Clinical Overview > Hormone > Triiodothyronine (T3)
You are looking at 51 - 59 of 59 items
Search for other papers by Milena S Pandrc in
Google Scholar
PubMed
Search for other papers by Stanko Petrović in
Google Scholar
PubMed
Search for other papers by Vanja Kostovski in
Google Scholar
PubMed
Search for other papers by Marijana Petrović in
Google Scholar
PubMed
Search for other papers by Miloš Zarić in
Google Scholar
PubMed
Summary
Immunoglobulin (Ig)G4-related sclerosing disease (IgG4-RSD) is a new disease entity first proposed with regard to autoimmune pancreatitis. A 67-year-old male patient was examined because of weight loss and an abdominal pain. Based on the clinical characteristics, laboratory parameters and ultrasound features, we identified the diagnosis of the IgG4-related systemic disease (IgG4-RSD), that was confirmed by the histopathological analysis after the biopsy of the head of pancreas. After confirmation, we started with the corticosteroid therapy with a good clinical, biochemical and morphological response. During the previous therapy, the disturbance of glucoregulation appeared, so we had to change the modality of treatment. We decided to add Azathioprine to the therapy in a dose of 150 mg/day. We achieved a stable phase of the disease with IgG 4.37 g/l and IgG4 0.179 g/l, and with no side effects from the therapy.
Learning points
-
There are potential clinical applications of identifying subsets of patients with IgG4 thyroiditis (FVHT and Riedel thyroiditis).
-
A trial of immunosuppressive therapy should be included if a resection is deemed inadvisable.
-
In particular, cases of FVHT that mimic malignancy, tissue and serum IgG4 may provide supportive diagnostic information.
Search for other papers by W C Candy Sze in
Google Scholar
PubMed
Search for other papers by Joe McQuillan in
Google Scholar
PubMed
Search for other papers by P Nicholas Plowman in
Google Scholar
PubMed
Search for other papers by Niall MacDougall in
Google Scholar
PubMed
Search for other papers by Philip Blackburn in
Google Scholar
PubMed
Search for other papers by H Ian Sabin in
Google Scholar
PubMed
Search for other papers by Nadeem Ali in
Google Scholar
PubMed
Search for other papers by William M Drake in
Google Scholar
PubMed
Summary
We report three patients who developed symptoms and signs of ocular neuromyotonia (ONM) 3–6 months after receiving gamma knife radiosurgery (GKS) for functioning pituitary tumours. All three patients were complex, requiring multi-modality therapy and all had received prior external irradiation to the sellar region. Although direct causality cannot be attributed, the timing of the development of the symptoms would suggest that the GKS played a contributory role in the development of this rare problem, which we suggest clinicians should be aware of as a potential complication.
Learning points
-
GKS can cause ONM, presenting as intermittent diplopia.
-
ONM can occur quite rapidly after treatment with GKS.
-
Treatment with carbamazepine is effective and improve patient's quality of life.
Hormones and Cancer Group, Garvan Institute of Medical Research, 384 Victoria Street, Sydney, New South Wales, 2010, Australia
Search for other papers by Sunita M C De Sousa in
Google Scholar
PubMed
Search for other papers by Peter Earls in
Google Scholar
PubMed
Hormones and Cancer Group, Garvan Institute of Medical Research, 384 Victoria Street, Sydney, New South Wales, 2010, Australia
Search for other papers by Ann I McCormack in
Google Scholar
PubMed
Summary
Pituitary hyperplasia (PH) occurs in heterogeneous settings and remains under-recognised. Increased awareness of this condition and its natural history should circumvent unnecessary trans-sphenoidal surgery. We performed an observational case series of patients referred to a single endocrinologist over a 3-year period. Four young women were identified with PH manifesting as diffuse, symmetrical pituitary enlargement near or touching the optic apparatus on MRI. The first woman presented with primary hypothyroidism and likely had thyrotroph hyperplasia given prompt resolution with thyroxine. The second and third women were diagnosed with pathological gonadotroph hyperplasia due to primary gonadal insufficiency, with histopathological confirmation including gonadal-deficiency cells in the third case where surgery could have been avoided. The fourth woman likely had idiopathic PH, though she had concomitant polycystic ovary syndrome which is a debated cause of PH. Patients suspected of PH should undergo comprehensive hormonal, radiological and sometimes ophthalmological evaluation. This is best conducted by a specialised multidisciplinary team with preference for treatment of underlying conditions and close monitoring over surgical intervention.
Learning points
-
Normal pituitary dimensions are influenced by age and gender with the greatest pituitary heights seen in young adults and perimenopausal women.
-
Pituitary enlargement may be seen in the settings of pregnancy, end-organ insufficiency with loss of negative feedback, and excess trophic hormone from the hypothalamus or neuroendocrine tumours.
-
PH may be caused or exacerbated by medications including oestrogen, GNRH analogues and antipsychotics.
-
Management involves identification of cases of idiopathic PH suitable for simple surveillance and reversal of pathological or iatrogenic causes where they exist.
-
Surgery should be avoided in PH as it rarely progresses.
Search for other papers by Christine Yu in
Google Scholar
PubMed
Search for other papers by Inder J Chopra in
Google Scholar
PubMed
Search for other papers by Edward Ha in
Google Scholar
PubMed
Summary
Ipilimumab, a novel therapy for metastatic melanoma, inhibits cytotoxic T-lymphocyte apoptosis, causing both antitumor activity and significant autoimmunity, including autoimmune thyroiditis. Steroids are frequently used in treatment of immune-related adverse events; however, a concern regarding the property of steroids to reduce therapeutic antitumor response exists. This study describes the first reported case of ipilimumab-associated thyroid storm and implicates iopanoic acid as an alternative therapy for immune-mediated adverse effects. An 88-year-old woman with metastatic melanoma presented with fatigue, anorexia, decreased functional status, and intermittent diarrhea for several months, shortly after initiation of ipilimumab – a recombinant human monoclonal antibody to the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4). On arrival, she was febrile, tachycardic, and hypertensive with a wide pulse pressure, yet non-toxic appearing. She had diffuse, non-tender thyromegaly. An electrocardiogram (EKG) revealed supraventricular tachycardia. Blood, urine, and stool cultures were collected, and empiric antibiotics were started. A computed tomography (CT) angiogram of the chest was negative for pulmonary embolism or pneumonia, but confirmed a diffusely enlarged thyroid gland, which prompted thyroid function testing. TSH was decreased at 0.16 μIU/ml (normal 0.3–4.7); free tri-iodothyronine (T3) was markedly elevated at 1031 pg/dl (normal 249–405), as was free thyroxine (T4) at 5.6 ng/dl (normal 0.8–1.6). With iopanoic acid and methimazole therapy, she markedly improved within 48 h, which could be attributed to lowering of serum T3 with iopanoic acid rather than to any effect of the methimazole. Ipilimumab is a cause of overt thyrotoxicosis and its immune-mediated adverse effects can be treated with iopanoic acid, a potent inhibitor of T4-to-T3 conversion.
Learning points
-
While ipilimumab more commonly causes autoimmune thyroiditis, it can also cause thyroid storm and clinicians should include thyroid storm in their differential diagnosis for patients who present with systemic inflammatory response syndrome.
-
Immune-related adverse reactions usually occur after 1–3 months of ipilimumab and baseline thyroid function testing should be completed before initiation with ipilimumab.
-
Conflicting data exist on the use of prednisone for treatment of CTLA4 adverse effects and its attenuation of ipilimumab's antitumor effect. Iopanoic acid may be considered as an alternative therapy in this setting.
Search for other papers by Stephanie Teasdale in
Google Scholar
PubMed
Search for other papers by Fahid Hashem in
Google Scholar
PubMed
Search for other papers by Sarah Olson in
Google Scholar
PubMed
Search for other papers by Benjamin Ong in
Google Scholar
PubMed
School of Medicine, The University of Queensland, Brisbane, Queensland, Australia
Search for other papers by Warrick J Inder in
Google Scholar
PubMed
Summary
A case of recurrent pituitary apoplexy is described in a 72-year-old man who initially presented with haemorrhage in a non-functioning pituitary adenoma. Five years later, he re-presented with a severe pituitary haemorrhage in an enlarging sellar mass invading both cavernous sinuses causing epistaxis and bilateral ocular paresis. Subsequent histology was consistent with a sellar malignant spindle and round cell neoplasm. Multiple pituitary tumours have previously been reported to coexist in the same individual, but to our knowledge this is the only case where two pathologically distinct pituitary neoplasms have sequentially arisen in a single patient. This case is also notable with respect to the progressive ocular paresis, including bilateral abducens nerve palsies, and the presentation with epistaxis.
Learning points
-
Ocular paresis in pituitary apoplexy can result from tumour infiltration of nerves, or by indirect compression via increased intrasellar pressure.
-
Epistaxis is a very rare presentation of a pituitary lesion.
-
Epistaxis more commonly occurs following trans-sphenoidal surgery, and can be delayed.
Search for other papers by Lauren J Baker in
Google Scholar
PubMed
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Search for other papers by Anthony J Gill in
Google Scholar
PubMed
Anatomical Pathology Department, Concord Hospital, Sydney, New South Wales, Australia
Search for other papers by Charles Chan in
Google Scholar
PubMed
Anatomical Pathology Department, Concord Hospital, Sydney, New South Wales, Australia
Search for other papers by Betty P C Lin in
Google Scholar
PubMed
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Search for other papers by Bronwyn A Crawford in
Google Scholar
PubMed
Summary
In 2006, a 58-year-old woman presented with thyrotoxicosis. She had undergone left hemithyroidectomy 14 years before for a benign follicular adenoma. Ultrasound imaging demonstrated bilateral cervical lymphadenopathy with enhanced tracer uptake in the left lateral neck on a Technetium-99m uptake scan. Fine-needle aspiration biopsy of a left lateral neck node was insufficient for a cytological diagnosis; however, thyroglobulin (Tg) washings were strongly positive. The clinical suspicion was of functionally active metastatic thyroid cancer in cervical lymph nodes. A completion thyroidectomy and bilateral cervical lymph node dissection were performed. Histology demonstrated benign multinodularity in the right hemithyroid, with bilateral reactive lymphadenopathy and 24 benign hyperplastic thyroid nodules in the left lateral neck that were classified as parasitic thyroid nodules. As there had been a clinical suspicion of thyroid cancer, and the hyperplastic/parasitic thyroid tissue in the neck was extensive, the patient was given ablative radioactive iodine (3.7 GBq). After 2 years, a diagnostic radioactive iodine scan was clear and the serum Tg was undetectable. The patient has now been followed for 7 years with no evidence of recurrence. Archived tissue from a left lateral neck thyroid nodule has recently been analysed for BRAF V600E mutation, which was negative.
Learning points
-
Thyrotoxicosis due to functional thyroid tissue in the lateral neck is very rare and may be due to metastatic thyroid cancer or benign parasitic thyroid tissue.
-
Parasitic thyroid nodules should be considered as a differential diagnosis of lateral neck thyroid deposits, particularly where there is a history of prior thyroid surgery.
-
Parasitic thyroid nodules may occur as a result of traumatic rupture or implantation from a follicular adenoma at the time of surgery.
-
The use of ablative radioactive iodine may be appropriate, as resection of all parasitic thyroid tissue can prove difficult.
-
BRAF mutational analysis of parasitic thyroid tissue may provide extra reassurance in the exclusion of papillary thyroid carcinoma.
Search for other papers by Gerald J M Tevaarwerk in
Google Scholar
PubMed
Summary
Low triiodothyronine (T3) concentrations in the presence of normal thyroxine (T4) and TSH levels, referred to as the low T3 syndrome (LT3S), are common. LT3S may be caused by starvation, various non-thyroidal illnesses (NTIs) and some medications. Reverse T3 (rT3) concentrations are elevated in the more severely ill, and they characteristically fail to respond to exogenous levothyroxine (l-T4) therapy. The biochemical abnormalities have been explained on the basis of altered peripheral deiodinase activities. Herein, we report on two patients with hypothyroid symptoms who on testing were found to have LT3S. They were atypical clinically in not having LT3S due to any of the usual causes, had no increased rT3 concentrations, and had a normal negative TSH feedback response to l-T4. One (patient 1) had previously been diagnosed with Hashimoto's autoimmune primary hypothyroidism and was on l-T4 therapy. Both had T4 concentrations in the reference range. TSH levels were elevated in patient 1 and in the reference range in patient 2. Starting or increasing l-T4 doses resulted in no clinical improvement and no increase in T3 levels in spite of a marked increase in T4 levels. It is suggested that in the absence of the usual causes, lack of elevated rT3 levels, response to treatment and intact negative TSH feedback these two patients differ from the usual secondary causes of decreases in deiodinase activity. It is speculated that they may represent primary alterations in deiodinase enzymes possibly due to genetic variations in the deiodinase-encoding genes.
Learning points
-
LT3S is commonly found secondary to starvation, NTIs and use of some medications.
-
Low T3 levels are the result of alterations in the activity of deiodinase enzymes.
-
LT3S without the usual causes may represent a primary disturbance in deiodinase activity.
Search for other papers by T Min in
Google Scholar
PubMed
Search for other papers by S Benjamin in
Google Scholar
PubMed
Search for other papers by L Cozma in
Google Scholar
PubMed
Summary
Thyroid storm is a rare but potentially life-threatening complication of hyperthyroidism. Early recognition and prompt treatment are essential. Atrial fibrillation can occur in up to 40% of patients with thyroid storm. Studies have shown that hyperthyroidism increases the risk of thromboembolic events. There is no consensus with regard to the initiation of anticoagulation for atrial fibrillation in severe thyrotoxicosis. Anticoagulation is not routinely initiated if the risk is low on a CHADS2 score; however, this should be considered in patients with thyroid storm or severe thyrotoxicosis with impending storm irrespective of the CHADS2 risk, as it appears to increase the risk of thromboembolic episodes. Herein, we describe a case of thyroid storm complicated by massive pulmonary embolism.
Learning points
-
Diagnosis of thyroid storm is based on clinical findings. Early recognition and prompt treatment could lead to a favourable outcome.
-
Hypercoagulable state is a recognised complication of thyrotoxicosis.
-
Atrial fibrillation is strongly associated with hyperthyroidism and thyroid storm.
-
Anticoagulation should be considered for patients with severe thyrotoxicosis and atrial fibrillation irrespective of the CHADS2 score.
-
Patients with severe thyrotoxicosis and clinical evidence of thrombosis should be immediately anticoagulated until hyperthyroidism is under control.
Search for other papers by Gemma Xifra in
Google Scholar
PubMed
Search for other papers by Silvia Mauri in
Google Scholar
PubMed
Search for other papers by Jordi Gironès in
Google Scholar
PubMed
Search for other papers by José Ignacio Rodríguez Hermosa in
Google Scholar
PubMed
Search for other papers by Josep Oriola in
Google Scholar
PubMed
Search for other papers by Wifredo Ricart in
Google Scholar
PubMed
CIBERobn, pathophysiology of obesity and nutrition, Spain
Search for other papers by José Manuel Fernández-Real in
Google Scholar
PubMed
Summary
Background: Thyroid hormone resistance (RTH) is a rare cause of thyroid dysfunction. High TSH levels, as described in RTH syndrome, are known to be associated with an increased risk of developing thyroid nodules with subsequent growth and malignancy.
Patient findings: In 2006, a 29-year-old Caucasian man presented with a palpable mass in the neck. Increased free thyroxine and triiodothyronine levels were found in the context of unsuppressed TSH levels, despite no signs or symptoms of hyperthyroidism. Ultrasonography revealed a multinodular and enlarged goitre, and fine-needle aspiration cytology revealed suspicious features of malignancy. After excluding pituitary tumour and levothyroxine (l-T4) treatment, the patient was diagnosed with generalized RTH. Screening for all the known mutations in thyroid hormone receptor-β (TR β (THRB)) was negative. Thyroidectomy disclosed five Hürthle adenomas and three hyperplasic nodules. Euthyroidism was achieved after surgery with 6.1 μg/kg per day of l-T4.
Conclusion: RTH may be a risk factor that predisposes to the development of multiple Hürthle cell adenomas. To our knowledge, this is the first case of multiple Hürthle cell adenomas in a patient with RTH.
Learning points
-
High TSH levels, as described in RTH syndrome, are known to be associated with an increased risk of developing thyroid nodules, with subsequent growth and malignancy.
-
The exact role of TR β mutants in thyroid carcinogenesis is still undefined.
-
We report the first case of multiple Hürthle cell adenomas associated with RTH.