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Thyroid Function Tests in Amyloid Goitre P Postgrad Med J (1990) 66, 304- 306 A) The Fellowship of Postgraduate Medicine, 1990 Postgrad Med J: first published as 10.1136/pgmj.66.774.304 on 1 April 1990. Downloaded from Thyroid function tests in amyloid goitre P. Duhra and J. Cassar West Middlesex University Hospital, Isleworth, Middlesex TW7 6AF, UK. Summary: We present two patients wth amyloid goitre due to primary systemic amyloidosis which was confirmed at post-mortem. Both were clinically euthyroid but had hyperthyroxinaemia and other thyroid function tests suggestive of thyrotoxicosis. Introduction Whereas minor amyloid infiltration of the thyroid 25.9 mmol/l, creatinine 519 p.mol/l. Creatinine gland is found in 50-80% of cases of generalized clearance was 12 ml/min and urinary protein excre- amyloidosis,' the induction of a goitre by amyloid tion 0.3 g/24 hours. invasion is rare.2 Amyloid is an inert substance3 and Assessment of thyroid function disclosed a infiltration ofthe thyroid does not usually interfere serum free thyroxine (FT4) of 32.5 pmol/l (NR with the endocrine function of the gland.4'5 In two 8.8-23), thyrotrophin releasing hormone (TRH) previous reports of possible hyperthyroidism in test showed thyroid stimulating hormone (TSH) amyloid goitre an elevated basal metabolic rate, on values) of 1.2, 0.6, 0.6 mU/I taken at time 0, 30, 60 which the diagnosis of hyperthyroidism rested, minutes after intravenous TRH bolus. could instead have been attributed to the underly- A technetium thyroid scan showed generalized ing chronic inflammatory disease producing the 'thyroid enlargement with homogenous distribu- secondary amyloidosis.6 Apart from these two tion "of radiaoactivity. The overall technetium copyright. reports thyroid over-activity has not been noted in uptake was 5.1% ofthe dose at 20 minutes (normal amyloid goitre. upper.level 3.5%). We describe two cases with amyloid goitre who Serum TSH receptor antibody activity was were clinically euthyroid but had hyperthyrox- determined using the Rapoport bioassay which inaemia. utilizes human thyroid cells in culture. The thyroid stimulating antibody level was 18 bovine TSH equivalents per ml (normal range under 2.8). Case reports Thyroglobin and microsomal antibodies were undetectable in the serum. http://pmj.bmj.com/ Case I Carbimazole therapy was introduced in April 1984 and FT4 three months later was reduced to A 50 year old manual worker presented in Feb- 7.5 pmol/l. In August 1984 carbimazole was ruary 1984 with an enlarging cervical swelling, inadvertently discontinued for 10 days and FT4, dysphagia for solids, change in voice, weight loss measured on the tenth day, had risen to 77.0 pmol/l. and feeling generally ill. Physical examination Carbimazole was promptly recommenced. Serum revealed a euthyroid man with pallor, a soft pitched immunoelectrophoresis showed a paraprotein, on October 1, 2021 by guest. Protected voice and a large, diffuse, hard goitre. There was no typed as IgG Kappa. Serum immunoglobulins cervical lymphadenopathy nor dysthyroid eye were assayed: IgG 28 g/l (NR 5.3-16.5); IgA disease and apart from moderate hepato- 0.2 g/l (NR 0.8-4.0) and IgM 0.3 g/l (NR 0.5-2.0). splenomegaly the rest of the examination was A skeletal survey showed no lytic defects typical of normal. multiple myeloma. A bone marrow aspirate con- Investigations showed a normochromic normo- tained 15% plasma cells with many abnormal cytic anaemia with haemoglobin 8.7 g/dl; mean forms. corpuscular volume 86.4 fl; erythrocyte sedimenta- A thyroid needle biopsy showed widely tion rate 39 mm in one hour. Biochemical profile separated thyroid follicles some ofwhich were filled was normal except total protein 71 g/l, albumin with colloid. The thyroid stroma stained with 28 g/l, plasma bicarbonate 18 mmol/l, urea congo red exhibited the characteristic apple-green birefringence of amyloid under polarized light. A renal biopsy performed in March 1985 confirmed Correspondence: J. Cassar, Ph.D, M.D., F.R.C.P. the diagnosis. By February 1985 he had progressed Accepted: 21 September 1989 to end-stage renal failure necessitating REPORTS 305 CLINICAL Postgrad Med J: first published as 10.1136/pgmj.66.774.304 on 1 April 1990. Downloaded from haemodialysis, and underwent a total thyroidec- Trephine biopsy revealed an excess ofmononucl- tomy in April 1985 for reliefof severe dysphagia. A ear cells staining positively for immunoglobulin pale, hard thyroid gland weighing 167 grammes lambda light chains. Only some cells were recog- was removed. There was gross amyloid infiltration nizably plasmacytoid. Free T4 was 8.7 pmol/l, accounting for approximately 90% of the thyroid TSH 0.6 mU/l. mass. In addition to separating individual follicles, There was a rapid deterioration in her clincial amyloid had obliterated many capillaries by state and she died 7 weeks after admission. Post- invasion of their wall. mortem confirmed the diagnosis of AL The follicles were atrophic with no hypertrophy amyloidosis. There was amyloid in the thyroid, of the follicular cells, and the only evidence of adrenal and pancreas. The thyroid weighed 360 g. thyroid hyperactivity was some papillary infolding On section there were multiple nodules without and scanty colloid. There was no significant cellular cystic change or haemorrhage. Histology showed infiltration of the interstitium. He developed amyloidosis of follicular basement membranes, rapidly worsening cardiac failure and died 3 weeks vessels, connective tissue septa and capsule. after thyroidectomy. Necropsy revealed cardiac failure due to amyloid invasion of the heart as the main cause of death. There was widespread AL amyloid deposition and no evidence of any under- Discussion lying chronic inflammatory disease. The presence of minor amyloid deposits in thyroid Case 2 gland in systemic amyloidosis was first recorded in 1855 by Ven Rekitansky. Greater amyloid invasion This patient was a school secretary and was first of the thyroid, sufficient to produce a clinically seen in 1950 when she was 40 years old. She had had detectable enlargement, was described by Von a goitre since the age of 12 which on examination Beckman in 1858. was multinodular. She was clinically euthyroid. In Amyloid goitre usually manifests clinically as a 1978 she was seen again because of onset of atrial rapidly enlarging cervical swelling with dysphagia, fibrillation. Total T4 was 140 pmol/l (NR 60-150). hoarseness ofvoice and dyspnoea, due to compres- copyright. Total triiodothyronine (T3) was 2.69 nmol/l. (NR sion of local structures. There may be additional 1.23-3.07). Over the years (1978-1982) her total symptoms related to amyloid deposition in other T4 fluctuated between 136 to 190 nmol/l (n = 14, organs. The goitre is firm to hard in consistency mean 162). Free T4 (1982-1984) fluctuated and this together with its rapid growth usually between 17.7 to 26.7 pmol/l (n = 13, mean 21.7, NR suggests malignancy7 and this suspicion may be 8.8-23). T3 was always within normal limits strengthened by the finding of regional lymph- (n = 15), except on one occasion. Thyroid anti- adenopathy5 also due to amyloid invasion. The bodies were a trial of correct is revealed after negative. During therapeutic diagnosis only thyroidec- http://pmj.bmj.com/ carbimazole at a dose of 15 mg/day between July to tomy but in some cases a needle biopsy of the November 1985 she quickly became hypothyroid thyroid has satisfactorily established the diag- with a free T4 down to 6.8 pmol/l. TSH at this stage nosis.8 was 2.4 mU/l (NR 0-5.5). Also at her last visit to Histologically, the thyroid parenchyma is the clinic free T4 was 7.6 pmol/l and TSH 1.3 mU/I. virtually replaced by amyloid, the follicles are A TRH test was carried out in 1981 and TSH distorted, containing scanty colloid and their lining response was basal 5.2 mU/l, 30 minutes 5.1 mU/I, epithelium is flattened.9 The lumen ofblood vessels 60 minutes 4.7 mU/l. This was repeated in 1985 and may be narrowed by infiltration of their wall with on October 1, 2021 by guest. Protected on this occasion TSH levels were basal 0.9 mU/1, 30 amyloid. Massive deposition of amyloid in the minutes 1.2 mU/1, 60 minutes 1.3 mU/l. Basal TSH thyroid may increase its size from five to ten times levels between 1983 to 1986 were between 1.3 to normal, and its weight from 150 to 250 grammes. 3 mU/1. Thyroid stimulating immunoglobulin The heaviest recorded weight being 573 grammes.6 levels were within normal limits. Despite such extensive amyloid infiltration the In May 1987 she complained of malaise and on endocrine function of the gland is remarkably well examination she had generalized oedema but was preserved. In a review of30 cases ofamyloid goitre, clinically euthyroid. Urinalysis showed + + + + Arien & Klein6 found no instance of hypo- proteinuria, full blood count was normal, blood thyroidism. However, they did find two cases of urea 7.9 mmol/l, creatinine 96Lmol/l, 24 hour possible hyperthyroidism, but this was based on an urine protein was 3.6 g. No Bence Jones proteins elevated basal metabolic rate which could instead were noted in the urine. Serum albumin was 17 g/l. be attributed to the underlying chronic Renal biopsy showed features of amyloidosis. inflammatory disease. Jaimet°' claims to have Plasma protein electrophoresis did not show para- described the first case of hypothyroidism in proteinaemia. amyloid goitre and another possible case of 306 CLINICAL REPORTS Postgrad Med J: first published as 10.1136/pgmj.66.774.304 on 1 April 1990. Downloaded from hypothyroidism was described by Danovitch et conversion of T4 to T3 is impaired by the presence al." However, their conclusion hinged on inade- of a non-thyroidal illness.'9 In our patients quate thyroid function tests.
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