scholarly journals How to Stop a Thyroid Storm When the Liver Is Bad: A Case Report and Literature Review

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A933-A934
Author(s):  
Ahmed Osman Saleh ◽  
Wajiha Gul ◽  
Mohammad Khair Ahmad Ibraheem Hamad ◽  
Emad Naem

Abstract Introduction: Patients with thyroid storm and resistance or contraindications to conventional medications may receive plasmapheresis until they have the definitive therapy. Case Presentation: A 42 years old lady with no past medical history was brought by the EMS with palpitations, shortness of breath, vomiting, and profuse diarrhea. She was found to have an atrial flutter with low blood pressure, received synchronized cardioversion, but unfortunately, she developed ventricular tachycardia, tonic-clonic seizure and went to pulseless electrical activity (PEA). Upon examination, the patient was intubated, heart rate of 200 beats/min, blood pressure of 80/60 on vasopressors. She had exophthalmos and icteric eyes. Neck examination revealed palpable goiter. There was bibasal fine cracked and mild lower limb edema. Laboratory showed FT4 39 (11.6-21.9 pmol/L), FT3 5 (3.7- 6.4 pmol/L), and TSH <0.01 (0.3-4.2 mIU/L). Burch- Wartofsky’s score was 55/140. Her presentation was suggestive of Graves’ disease with thyroid storm. Further labs showed high liver enzymes, high INR, ammonia as well as high creatinine. She was started on IV hydrocortisone and cholestyramine. Thionamides were contraindicated due to liver impairment. Extracorporeal membrane oxygenation (ECMO) was initiated for cardiopulmonary support and continued for 6 days. TSH receptor antibodies result was pending, thus a thyroid uptake scan was done while the patient connected to ECMO to confirm the diagnosis. Thyroid scan showed increased uptake suggestive of grave’s disease despite iodine contrast received for CT scan chest two days back. After 5 sessions of plasmapheresis, FT3 2.8, and FT4 30, Lugol’s iodine started and she underwent total thyroidectomy. She was successfully extubated and thyroxine replacement was started after normalization of thyroid hormones Discussion: The raised liver enzymes (shock liver) were a barrier to thioamides. With the contraindication to antithyroid medications, plasmapheresis was a rapid and safe option before thyroidectomy. The mechanism of plasmapheresis is to eliminate thyroid hormones, TSH-receptor antibodies, and cytokines. The current guidelines lack clear indications, the timing of initiation, and patient selection for plasmapheresis. Conclusion: Plasmapheresis should be considered as a stabilising measure, especially when patients cannot tolerate conventional medications. Plasmapheresis leads to rapid decline in thyroid hormone levels, providing a window to treat definitively with thyroidectomy.

2021 ◽  
Author(s):  
Artur Bossowski ◽  
Karolina Stożek

Hyperthyroidism is the state of excessive synthesis and release of the thyroid hormones by thyrocytes. Graves’ disease is the most common cause of hyperthyroidism in children. The condition may occur at any age but the prevalence increases with age. According to the classical paradigm, coexistence of genetic susceptibility, environment triggers and immunological dysfunction are responsible for its development. Diagnosis of Graves’ disease is based on presence of characteristic clinical symptoms, TSH receptor antibodies and excess of thyroid hormones. The management in pediatric population involves mainly pharmacotherapy (thyrostatics, β-adrenolitics), in resistant cases radical radioiodine I131 therapy or surgical treatment is necessary.


Thyroid ◽  
2007 ◽  
Vol 17 (10) ◽  
pp. 923-938 ◽  
Author(s):  
Bernard Rees Smith ◽  
Jane Sanders ◽  
Jadwiga Furmaniak

1989 ◽  
Vol 120 (1) ◽  
pp. 99-106 ◽  
Author(s):  
B. Y. Cho ◽  
Y. K. Shong ◽  
H. K. Lee ◽  
C.-S. Koh ◽  
H. K. Min

Abstract. We studied the blocking type TSH receptor antibodies in 28 patients with primary myxedema and 21 patients with goitrous Hashimoto's thyroiditis by measuring the ability of their IgGs to inhibit TSH binding to its receptor, and to inhibit TSH-stimulated cAMP increase and [3H] thymidine incorporation in a rat thyroid cell line, FRTL-5. The incidences of TSH binding inhibitor immunoglobulin, thyroid stimulation inhibiting immunoglobulin and thyroid growth inhibiting immunoglobulin in patients with primary myxedema were 54.6, 75 and 65.2%, respectively, against 14.3,0 and 17.7%, respectively, in goitrous Hashimoto's thyroiditis. The antibodies inhibited dose-dependently not only TSH stimulated but also Graves' IgG-stimulated cAMP increase and [3H] thymidine incorporation. The TSH binding inhibitor immunoglobulin activities in patients with primary myxedema were significantly correlated with both the thyroid stimulation inhibiting immunoglobulin (r = 0.665; P<0.01) and the thyroid growth inhibiting immunoglobulin (r = 0.618; P<0.01) activity. Thirteen patients whose TSH binding inhibitor immunoglobulin activities were more than 50% had both strong thyroid stimulation inhibiting immunoglobulin (75.1–100%) and thyroid growth inhibiting immunoglobulin (57.4–100%) activities. These data suggest that the vast majority of patients with primary myxedema have potent blocking type TSH receptor antibodies. These might play a role in primary myxedema causing hypothyroidism and thyroid atrophy through inhibiting TSH-stimulated cAMP generation.


1984 ◽  
Vol 105 (3) ◽  
pp. 330-340 ◽  
Author(s):  
Tjerk W. A. de Bruin ◽  
Daan van der Heide ◽  
Maria C. Krol

Abstract. The effect of the anti-TSH receptor antibodies present in the sera of 8 patients with Graves' disease on the affinity constant (Ka) and the number (R) of TSH receptors in autologous human thyroid plasma membranes was investigated. Kinetic analysis of [125I]bTSH binding to human thyroid plasma membranes in the presence of autologous Graves' and normal gammaglobulins was carried out by means of a computer fitting programme. Analysis of the TSH-TSH receptor interaction in the presence of TSH alone yielded curvilinear Scatchard plots, indicating the existence of two independent classes of binding sites (high affinity Ka: 8.5 ± 4.8 × 108 m−1; low affinity Ka: 5.3 ± 2.7 × 106 m−1). Similarly the Scatchard plot for this interaction in the presence of normal gammaglobulins is also curvilinear. Linear Scatchard plots, indicating the existence of only one class of high affinity TSH binding sites (Ka: 3.5 ± 1.8 × 108 m−1), were obtained for both autologous gammaglobulins and pure IgG from 8 patients with Graves' disease. The number of high affinity TSH binding sites in the presence of Graves' gammaglobulins had increased on the average by a factor 3.76 ± 0.74 (sd) with respect to the number found in the presence of normal gammaglobulins. This marked change in the kinetic behaviour of the TSH binding sites provided evidence that there is a direct interaction between anti-TSH receptor antibodies and autologous TSH receptors. Divalency of Graves' IgG or linkage of Fab fragments by anti-Fab antiserum proved to be necessary to produce this specific change in the kinetic behaviour of TSH binding sites. Graves' IgG monovalent Fab and Fc fragments had no effect. We suggest that the mechanism by which anti-TSH receptor antibodies in Graves' disease mimick the biological action of TSH is the IgG-induced cross-linkage of TSH receptors.


Thyrotropin ◽  
1987 ◽  
pp. 307-314 ◽  
Author(s):  
P. Vitti ◽  
G. F. Fenzi ◽  
L. Chiovato ◽  
C. Marcocci ◽  
A. Pinchera

2009 ◽  
Vol 100 (04/05) ◽  
pp. 73-74 ◽  
Author(s):  
M. Ludgate ◽  
S. Costagliola ◽  
D. Danguy ◽  
J. Perret ◽  
G. Vassart

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