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Hypothyroidism
- 1. Primary Hypothyroidism: Management Mathew John, MD, DM, DNB Consultant Endocrinologist Providence Endocrine & Diabetes Specialty Centre www.endocrinologydiabetes.com www.providence.co.in
- 2. Case 32 year oldlady was evaluated for generalized paraesthesias with aches and pains in different joints. No arthritis was noted. No fever/red eyes/ extraarticular manifestations of collagen vascular diseases Seen by a neurologist and investigated Blood sugars : normal CPK: 300 U/L ( Normal < 200 ) Calcium parameters: normal ANA/ dsDNA : negative RA factor : 86 ( Normal< 60 ) ESR: 26 mm / 1 hr Uric acid : 8.6 mg/dl (< 6 ) CBC: normal except for Hb: 9.8 gm/dl , MCV: 104 NCV: bilateral CTS
- 3. Vague Multiple symptoms symptoms Mild anemia Dimentia Postpartum Think Thyroid period Carpal Tunnel Mild hyperuricemia Syndrome Altered lipid profile Elevated CPK
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- 5. What further tolook before starting treatment ? • Diagnosis • Coexistent conditions age of patient severity of hypothyroidism coexistent drugs coexistent medical conditions
- 6. The patient wasseen by physician Additional information generated • Strong family history of hypothyroidism • Delivered 6 months back and breast feeding • Taking iron and calcium tablets • Small firm goiter • TSH > 100 IU/ml Free T4: 0.45 ng/dl
- 7. Diagnosis Primary hypothyroidism Postpartum thyroiditis
- 8. Etiology PRIMARY HYPOTHYROIDISM • Hashimoto’sthyroiditis-most common Post partum thyroiditis • Atrophic hypothyroidism • Irradiation of thyroid • Surgical removal • Late stage invasive fibrous thyroiditis • Iodine deficiency • Drug therapy (Lithium, Interferon) • Infiltrative Diseases:Sarcoidosis, Amyloidosis Scleroderma, Hemochromatosis
- 9. Diagnosis Thyroid hormones feedback inhibit TSH So If T3, T4 reduces TSH increases Primary hypothyroidism
- 10. The spectrum ofdisease Euthyroid Free T4/ T4: normal TSH : normal Subclinical hypothyroidism Free T4/ T4 : normal TSH : elevated Overt Hypothyroidism Free T4/ T4 : low TSH : elevated
- 11. The spectrum ofdisease Euthyroid Free T4/ T4: normal TSH : normal Subclinical hypothyroidism Free T4/ T4 : normal TSH : elevated Overt Hypothyroidism Free T4/ T4 : low TSH : elevated
- 12. The spectrum ofdisease Euthyroid Free T4/ T4: normal TSH : normal Subclinical hypothyroidism Free T4/ T4 : normal TSH : elevated Overt Hypothyroidism Free T4/ T4 : low TSH : elevated
- 13. Further testing • AntiTPO antibody (Thyroid Peroxidase) • Anti Tg( Thyroglobulin) antibody marker of autoimmunity • Ultrasound thyroid : usually not needed • FNAC thyroid: usually not needed in autoimmune thyroiditis needed in infiltrative diseases
- 14. Treatment • Treated withthyroid replacement • Normal thyroid produces both T4 and T3 , predominantly T4 • T3 is formed in periphery by deiodination of T4 • Commercial preparations are usually only L-thyroxine ( T4)
- 15. Dose Thyroxine ( T4) •Strengths: 25 mcg, 50 mcg, 75 mcg,88 mcg, 100 mcg and 125 mcg • Adults require 1.6 mcg/kg/day • Elderly : 1.0 mcg/kg/day T3 (Triodothyronine) : available as Tetroxin/ Cytomel T3 as compare to T4 is • 4 times more potent. • Short duration of activity. • Rapid onset of action • Can be used for myxedema coma
- 16. Starting therapy • Adults 50 to 100 mcg/day of thyroxine • Elderly / Cardiac disease 25 mcg/day of thyroxine • 80% bioavailability • t1/2 1 week. Need 6 weeks for equilibration
- 17. Titrating therapy • Callback after 6 –12 weeks with TSH • Titrate 25-50 mcg/ day increments • Repeat testing only by 3 months • Only TSH is usually required for monitoring • Target TSH – lower half of the normal range (~2.5- 3mU/L) • Once TSH stable, repeat TFT annually. Ensure compliance
- 18. Changes with treatment •Begin to feel better within 2 weeks • Full symptom relief may take 3-6 months after TSH levels are normal • Risk of over treatment – atrial fibrillation – osteoporosis
- 19. Our patient • Startedon 100 mcg/day thyroxine in empty stomach • Called back after 6 weeks TSH : 63 mIU/L • Patient reports good compliance • Increased doses to 125 mcg/day • Called back after 3 months TSH : 38 mIU/L Not controlled ?
- 20. Follow up • Whatare the cause for high dose requiremts ? • Is thyroxine treatment during breast feeding harmful to baby ? • How long to continue treatment ?
- 21. High dose requirementof thyroxine • Malabsorption (celiac disease, small bowel surgery) • Compliance • Medications – Estrogen – Aluminium hydroxide – Cholestyramine – Rifampicin – Ferrous sulfate – Amiodarone – Calcium –Carbamazepine – Lovastatin – Phenytoin – Colsevelam –Magnesium containing laxatives – Lanthanum carbonate –Bulk laxatives with fiber – PPI ( ?)
- 22. What to do? • Space out tablets of thyroxine from other offending drugs • Can be converted to night dosing • Empty stomach : 30-60 minutes before breakfast • To minimize interference with food • No dose adjustment for kidney and liver disease
- 23. Hashimoto’s thyroiditis Chronic lymphocytic thyroiditis • Most common cause of hypothyroidism • Can be goitrous or non goitrous • Anti TPO antibody positive • Euthyroid Hashimoto’s : no treatment/ LT4 to reduce goiter size and antibody levels • Very rarely associated with thyroid lymphoma • Can have co-existent papillary carcinoma
- 24. Postpartum thyroiditis • Usually2-6 months after delivery • Transient thyrotoxicosis followed by hypothyroidism /hypothyroidism • Silent thyroiditis in postpartum period • 23 % progress to permanent hypothyroidism • More common with severe hypothyroidism higher Anti TPO antibody titre
- 25. Postpartum thyroiditis Clinical course
- 26. Case continued • Patientevaluated after spacing out the iron/calcium tablets • TSH : reduced to 2.8 mU/L • Continued same dose of LT4 125 mcg/day • Asked to come back after 3 months TSH: < 0.01 mU/L Next ?
- 27. Reversibility of primary hypothyroidism • Reversible hypothyroidism: Post partum Drug induced( alfa interferon, Li ) Infectious ( Whipple’s disease, Sub acute thyroiditis) ) • 20 % of autoimmune hypothyroidism has been found to be reversible • Spontaneous disappearance of blocking antibodies
- 28. Do you needto treat subclinical hypothyroidism • 3-8 % of individuals have subclinical thyroid disease • • Most common cause is autoimmune thyroid disease • 4.3 % progress to hypothyroidism is anti TPO antibody present 1. TSH > 10 mU/ml • Therapy indicated if 2. Anti TPO positive 3. Goiter present 4. Menstrual irregularities/ infertility 5. Childhood 6. Bipolar disease/ depression 7. Increasing TSH
- 29. Hypothyroid symptoms andnormal TFT (functional hypothyroidism) • Many patients, especially in internet era • Wilson's syndrome ( not Wilson’s disease) refers to the presence of common and nonspecific symptoms, relatively low body temperature, and normal levels of thyroid hormones in blood. ATA : no scientific basis for Wilson Syndrome American Thyroid Association Statement on "Wilson's Syndrome" , Updated May 24, 2005
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- 31. Functional somatic syndromes. •More than 20% of adults report significant fatigue • 30% have current musculoskeletal symptoms • Typical adult has one of the symptoms every 4 to 6 days • More than 80% of the general population has one of these symptoms during any 2 to 4 week period. Barsky AJ, Borus JF. Functional somatic syndromes Ann Intern Med 1999;130:910-21
- 32. Deja vu • A lady with weight gain • A lady with lowish resting heart rates • Lady with tiredness • Lady with memory loss • Lady with “ low” pressure • A lazy boy with poor school performance Have you ever started thyroxine for these people ?
- 33. Messages • Suspect hypothyroidism •Thyroxine is the treatment for primary hypothyroidism • Dose changes in thyroxine according to TSH • Some causes of primary hypothyroidism are reversible • Treat patients only with abnormal thyroid functions
- 34. Thank you www.providence.co.in: forpatient information materials twitter.com/providenceendo : for slide presentations
- 35. Diagnosis 2.0 ng/dl TSH Normal range for patient Normal range of population 0.8 ng/dl Free T4 4 mIU/L Free T4 0.3 mIU/L Euthyroid Subclinical hypothyroidism Not drawn to scale
- 36. Disclaimer The material forthese slides were derived from various sources including pictures and cartoons from the world wide web. I have tried my best to acknowledge all possible sources and references. However, if I have overlooked any particular reference, it is not done intentionally. Anyone reproducing materials from this presentations should acknowledge the author of the original work. The case given is imaginary and is given only to support the purpose of this talk. Any similarity to published case report/ patient is unintentional.