascularity. In 1830 AD Graves and von Basedow describe a toxic goiter condition they referred to as “Merseburg Triad” – goiter, exopthalmos, and palpitations. In 1866, Samuel David Gross said, “If a surgeon should be so foolhardy as to undertake it [thyroidectomy] … every step of the way will be environed with difficulty, every stroke of his knife will be followed by a torrent of blood, and lucky will it be for him if his victim lives long enough to enable him to finish his horrid butchery.” In 1883, Theodor Kocher while addressing the German Medical Congress stated, “The thyroid gland in fact had a function”. In the same year Kocher’s performed a retrospective review on 5000 career thyroidectomies. The thyroxine was discovered somewhere in 19th century and a remarkable turning point started with this in management of thyroid disorders by allopathic counterparts.
REFERENCES FROM THE LITERATURE2
The homoeopathic literature is loaded with vast examples of thyroid diseases and their cure with homoeopathy. It was the insight of our great masters that they have so beautifully described thyroid related disorders and their management in Homoeopathy. In his great work, Master Samuel Hahnemann has quoted, “What action is exerted on the skin by certain diseases of the glands with an internal secretion (thyroid gland, ovaries, testicles, supra-renal capsules, pituitary gland, etc.) must remain reserved for future research. So much, however, is established to-day to prove that some of these disturbances (Addison’s disease) cause considerable alterations of the skin.” Below are some of the references from the history regarding thyroid disorders and their Homoeopathic cure.
CASE STUDIES PRESENTED SO FAR2
- Journal of Homoeopathic Clinics, Vol 3, Sep N’1, Case 458, 1869-1870: A 19 years old female with large swelling of the thyroid gland was treated with Bromine 3, several times a day following by Calc Carb 3 and was relieved in three weeks of time.
- International Hanhnemannian Association 1902: A case of thyrotoxicosis was treated by Homoeopathically chosen remedies: China, Lachesis, Sul.
- Clinical Illustrations Homoeopathician (A Journal Of Pure Homoeopathy) 1914: presented 3 cases of thyroid enlargement with thyroid dysfunction and were reported cured by Iodum and Baryta carb.
- International Hahnemannian Association 1919: “Our knowledge of the endocrine remedies is as yet in a formative stage, but the therapeutic use of the ductless glands is steadily growing. We know more of the thyroid gland and of its therapeutic applications, than of any of the other ductless glands.” There is also a case presented which was treated using 2x and 3x trituration of thyroidinum.
- International Foundation for Homoeopathy: Case Conference Proceedings 1995: A case of primary hypothyroidism aged 30 female was presented by Dr. George Guess.
- Master F. J. , 1995: A case of a lady aged 51 years with migraine of 15 years standing, hypothyroidism since 10 years and leucoderma since 5 years and a diagnosed as a case of Hypothyroidism was given Staphisgaria.
REFERENECES FROM MATERIA MEDICA2
- Blackwood A. L. Manual of materia medica therapeutics: “A normal thyroid has much to do with the function of the ovaries; with a hypothyroid condition, although the ovaries and uterus are normal, menstruation may not appear and the patient becomes obese, the skin dry; should the pituitary show disturbance, the skin will be moist and soft”.
- American Homoeopath described the concept of Hypothyroidism, cancer and clinical depression.
- Boericke W. Pocket manual of homoeopathic materia medica: Kali Carb: “Pain in small spot on left side Hypothyroidism”. Thryroidinum: “Marked sensitiveness to cold, Hypothyroidism after acute diseases, i.e. weakness.
- Grand George D. The spirit of homoeopathic medicines: “At times the remedy is suggested by hypertrophied glands or the beginning of goiter. Homeopathic treatment will remedy a slight disorder in the glandular system, but when the disorder is too great, hormonal treatment will be necessary.
- Lesser O. Textbook of Homoeopathic Materia Medica: “If the alkali and earthy alkali metals, Na, K, Mg, Ca, as cations determine the drug picture, then they shape it as hydrogenoid, cold, sensitive to cold, relaxed torpid lymphatic constitutional types stigmatized along the side of the parasympathetic system. Seen from an endocrine side, they tend toward the hypothyroid side, the function of the lymphocytic apparatus (thymus) is increased.”
- Master F. J. The bed side Organon of Medicine: “Never give thyroidinum as a routine or specific for all patients who come with thyroid problem.”
REFERENCES FROM REPERTORY3
There are 32 references in the forms of rubrics and subrubrics given in Synthesis treaure edition. Whereas Kent’s repertory, Murphy repertory and Complete repertory consists of 9, 13 and 37 rubrics in relation to thyroid and other rubrics and vice versa respectively.
The thyroid gland starts developing by 3-4 weeks of gestation, appearing as an epithelial proliferation in the floor of the pharynx. Follicles of the thyroid begin to make colloid in the by 12th week of gestation and thus contribute in development of physical and neurological features. Failure of synthesis of hormones and TSH by thyroid gland may result in arrested or abnormal growth of the fetus. At birth, a cold-stimulated short-lived TSH surge is observed, followed by a TSH decrease until day 3 or 4 of life by T4 feedback inhibition.
ANATOMY OF THYROID GLAND5
FUNCTIONS OF THYROID GLAND6
The thyroid gland is one of the most important endocrine gland which secrets two major hormones, thyroxine and triiodothyronine. It is situated in the anterior part of the neck just above the lower part of the trachea, situated in between the cricoid cartilage and suprasternal notch. Normally it is not palpable but may be palpated in conditions in which it is enlarged. Enlargement of the gland may not be a sign of its under or over functioning, but association of goiter with thyroid function status and other investigative modalities helps us to understand disease in a better term. Goiter is assessed by palpation by fingers of both hands for size, consistency and presence of nodules if any.
Thyroid palpation method
Thyroxine (T4) and tri-iodothyronine (T3) are two major hormones that are secreted in pulsatile manner under feedback mechanism controlled by hypothalamic-pituitary-thyroid-pituitary axis.
DIAGNOSING VARIOUS THYROID DISORDERS
The diagnosis of thyroid disorder is primarily done on following points:
- Complete homoeopathic case taking.
- Family history of systemic disorders particularly thyroid and autoimmune disorders. It is seen that the individuals who have family history positive of thyroid dysfunction are at greater risk of developing thyroid disorders.
- Consistancy and size of thyroid gland, as it may give us some hint about the underlying pathology, e.g. firm gland are suggestive of Hashimoto’s thyroiditis, goiter in high grades can induce pressure symptoms on trachea and other adjacent tissues, painful gland suggests acute or subacute inflammatory condition.
- Presence of anti thyroid antibodies, may suggest some of the thyroid dysfunction.
- Other investigations also help in arriving at diagnosis of thyroid disorders. Some of the investigations are: Radioactive iodine uptake (RAIU), Technetium scan (Tc Scan), Fine needle biopsy (FNB). These investigations are condition specific and are to be advised as per requirement of the case. The detailed description of these investigative modalities is described later in the following text.
The ultimate and ground level workers in thyroid-body axis are the two hormones secreted by thyroid gland. These hormones are responsible for various activities in almost the entire body. Every organ and tissue thus needs these hormones (particulary T3) for proper functioning. Thyroid hormones acts by crossing the cell membrane and binding to intracellular receptors (?1, ?2, ?1 and ?2), which act alone, in pairs or together with the retinoid X-receptor as transcription factors to modulate DNA transcription and thus various metabolic and other functions are performed. There are two variants of thyroid hormones circulating in body; free and bounded hormones, as hormones are circulated along the body in protein-bound form. These proteins are majorly thyroid binding globulins (TBG) and less commonly albumin. According to extensive research studies done on this reveals that free hormone assay is more reliable as bound hormones level may vary in conditions in which there is pooling of TBG in body eg.,
- Estrogen therapy
- Oral contraceptive pills
- Acute viral hepatitis
- Primary biliary cirrhosis
- Hepatocellular cancer
- Collagen vascular disease
On the other hand TBG in decreased in
- Nephrotic syndrome
- Protein-losing enteropathy
- Critical illness/starvation
T4 (thyroxine) is the major circulating hormone whereas T3 is more biologically active. Both T3 and T4 give a feedback to pituitary to release or suppress secretion of TSH. TSH is ultrasensitive to even smaller amouts of circulating T3 and T4 levels, this phenomenon is to be understood at the ground level to understand the diagnosing and follow up cases of thyroid disorders. This can be understood by the following simple yet informative flow chart:
TSH is one of the most reliable marker of thyroid disorders along with FT4 estimation. Other diagnostic modalities used to diagnose various thyroid dysfunctions are given below with their advantages and description:
|TSH||Most reliable marker to assess thyroid dysfunction with FT4 as TSH is the precursor of release of FT3 & FT4|
|Free T3, T4||Circulating un-bound hormone assays depicts the actual level of thyroid hormones thus prognosis can further be made along with the clinical and confirmed diagnosis.|
|Antibodies: Anti-TPO, Anti-TSHr||Presence of antibodies may sometime help us to understand the natural history of thyroid functions, as their presence confirms the undergoing pathological conditions.|
|Thyroid ultrasonography||Thyroid Ultrasonography is done to see the consistency of thyroid gland. It is also done to rule out the presence of nodules. Ultrasonography can also be suggestive of congenital anomalies e.g. absence of one or both lobes of thyroid gland.|
|RAIU||Scintillation counter measures radioactivity after I123 administration. Uptake varies greatly by iodine status, e.g. indigenous diet (normal uptake 10%).|
Elevated RAIU with hyperthyroid symptoms may be presented in:
Low RAIU with hyperthyroid symptoms is used to distinguish:
The RAIU technique is also used as a therapy to suppress the hyperactive gland in thyrotoxicosis and hyperthyroidism.
|Technetium scan (Tc Scan)||Technetium scan is also based on the uptake phenomenon of Tc by thyroid gland that is then use to differentiate various nodules and hyper functioning and hyperactive thyroid gland.|
|Final Needle Biopsy (FNB)||FNB is used to study the morphological and pathophysiology of glandular tissue. By this technique we can differentiate various types of carcinomas, dysplasia, and chronic lymphatic infiltration.|
- TSH is a good screening test to assess thyroid function in an outpatient setting.
- If TSH is abnormal, the diagnosis is confirmed with thyroid hormone levels.
- Change in thyroid binding proteins could alter total thyroid hormone levels.
- 99% of thyroid hormones are protein bound.
- In order to assess the thyroid hormone levels unaffected by the binding proteins, free thyroid hormone levels assessment is more reliable.
- T4 is the major thyroid hormone in circulation; therefore assessing T4 status alone is usually sufficient to assess the thyroid hormone status.
- In certain situations, T3 level becomes abnormal without changes in T4, as in T3 thyrotoxicosis where there are elevated levels of T3 along with normal T4 levels and low TSH level.
- Acute illnesses can alter thyroid function tests without thyroid disease as they tend to increase binding proteins, also TSH can also be influenced by stress and anxiety.
- Thyroglobulin is a good cancer marker for papillary and follicular cancer after total thyroidectomy.
- Thyroid antibodies can assess the risk of developing autoimmune thyroid diseases.
SPECTRUM OF THYROID DISORDERS7
Chronic enlargement of the thyroid gland not due to neoplasm is called as goiter.
- Endemic goiter-Areas where > 5% of children of 6-12 years of age have goiter, very common in China and central Africa.
- Sporadic goiter –Areas where < 5% of children 6-12 years of age have goiter. Multinodular goiter in sporadic areas often denotes the presence of multiple nodules rather than gross gland enlargement.
- Hashimoto’s thyroiditis
- Early stages only, late stages show atrophic changes
- May present with hypo, hyper or euthyroid states
- Graves’ disease – Due to chronic stimulation of TSH receptor
- Diet – Brassica (cabbage, turnips, cauliflower, broccoli), Cassava, Lithium prevents release of hormone, causes goiter in 6% of chronic users
- Chronic Iodine excess – Iodine excess leads to increased colloid formation and can prevent hormone release. If a patient does not develop iodine leak, excess iodine can lead to goiter.
– Palpable: 4-7%
– Non-Palpable: >50%
– Cancer in nodules: 5%
- Women affected more than men
- Most subjects are euthyroid and/or asymptomatic
- Prevalence is less than 1% with thyrotoxicosis
- Historical Red Flags are defined as:
– Extremes of age (<20 or >65)
– Rapid Growth
– Symptoms of local invasion (hoarseness, dysphagia, neck pain)
– History of radiation to the head or neck dispose an individual to develop nodules
– Family history of Thyroid Cancer or Polyposis
SOLITARY THYROID NODULE
- More likely to be malignant in men, patients over 60 and patients with a h/o head or neck irradiation are at more risk.
- No growth for years almost always indicative of benign nodule as it is not a nodule that appears suddenly (likely a cyst or adenoma hemorrhage)
- Malignant nodule develops in weeks to months.
- Virtually all patients with thyroid carcinoma are euthyroid as are those with benign nodules. Nodule of >1.5 cms., are usually detectable on examination and are confirmed in the Ultrasonography. Lifetime risk for developing a nodule is 5-10%. Studies show 50% of people during autopsy have either single or multiple nodules. 5-10% of clinically detectable hypofunctioning (cold) nodules can be malignant. The laboratory/imaging techniques used are: TSH, Calcitonin, Ultrasound, FNB for characterization of Nodules, Nuclear Scan to see whether nodule is “Hot” or “Cold.” If FNB is suggestive of malignancy then surgery is advised, and if it is suspicious or negative then a follow up of few months is given to the patient with repeat investigations. In case there are indeterminant reports then FNB is repeated, if still indeterminant, surgery is recommended.
Definition – disorder of the thyroid gland causing decreased thyroid hormone production and secretion. It is the most common disorder of thyroid dysfunction. The factors attributed to these are:
- Worldwide – iodine deficiency is most common cause.
- Iodine depleted areas – chronic autoimmune thyroiditis is commonly present in these areas.
- Associated with elevated serum cholesterol, CPK, AST and LDH
Definition – It is caused by decreased thyroidal stimulation by TSH.
- Also referred to as central or hypothyrotropic hypothyroidism.
- Caused by either pituitary or hypothalamic diseases.
- Very uncommon.
- TSH is usually low or inappropriately normal.
Symptoms of hypothyroidism
It includes – Fatigue, lethargy, mental impairment, depression, cold intolerance, hoarseness, dry skin, decreased perspiration, weight gain, decreased appetite, constipation, menstrual irregularities, arthralgias and parasthesias.
Slow movements, slow speech, hoarseness, bradycardia, dry skin, non-pitting edema, hyporeflexia, delayed relaxation of reflexes are some of the signs of hypothyroidism.
N. B.: Older patients tend to have fewer signs and symptoms of hypothyroidism and those they have tend to be less specific.
- Low FT4, High TSH (Primary, antibodies estimation suggested)
- Low FT4, Low TSH (Secondary or Tertiary, TRH stimulation test, MRI)
- It is the most common cause of hypothyroidism.
- It is due to action of auto- antibodies to TPO, TBG thus by inhibiting/diminishing the production and secretion of thyroid hormones.
- Commonly presents in subjects from 30-50 yrs, female affected more than males.
- It is usually non-tender and asymptomatic.
- Lab values
- High TSH
- Low T4
- Anti-TPO Ab, Anti-TBG Ab
SILENT THYROIDITIS (POST-PARTUM THYROIDITIS)
Silent thyroiditis is termed post-partum thyroiditis if it occurs within one year of delivery. Patient comes with hyperthyroid symptoms. Soon there is progression to euthyroidism followed by hypothyroidism for up to 1 year. Later on hypothyroidism generally resolves.
SUBACUTE THYROIDITIS (DEQUERVAIN’S, GRANULOMATOUS)
It is the most common cause of painful thyroiditis. It often follows a URI. FNA may reveal multinuleated giant cells or granulomatous change.
– It starts with pain and thyrotoxicosis (3-6 weeks) followed by asymptomatic euthyroidism.
– Then there is period of hypothyroid state(weeks to months).
– It is followed by phase of recovery (complete in 95% after 4-6 months).
– Elevated ESR
– Anemia (normochromic, normocytic)
– Low TSH, Elevated T4 > T3, Low anti-TPO/Tgb
– Low RAI uptake (same as silent thyroiditis)
– Graves’ disease may occasionally develop as a late sequellae
– 68% Bacterial (S. aureus, S. pyogenes)
– 15% Fungal
– 9% Mycobacterial
It may occur secondary to Pyriform sinus fistulae, Pharyngeal space infections, Persistent Thyroglossal remnants, Thyroid surgery wound infections (rare) and in HIV.
– Warm, tender, enlarged thyroid