BACKGROUND: Central diabetes insipidus (CDI) occurs in 20% of cases of traumatic brain injury (TBI). Most cases of post-TBI CDI resolve within 2–5 days. Only 6% of long-term survivors of TBI have evidence of persistent CDI.1 We report a patient with persistent CDI after TBI. Clinical Case: A 27 year old male was referred for polyuria. Three months prior he was in a rollover motor vehicle accident. At that time, CT head revealed frontal and occipital contusions with scattered subarachnoid, subdural, and intraventricular blood. There was no evidence of skull fracture, mass-effect, or midline shift. On hospital day 4, his urine output increased to > 3L/day, with serum sodium of 146 mEq/L (n 135–145) and urine specific gravity of 1.015 (n 1.005–1.030). Repeat head CT revealed bilateral subdural hematomas causing mild mass effect. During the rest of his 2-month hospitalization, he continued to have polyuria with specific gravity as low as 1.005, and occasional hypernatremia, with a peak serum sodium of 149 mEq/L. Serum sodium on discharge was 144 mEq/L. On presentation to our clinic, his family and caretakers reported polydipsia, polyuria and nocturia. He had no history of diabetes mellitus or lithium use. On exam he was tachycardic but normotensive with no signs of dehydration. Neurologic exam was normal except for distractibility and impaired long- and short-term memory. After 3 hours of water deprivation, laboratory testing revealed serum sodium 150 mEq/L, serum osmolality 307 mOsmol/kg (n 270–295), urine osmolality 119 mOsmol/kg (n 300–900), and ADH 3 pmol/L (n </= 14); consistent with CDI. Oral desmopressin led to resolution of polydipsia and polyuria. Evaluation of anterior pituitary function was normal. Six months post TBI, CT head revealed increased left frontal subdural hematoma with effacement of the right lateral ventricle and 1cm left-to-right midline shift. A burr hole procedure was performed but CDI persisted. Conclusion: Animal studies have shown that neurohypophyseal apoptosis occurs by inducing intracranial hypertension lasting 12 hours or more.2 Persistent DI may herald rising intracranial pressure (ICP), as reflected by our patient’s case.1 Clinicians should be aware of the reciprocal association between increased ICP and persistent CDI following TBI. References: (1) Tudor R. M., Thompson C. J. Posterior pituitary dysfunction following traumatic brain injury: review. Pituitary. 2019 Jun; 22(3):296–304. (2) Tan H., et al. Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI. Sci Rep. 2017 Jun; 7(1):3805.
Background Diabetes insipidus (DI) occurs in 1/30,000 pregnancies and can be difficult to recognize due to normal peripartum physiology. The most common etiology is excess production of placental vasopressinase, which degrades maternal anti-diuretic hormone. Although rare, hypothalamic and pituitary disorders must also be considered in pregnant patients presenting with DI. We present the case of a pregnant woman presenting with diabetes insipidus and pituitary apoplexy. Clinical case We were called to see a 33 year old female with polyuria and polydipsia on post-partum day #2. She had presented to the ED at 29.4 weeks of her 5th pregnancy (G5P4) with an unrelenting headache, nausea, and vomiting for 12 hours. She was tachycardic, hypertensive, and had no focal neurologic deficits. Fetal evaluation was reassuring. Admission labs included serum sodium of 147 mEq/L (n 136-145), serum potassium 2.8 mEq/L (n 3.4-4.4), and urine specific gravity of 1.003 (n 1.005-1.030). Glycemic parameters, renal function, and hepatic function were normal. She remained tachycardic despite vigorous IV fluid administration. Overnight into hospital day #3 she began to have uterine contractions with fetal decelerations, and betamethasone was given. It was noted that she had produced 8L of urine over the preceding 24 hours. Serum sodium was 159 mEq/L with urine osmolality of 78 mOsmol/kg (n 300-900). A presumptive diagnosis of gestational DI was made and 2 mcg of subcutaneous DDAVP was given. Shortly thereafter she delivered a healthy infant. Maternal blood loss was minimal. Over the next 12 hours her urine became concentrated and her serum sodium decreased, but by the next morning she re-developed dilute polyuria. At the time of our evaluation, her headache had resolved and she had no focal neurologic deficits. She had no apparent signs of glucocorticoid or thyroxine deficiency but had not begun to lactate. Biochemical evaluation included early morning cortisol of 4.6 ug/dL (n 3.5-18.3), TSH 0.46 uIU/mL (n 0.35-4.94), free T4 0.76 ng/dL (n 0.70-1.48), and prolactin 26.6 ng/mL (n 5.2-26.5). Pituitary MRI showed a mildly enlarged gland with central T1 hyperintensity, consistent with apoplexy. A regimen of hydrocortisone and DDAVP was initiated. Conclusion Pituitary apoplexy is uncommon during pregnancy but is potentially life-threatening for the mother and fetus if it goes unrecognized. The significant physiologic growth of the pituitary during pregnancy may increase the risk of apoplexy. A severe headache is the most common symptom and may be accompanied by signs of pituitary dysfunction. Although diabetes insipidus is more often caused by placental physiology, pituitary apoplexy must also be considered in a pregnant woman who has concurrent neurologic symptoms.
Background Squamous cell carcinoma of the thyroid (SCCT) is a very rare malignant neoplasm of the thyroid with distinct squamous differentiation of tumor cells. Only 84 cases of primary SCCT were diagnosed worldwide up until 2012. The number has now increased to around 200. The incidence of SCCT is less than 1% out of all thyroid malignancies, but it has one of the fastest increasing incidences of cancer worldwide 1 . With no standard consensus to guide the management plan and 3 year survival rate of 43%, primary SCCT is challenging to treat 1 . Here we describe a case of primary SCCT. Case Summary A 65 year old white female with a medical history of longstanding Hashimoto's thyroiditis on Levothyroxine was initially evaluated for left neck enlargement and compressive symptoms. She had no significant risk factors for malignancy. TFTs were normal on Levothyroxine 100 mcg daily. CT neck showed a left thyroid cyst measuring 4.4×7 cm. Biopsy showed cystic material. Left hemithyroidectomy pathology showed moderately differentiated squamous cell carcinoma stage pT3aN0a, 4.5 cm without lymph node involvement. The cells stained positive for p40, Ck5/6, p63 and TTF1, but negative for thyroglobulin and calcitonin. Subsequently, completion thyroidectomy with central lymph node dissection resulted in benign pathology. Postoperative imaging was without evidence of residual neoplasm or pathologic cervical adenopathy. Levothyroxine was continued to maintain a TSH in the normal range. SCCT is not radioiodine avid and is therefore resistant to I-131 treatment. For this reason, the patient was referred to radiation-oncology and completed 6 weeks of XRT. Oncology recommended supportive care due to the aggressive nature of this tumor subtype. Conclusion SCCT is a very rare cancer of the thyroid with a mortality rate of 57% at 3 years. Overall survival rate, although poor, is dependent on the extent of the tumor resection and adjuvant radiotherapy/chemotherapy. Experts predict a 6 month average life expectancy with SCCT. At the time of this abstract, there is no evidence of recurrence or metastasis for our patient. There are no official guidelines on the diagnosis and treatment of SCCT, and more research is needed to better manage this rare cancer. Reference: 1. Primary Squamous Cell Carcinoma of the Thyroid Gland. Mohd-Irman-Shah Ibrahim et al. Iranian Journal of Otorhinolaryngology 2018 Jan; 30(96): 65–68 Presentation: No date and time listed
Background In 2011, Shoenfeld and Agmon-Levin described a distinct clinical entity called the autoimmune/inflammatory syndrome induced by adjuvants (ASIA). Adjuvants are primarily used in vaccines for directing the adaptive immune response. However, adjuvants sometimes trigger undesirable autoimmune effects, especially in genetically predisposed individuals such as those with DRB1 allele mutations. The mRNA vaccine may exert "self-adjuvant" properties through activation of tumor necrosis factor, interferon-alpha and other cytokines secreted by immune cells or cross reactivity of mRNA targeting CoV-2 spike protein with thyroid tissue antigens. With the recent widespread use of SARS-CoV-2 mRNA vaccine, cases of vaccine associated thyroid disorders are becoming more apparent. Case Summary A 45-year-old male with well controlled hypertension and type 2 diabetes mellitus was evaluated for abnormal thyroid function tests with a TSH of 0.078 uIU/mL and Free T4 of 2.17 ng/dl. He reported a history of Hashimoto's chronic thyroiditis. He received the second dose of mRNA COVID-19 vaccine one month prior to presentation. He denied any change in the size of his thyroid gland. He also reported no local neck symptoms, dysphagia, odynophagia or change in voice. A nuclear thyroid uptake and scan showed mildly asymmetric thyroid lobes with markedly decreased 24-hour uptake of 0.7%. Based on his clinical presentation, labs and nuclear imaging he was diagnosed with painless thyroiditis. His thyroid function normalized to a TSH of 0.96uIU/ml and Free T4 of 1.29 ng/dl within 2 months without any intervention. There is a strong possibility that the SARS-CoV-2 vaccine accentuated his underlying Hashimoto's chronic thyroiditis enough to cause this transient episode of painless thyroiditis, particularly considering the close interval between the vaccine and onset of his thyroid abnormalities. Conclusion Autoimmune thyroid abnormalities induced by vaccines have been historically associated with protein vaccines for protection from HPV, HBV, seasonal influenza, etc. The spectrum of these disorders can potentially manifest as a transient side effect or even years later with non-specific findings. The SARS-CoV-2 mRNA vaccine may incite similar immunogenicity though yet unestablished, and physicians should be mindful of this phenomenon. Due to limited data, more rigorous studies are needed to fully understand the underlying pathogenesis of thyroiditis following SARS-CoV-2 vaccine in future. As there have been minimal cases of thyroiditis reported, SARS-CoV-2 vaccine should still be strongly recommended. References Bragazzi NL, Hejly A, Watad A, Adawi M, Amital H, Shoenfeld Y. ASIA syndrome and endocrine autoimmune disorders. Best Pract Res Clin Endocrinol Metab. 2020 Jan;34(1): 101412. doi: 10.1016/j.beem.2020.101412. Epub 2020 Mar 11. PMID: 32265102. Watad A, David P, Brown S, Shoenfeld Y. Autoimmune/Inflammatory Syndrome Induced by Adjuvants and Thyroid Autoimmunity. Front Endocrinol (Lausanne). 2017 Jan 24;7: 150. doi: 10.3389/fendo.2016.00150. PMID: 28167927; PMCID: PMC5256113. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m., Monday, June 13, 2022 1:12 p.m. - 1:17 p.m.
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