Browsing by Author "Lithgow, Kirstie"

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    Severe Thyrotoxicosis Secondary to Povidone-Iodine from Peritoneal Dialysis
    (2017-08-24) Lithgow, Kirstie; Symonds, Christopher
    A 73-year-old male on home peritoneal dialysis (PD) with recent diagnosis of atrial fibrillation presented with fatigue and dyspnea. Hyperthyroidism was diagnosed with TSH ud_less_than 0.01 mIU/L and FT4 > 100 pmol/L. He had no personal or family history of thyroid disease. There had been no exposures to CT contrast, amiodarone, or iodine. Technetium thyroid scan showed diffusely decreased uptake. He was discharged with a presumptive diagnosis of thyroiditis. Three weeks later, he had deteriorated clinically. Possible iodine sources were again reviewed, and it was determined that povidone-iodine solution was used with each PD cycle. Methimazole 25 mg daily was initiated; however, he had difficulty tolerating the medication and continued to clinically deteriorate. He was readmitted to hospital where methimazole was restarted at 20 mg bid with high dose prednisone 25 mg and daily plasma exchange (PLEX) therapy. Biochemical improvement was observed with FT4 dropping to 48.5 pmol/L by day 10, but FT4 rebounded to 67.8 pmol/L after PLEX was discontinued. PLEX was restarted and thyroidectomy was performed. Pathology revealed nodular hyperplasia with no evidence of thyroiditis. Preoperative plasma iodine levels were greater than 5 times the upper limit of normal range. We hypothesize that the patient had underlying autonomous thyroid hormone production exacerbated by exogenous iodine exposure from a previously unreported PD-related source.
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    Utility of serum IGF-1 for diagnosis of growth hormone deficiency following traumatic brain injury and sport-related concussion
    (2018-04-02) Lithgow, Kirstie; Chin, Alex; Debert, Chantel T; Kline, Gregory A
    Abstract Background Growth hormone deficiency (GHD) is a potential consequence of traumatic brain injury (TBI), including sport-related concussion (SRC). GH stimulation testing is required for definitive diagnosis; however, this is resource intensive and can be associated with adverse symptoms or risks. Measurement of serum IGF-1 is more practical and accessible, and pituitary tumour patients with hypopituitarism and low serum IGF-1 have been shown to have a high probability of GHD. We aimed to evaluate IGF-1 measurement for diagnosing GHD in our local TBI population. Methods We conducted a retrospective chart review of patients evaluated for GHD at the TBI clinic and referred for GH stimulation testing with insulin tolerance test (ITT) or glucagon stimulation test (GST) since December 2013. We obtained demographics, TBI severity, IGF-1, data pertaining to pituitary function, and GH stimulation results. IGF-1 values were used to calculate z-scores per age and gender specific reference ranges. Receiver operator curve analysis was performed to evaluate diagnostic threshold of IGF-1 z-score for determining GHD by GST or ITT. Results Sixty four patient charts were reviewed. 48 patients had mild, six had moderate, eight had severe TBI, and two had non-traumatic brain injuries. 47 patients underwent ITT or GST. 27 were confirmed to have GHD (peak hGH < 5 μg/L). IGF-1 level was within the age and gender specific reference range for all patients with confirmed GHD following GH stimulation testing. Only one patient had a baseline IGF-1 level below the age and gender specific reference range; this patient had a normal response to GH stimulation testing. ROC analysis showed IGF-1 z-score AUC f, confirming lack of diagnostic utility. Conclusion Baseline IGF-1 is not a useful predictor of GHD in our local TBI population, and therefore has no value as a screening tool. TBI patients undergoing pituitary evaluation will require a dynamic test of GH reserve.
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    Xanthogranulomatous pyelonephritis presenting as acute pleuritic chest pain: a case report
    (2017-04-12) Chow, Justin; Kabani, Rameez; Lithgow, Kirstie; Sarna, Magdalena A
    Abstract Background Xanthogranulomatous pyelonephritis is a rare and serious manifestation of chronic kidney inflammation that can be life-threatening if not recognized and treated appropriately, often with antibiotics and surgery. Affected patients are most commonly females in their fifth or sixth decade of life with a background of obstructive uropathy, nephrolithiasis, or recurrent urinary tract infections who present with vague nonspecific symptoms. Case presentation A 43-year-old woman of Russian ethnicity with a history of nephrolithiasis presented to our emergency department with new left-sided pleuritic chest pain amid a 6-week history of constitutional symptoms including fevers, night sweats, and 7 kg of weight loss. Workup for acute coronary syndrome and pulmonary embolism in our emergency department was negative. Given that she was clinically unwell, she was admitted to internal medicine to expedite workup for the cause of her symptoms. A broad differential diagnosis for various infectious, inflammatory/autoimmune, and neoplastic processes was considered. Based on classic radiographic and histopathologic findings, she was ultimately diagnosed with xanthogranulomatous pyelonephritis of her left kidney, which was a direct consequence of chronic inflammation. This inflammation exhibited spread to local tissues and across her left hemidiaphragm, resulting in a unilateral pleural effusion which explained her chest discomfort. She was treated with antibiotics administered intravenously and urgent total nephrectomy with a good functional outcome. Conclusions Our case illustrates an uncommon but clinically important do-not-miss diagnosis that underlies a common clinical presentation of pleuritic chest pain. The case underscores the importance of maintaining a broad differential diagnosis and organized approach when treating patients with undifferentiated clinical presentations.