scholarly journals Exophthalmos and multinodular goitre, an unusual combination

2019 ◽  
Vol 2019 ◽  
Author(s):  
Kingsley Okolie ◽  
Daniel Chen ◽  
Raf Ghabrial ◽  
Robert Schmidli
Keyword(s):  
Thyroid Stimulating Hormone ◽  
Eye Disease ◽  
List Type ◽  
Multinodular Goitre ◽  
Diagnostic Dilemma ◽  
Graves Orbitopathy ◽  
Eye Symptoms ◽  
Possible Cause ◽  
Learning Points ◽  
Rule Out

Summary Multinodular goitre is not associated with eye disease, unless in a rare case of Marine–Lenhart syndrome where it coexists with Grave’s disease. Therefore, other causes of exophthalmos need to be ruled out when the eye disease is seen in a patient with multinodular goitre. Confusion can arise in patients with features suggestive of Graves’ ophthalmopathy in the absence of thyroid-stimulating hormone receptor autoantibodies and no evidence of other causes of exophthalmos. We present a case of multinodular goitre in a patient with exophthalmos which flared up after iodine contrast-based study. A 61-year-old Australian presented with a pre-syncopal attack and was diagnosed with toxic multinodular goitre. At the same time of investigations, to diagnose the possible cause of the pre-syncopal attack, computerised tomographic (CT) coronary artery angiogram was requested by a cardiologist. A few days after the iodine contrast-based imaging test was performed, he developed severe eye symptoms, with signs suggestive of Graves’ orbitopathy. MRI of the orbit revealed features of the disease. Although he had pre-existing eye symptoms, they were not classical of thyroid eye disease. He eventually had orbital decompressive surgery. This case poses a diagnostic dilemma of a possible Graves’ orbitopathy in a patient with multinodular goitre. Learning points: Graves’ orbitopathy can occur in a patient with normal autothyroid antibodies. The absence of the thyroid antibodies does not rule out the disease in all cases. Graves’ orbitopathy can coexist with multinodular goitre. Iodine-based compounds, in any form, can trigger severe symptoms, on the background of Graves’ eye disease.

scholarly journals Acute milk-alkali syndrome

2018 ◽  
Vol 2018 ◽  
Author(s):  
Bidhya Timilsina ◽  
Niranjan Tachamo ◽  
Prem Raj Parajuli ◽  
Ilan Gabriely
Keyword(s):  
Renal Failure ◽  
Metabolic Alkalosis ◽  
List Type ◽  
Over The Counter ◽  
Excess Calcium ◽  
Severe Hypercalcemia ◽  
History Of ◽  
High Index Of Suspicion ◽  
Learning Points ◽  
Rule Out

Summary A 74-year-old woman presented with progressive lethargy, confusion, poor appetite and abdominal pain. She was found to have non-PTH-mediated severe hypercalcemia with renal failure and metabolic alkalosis. Extensive workup for hypercalcemia to rule out alternate etiology was unrevealing. Upon further questioning, she was taking excess calcium carbonate (Tums) for her worsening heartburn. She was diagnosed with milk-alkali syndrome (MAS). Her hypercalcemia and alkalosis recovered completely with aggressive hydration along with improvement in her renal function. High index of suspicion should be maintained and history of drug and supplements, especially calcium ingestion, should be routinely asked in patients presenting with hypercalcemia to timely diagnose MAS and prevent unnecessary tests and treatments. Learning points: Suspect milk-alkali syndrome in patients with hypercalcemia, metabolic alkalosis and renal failure, especially in context of ingestion of excess calcium-containing supplements. Careful history of over-the-counter medications, supplements and diet is crucial to diagnose milk-alkali syndrome. Milk-alkali syndrome may cause severe hypercalcemia in up to 25–30% of cases.

scholarly journals Pseudohyperkalaemia in essential thrombocytosis: an important clinical reminder

2021 ◽  
Vol 2021 ◽  
Author(s):  
Jean Marc Mizzi ◽  
Christopher Rizzo ◽  
Stephen Fava
Keyword(s):  
Venous Blood ◽  
Elevated Serum ◽  
Plasma Potassium ◽  
List Type ◽  
Limb Weakness ◽  
Clinical Reminder ◽  
Bilateral Lower Limb ◽  
Venous Blood Gas ◽  
Learning Points ◽  
Rule Out

Summary An 82-year-old female was admitted to a general hospital due to progressive bilateral lower limb weakness. A T8–T9 extramedullary meningioma was diagnosed by MRI, and the patient was referred for excision of the tumour. During the patient’s admission, she was noted to have persistent hyperkalaemia which was refractory to treatment. Following a review by an endocrinology team, a diagnosis of pseudohyperkalaemia secondary to thrombocytosis was made. This case demonstrates the importance of promptly identifying patients who are susceptible to pseudohyperkalaemia, in order to prevent its potentially serious consequences. Learning points Pseudohyperkalaemia should be considered in patients with unexplained or asymptomatic hyperkalaemia. It should also be considered in those patients who are resistant to the classical treatment of hyperkalaemia. A diagnosis of pseudohyperkalaemia is considered when there is a difference of >0.4 mmol/L of potassium between serum and plasma potassium in the absence of symptoms and ECG changes. In patients who are presenting with consistently elevated serum potassium levels, it may be beneficial to take venous blood gas and/ or plasma potassium levels to rule out pseudohyperkalaemia. Pseudohyperkalaemia may subject patients to iatrogenic hypokalaemia which can be potentially fatal. Pseudohyperkalaemia can occur secondary to thrombocytosis, red cell haemolysis due to improper blood letting techniques, leukaemia and lymphoma.

scholarly journals Targeting TSH and IGF-1 Receptors to Treat Thyroid Eye Disease

2020 ◽  
Vol 9 (Suppl. 1) ◽  
pp. 59-65
Author(s):  
Susanne Neumann ◽  
Christine C. Krieger ◽  
Marvin C. Gershengorn
Keyword(s):  
Thyroid Stimulating Hormone ◽  
Thyroid Eye Disease ◽  
Therapeutic Interventions ◽  
Eye Disease ◽  
Thyroid Cells ◽  
Hormone Synthesis ◽  
Dependent Component ◽  
Graves Orbitopathy ◽  
Blocking Antibodies ◽  
Orbital Fibroblasts

Graves’ disease (GD) is an autoimmune disease caused in part by thyroid-stimulating antibodies (TSAbs) that activate the thyroid-stimulating hormone receptor (TSHR). In Graves’ hyperthyroidism (GH), TSAbs cause persistent stimulation of thyroid cells leading to continuous thyroid hormone synthesis and secretion. Thyroid eye disease (TED), also called Graves’ orbitopathy, is an orbital manifestation of GD. We review the important roles of the TSHR and the insulin-like growth factor 1 receptor (IGF-1R) in the pathogenesis of TED and discuss a model of TSHR/IGF-1R crosstalk that considers two pathways initiated by TSAb activation of TSHR in the eye, an IGF-1R-independent and an IGF-1R-dependent signaling pathway leading to hyaluronan (HA) secretion in orbital fibroblasts. We discuss current and future therapeutic approaches targeting the IGF-1R and TSHR. Teprotumumab, a human monoclonal anti-IGF-1R-blocking antibody, has been approved as an effective treatment in patients with TED. However, as the TSHR seems to be the primary target for TSAbs in patients with GD, future therapeutic interventions directly targeting the TSHR, e.g. blocking antibodies and small molecule antagonists, are being developed and have the advantage to inhibit the IGF-1R-independent as well as the IGF-1R-dependent component of TSAb-induced HA secretion. Antigen-specific immunotherapies using TSHR peptides to reduce serum TSHR antibodies are being developed also. These TSHR-targeted strategies also have the potential to treat both GH and TED with the same drug. We propose that combination therapy targeting TSHR and IGF-1R may be an effective and better tolerated treatment strategy for TED.

scholarly journals Lugol's solution-induced painless thyroiditis

2017 ◽  
Vol 2017 ◽  
Author(s):  
Ji Wei Yang ◽  
Jacques How
Keyword(s):  
Thyroid Stimulating Hormone ◽  
Thyroid Storm ◽  
Graves Disease ◽  
List Type ◽  
Free T4 ◽  
Iodine Excess ◽  
Thyroid Glands ◽  
Painless Thyroiditis ◽  
Learning Points ◽  
Painful Thyroiditis

Summary Lugol’s solution is usually employed for a limited period for thyroidectomy preparation in patients with Graves’ disease and for the control of severe thyrotoxicosis and thyroid storm. We describe a rare case of Lugol’s solution-induced painless thyroiditis. In November 2014, a 59-year-old woman was prescribed Lugol’s solution four drops per day for the alleviation of menopausal symptoms. She was referred to our clinic in June 2015 for fatigue, hair loss, and a 20-lb weight loss without thyroid pain or discomfort. Physical examination revealed a normal thyroid gland. On 7 May 2015, laboratory tests revealed a suppressed thyroid-stimulating hormone (TSH) 0.01 U/L with elevated free T4 3.31 ng/dL (42.54 pmol/L). Repeat testing on 25 May 2015 showed spontaneous normalization of the free thyroid hormone levels with persistently low TSH 0.10 U/L. Following these results, a family physician prescribed methimazole 10 mg PO TID and very soon after, the TSH concentration rose to >100 U/L along with subnormal free T4 and T3 levels. Methimazole was promptly discontinued, namely within 18 days of its initiation. Over the course of the next few months, the patient spontaneously achieved clinical and biochemical euthyroidism. To our knowledge, this is a unique case of painless thyroiditis induced by Lugol’s solution, which has not been reported before. Lugol’s solution is a short-term medication given for the preparation of thyroidectomy in patients with Graves’ disease and for the control of severe thyrotoxicosis. Iodine excess can cause both hyperthyroidism and hypothyroidism. Rarely, Lugol’s solution can cause acute painless thyroiditis. Learning points: Lugol’s solution is used for thyroidectomy preparation in patients with Graves’ disease and for the control of severe thyrotoxicosis and thyroid storm. Iodine excess can cause both hypothyroidism and thyrotoxicosis. Thyroid glands with an underlying pathology are particularly susceptible to the adverse effect of iodine. The prolonged off-label use of Lugol’s solution can be harmful. Rarely, Lugol’s solution can cause acute painful thyroiditis.

Recurring thyroid eye disease: a diagnostic dilemma

2015 ◽  
Author(s):  
Pauline McAleer ◽  
Emma Turtle ◽  
Jan Kerr ◽  
Karen Adamson
Keyword(s):  
Thyroid Eye Disease ◽  
Eye Disease ◽  
Diagnostic Dilemma

Outcome and Safety of Different Cumulative Doses and Protocols of Intravenous Methylprednisolone in Moderate to Severe and Active Graves’ Ophthalmopathy

2019 ◽  
Vol 43 (1) ◽  
pp. 15
Author(s):  
Amelya Permata Sari ◽  
M Sidik ◽  
Syntia Nusanti
Keyword(s):  
Clinical Outcome ◽  
Literature Search ◽  
Oral Route ◽  
Eye Disease ◽  
Aperture Size ◽  
Journal Articles ◽  
Inclusion Criteria ◽  
Intravenous Methylprednisolone ◽  
Graves Ophthalmopathy ◽  
Graves Orbitopathy

Background: Graves’ ophthalmopathy (GO), also known as Graves’ orbitopathy or thyroid eye disease, has a potential sight-threatening complications. The activity and severity are important determinants in GO and are implications for treatment. Intravenous Glucocorticoid (GC) was associated with significantly greater efficacy and was better tolerated than oral route in the treatment of patients with moderate to severe and active GO. Intravenous GC has a variation cumulative dose and protocols; meanwhile the optimal treatment is still undefined. The aim of this literature review was to analyze the outcome and safety of different cumulative doses and protocols of intravenous methylprednisolone of patients with moderate to severe and active GO. Methods: The literature search was conducted from Google Scholar and Pubmed for journal articles that were published and related to the use of IVGC in moderate to severe and active GO Results: From the keywords mentioned, titles were screened for eligibility and seventeen articles were found. After being checked for the duplication, the articles were screened based on the abstracts and/or full texts. As many as eight articles met the inclusion criteria, others were excluded. Conclusion: Intravenous GC therapy in moderate to severe and active GO provide effect in reducing CAS, decreasing lid aperture size, decreasing proptosis size, and disappearing diplopia. A protocol uses a low cumulative doses (<5 g) of methylprednisolone weekly for 6 weeks and then halved dose weekly for another 6 weeks are preferred due to higher response in clinical outcome and safety profile.

scholarly journals Unilateral mydriasis in a child with a ventriculoperitoneal shunt for obstructive hydrocephalus: a diagnostic dilemma

2020 ◽  
Vol 13 (12) ◽  
pp. e237257
Author(s):  
Monidipa Banerjee ◽  
Eiman Haj Ahmed ◽  
Kathryn Foster ◽  
Arundoss Gangadharan
Keyword(s):  
Ipratropium Bromide ◽  
Obstructive Hydrocephalus ◽  
Sudden Onset ◽  
Unique Case ◽  
Diagnostic Dilemma ◽  
Vp Shunt ◽  
Life Threatening ◽  
Unilateral Mydriasis ◽  
The Brain ◽  
Rule Out

There are several causes for sudden onset unilateral mydriasis, however impending transtentorial uncal herniation needs to be ruled out. This unique case highlights an uncommon adverse response to a common mode of treatment that leads to a diagnostic dilemma. A 3-year-old boy with a ventriculoperitoneal (VP) shunt for an obstructive hydrocephalus presented with an acute respiratory distress. He developed unilateral mydriasis with absent light reflex during treatment with nebulisers. An urgent CT scan of the brain did not show any new intracranial abnormality. A case of pharmacological anisocoria was diagnosed that resolved completely within 24 hours of discontinuation of ipratropium bromide. Although ipratropium-induced anisocoria has been reported in children, but to our knowledge none in a child with VP shunt for hydrocephalus. This emphasises the urgency in evaluating unilateral mydriasis to rule out life-threatening conditions. Clinicians should remember that ipratropium administered through ill-fitting face masks could cause this completely reversible adverse effect.

Infants Diagnosed with Athyreosis on Scintigraphy May Have a Gland Present on Ultrasound and Have Transient Congenital Hypothyroidism

2021 ◽  
pp. 1-8
Author(s):  
Niamh McGrath ◽  
Colin Patrick Hawkes ◽  
Stephanie Ryan ◽  
Philip Mayne ◽  
Nuala Murphy
Keyword(s):  
Thyroid Gland ◽  
Congenital Hypothyroidism ◽  
Thyroid Tissue ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Ultrasound ◽  
Free T4 ◽  
Median Serum ◽  
Thyroid Glands ◽  
Rule Out

Scintigraphy using technetium-99m (<sup>99m</sup>Tc) is the gold standard for imaging the thyroid gland in infants with congenital hypothyroidism (CHT) and is the most reliable method of diagnosing an ectopic thyroid gland. One of the limitations of scintigraphy is the possibility that no uptake is detected despite the presence of thyroid tissue, leading to the spurious diagnosis of athyreosis. Thyroid ultrasound is a useful adjunct to detect thyroid tissue in the absence of <sup>99m</sup>Tc uptake. <b><i>Aims:</i></b> We aimed to describe the incidence of sonographically detectable in situ thyroid glands in infants scintigraphically diagnosed with athyreosis using <sup>99m</sup>Tc and to describe the clinical characteristics and natural history in these infants. <b><i>Methods:</i></b> The newborn screening records of all infants diagnosed with CHT between 2007 and 2016 were reviewed. Those diagnosed with CHT and athyreosis confirmed on scintigraphy were invited to attend a thyroid ultrasound. <b><i>Results:</i></b> Of the 488 infants diagnosed with CHT during the study period, 18/73 (24.6%) infants with absent uptake on scintigraphy had thyroid tissue visualised on ultrasound (3 hypoplastic thyroid glands and 15 eutopic glands). The median serum thyroid-stimulating hormone (TSH) concentration at diagnosis was significantly lower than that in infants with confirmed athyreosis (no gland on ultrasound and no uptake on scintigraphy) (74 vs. 270 mU/L), and median free T4 concentration at diagnosis was higher (11.9 vs. 3.9 pmol/L). Six of 10 (60%) infants with no uptake on scintigraphy but a eutopic gland on ultrasound had transient CHT. <b><i>Conclusion:</i></b> Absent uptake on scintigraphy in infants with CHT does not rule out a eutopic gland, especially in infants with less elevated TSH concentrations. Clinically, adding thyroid ultrasound to the diagnostic evaluation of infants who have athyreosis on scintigraphy may avoid committing some infants with presumed athyreosis to lifelong levothyroxine treatment.

scholarly journals Updates on the understanding and management of thyroid eye disease

2021 ◽  
Vol 13 ◽  
pp. 251584142110277
Author(s):  
Clara J. Men ◽  
Andrea L. Kossler ◽  
Sara T. Wester
Keyword(s):  
Autoimmune Diseases ◽  
Immune Modulation ◽  
Complex Disease ◽  
Vision Loss ◽  
Treatment Options ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Eye Disease ◽  
Eye Disease ◽  
Signaling Complex ◽  
Clinical Trial Results

Thyroid eye disease (TED) is a complex disease associated with myriad clinical presentations, including facial disfigurement, vision loss, and decreased quality of life. Traditionally, steroid therapy and/or radiation therapy were commonly used in the treatment of active TED. While these therapies can help reduce inflammation, they often do not have a sustainable, significant long-term effect on disease outcomes, including proptosis and diplopia. Recent advances in our understanding of the pathophysiology of TED have shifted the focus of treatment toward targeted biologic therapies. Biologics have the advantage of precise immune modulation, which can have better safety profiles and greater efficacy compared to traditional approaches. For instance, the insulin-like growth factor-1 receptor (IGF-1R) has been found to be upregulated in TED patients and to colocalize with the thyroid-stimulating hormone receptor (TSHR), forming a signaling complex. Teprotumumab is an antibody targeted against IGF-1R. By inhibiting the IGF-1R/TSHR signaling pathway, teprotumumab may reduce the production of proinflammatory cytokines, hyaluronan secretion, and orbital fibroblast activation in patients with TED. Due to promising phase II and III clinical trial results, teprotumumab has become the first biologic US Food and Drug Administration (FDA)-approved for the treatment of TED. In addition, there are currently ongoing studies looking at the use of antibodies targeting the neonatal Fc receptor (FcRn) in various autoimmune diseases, including TED. FcRn functions to transport immunoglobulin G (IgG) and prevent their lysosomal degradation. By blocking the recycling of IgG, this approach may dampen the body’s immune response, in particular the pathogenic IgG implicated in some autoimmune diseases. Advances in our understanding of the pathophysiology of TED, therefore, are leading to more targeted therapeutic options, and we are entering an exciting new phase in the management of TED. This review will cover recent insights into the understanding of TED pathophysiology and novel treatment options as well as ongoing studies of new potential treatment options for TED.

scholarly journals A case of pituitary apoplexy in pregnancy

2014 ◽  
Vol 2014 ◽  
Author(s):  
Aimee R Hayes ◽  
Anthony J O'Sullivan ◽  
Mark A Davies
Keyword(s):  
Pituitary Apoplexy ◽  
Rare Event ◽  
Visual Disturbance ◽  
List Type ◽  
The Subject ◽  
Magnetic Resonance Imaging Mri ◽  
Evidence Of Impact ◽  
Learning Points ◽  
Visual Abnormalities ◽  
In Pregnancy

Summary Pituitary apoplexy is a rare event in pregnancy. A 41-year-old woman with a known pituitary microadenoma presented with visual disturbance and headache during the second trimester of pregnancy. Magnetic resonance imaging (MRI) demonstrated pituitary apoplexy with chiasmal compression. After treatment with corticosteroid therapy, she underwent transsphenoidal excision of the pituitary adenoma. Visual abnormalities were completely restored and pituitary function preserved. There was no evidence of impact on the foetus. The literature on the subject is reviewed with emphasis on the management of the apoplectic patient with mild and stable neuro-ophthalmological signs. Learning points There are no clear guidelines on the management of pituitary apoplexy in pregnancy. A multidisciplinary approach can minimise morbidity and mortality. Pituitary apoplexy has an unpredictable clinical course and determining which clinical situations warrant early surgery needs to take into consideration the presence and severity of neurological signs and their stability. The management of conscious apoplectic patients with absent or mild and stable neuro-ophthalmological signs is controversial.

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