Introduction To date, case reports have shown an association between paraganglioma and primary hyperaldosteronism, and primary hyperparathyroidism with primary aldosteronism, but not for all three of the aforementioned endocrinopathies combined. Clinical Case A 54-year-old woman with history of uncontrolled HTN, hypokalemia, DM2, CKD stage III, Takotsubo cardiomyopathy and primary hyperparathyroidism presented to the hospital with back pain. CT scan showed a 4.3 cm necrotic retroperitoneal mass. Due to her labile blood pressure, ranging from 194/102 mmHg to 106/60 mmHg, endocrinology was consulted for evaluation of secondary hypertension. Plasma normetanephrines were 3447 pg/mL (n ≤ 57 pg/mL), 24-hour urine normetanephrines 5954 mcg/24 hours (n 122-676 mcg/24 hours) and 24-hour urine norepinephrines 476 mcg/24 hours (n 15-100 mcg/24 hours). 24-hour urine cortisol and 24-hour urine metanephrines were within normal limits. Plasma aldosterone level and plasma renin activity (PRA) were 19 ng/dL and 0.78 ng/mL/h (n 0.25-5.82 ng/mL/h),. However, the patient was also taking spironolactone and telmisartan which interfered with results, and withdrawal of interfering medications was considered unsafe. 68Ga-DOTATATE PET/CT showed mild uptake in a left para-aortic mass. Genetic testing did not show pathogenic mutations of AP2S1, CASR, MEN1, NF1, RET, SDHA, SDHAF2, SDHB, SDHC, TMEM127 or VHL genes. The patient was started on doxazosin and underwent successful removal of the left retroperitoneal mass consistent with paraganglioma. Six months later, surveillance testing showed normalization of fractionated plasma metanephrines and of 24-hour urine metanephrines. However, due to blood pressure of 152/100 mmHg and K of 2.8 mmol/L (n 3.5-4.7 mmol/L), concern was raised for primary hyperaldosteronism. After potassium repletion, labs showed plasma aldosterone of 37 ng/dL, PRA of 0.2 ng/mL/h (n 0.25-5.82 ng/mL/h) and ARR of 185 with potassium of 4.1 mmol/L (n 3.5-4.7 mmol/L) consistent with primary hyperaldosteronism. MRI of adrenal glands showed a left adrenal gland that was thickened and nodular but without discrete nodules > 1 cm. The patient was referred for adrenal vein sampling. Five years previously, the patient had been diagnosed with primary hyperparathyroidism, with PTH of 188.5 pg/mL (n 14-64 pg/dL), Calcium of 10.6 mg/dL (n 8.5-10.1 mg/dL) and GFR of 39. Pre-operative imaging with MRI neck had shown enlargement of two parathyroid glands. She had undergone two-gland parathyroidectomy with intraoperative PTH decrease of > 50% and normalization of calcium. However two weeks later, her PTH returned to pre-operative levels (with normal 25(OH)D) and continues to remains elevated. This has been attributed to underlying secondary hyperparathyroidism from her chronic kidney disease. Conclusion To our knowledge, this is a unique case of combined paraganglioma, primary hyperaldosteronism and primary hyperparathyroidism, as thorough literature review has not shown such a coexistence in the past. Presentation: No date and time listed
Rhabdomyolysis has an initial oliguric stage characterized by hypocalcemia and a recovery stage characterized by hypercalcemia. The latter can be severe, and cause altered mental status, arrhythmias and even death. Immobilization can also contribute to hypercalcemia, as in this patient with severe rhabdomyolysis with complication of bilateral foot drop and prolonged hypercalcemia after renal function recovered. We present a 19-year-old male with history of sickle cell trait and G6PD deficiency, admitted to ICU for acute renal failure and hemolytic crisis after intense exercise training. Labs were pertinent for: K 6.9 mmol/L(n=3.5-4.7), lactate 34.8 mmol/L(n=0.5-2.2), phosphorus 17.5mg/dL(n=2.5-4.9), CPK 5420U/L(n=39-308), magnesium 5. 0 mg/dL(n=1.7-2.4), calcium 5.3 mg/dL(n=8.5-10.1), albumin 3.1 g/dL(n=3.4-5), ionized calcium 0.86 nmol/L(n=1.13-1.32), Cr 1.9 mg/dL(n=0.67-1.17), AST 15064 U/L(n=10-37), ALT 3687 U/L(n-10-65), myoglobin 240000mcg/L(n=<95). Creatine peaked to 7.9mh/dL. He required 8 weeks of hemodialysis, multiple pRBC transfusions, calcium supplementation, and high dose steroids. Once off hemodialysis, he steadily became hypercalcemic over the span of 40 days (10.1–11.9 mg/dL). Endocrinology was consulted: PTH was 2 pg/mL (n=18.4-80.1); Calcitriol <8pg/ml (n=18-72); 25-OH vit D <4.2 ng/mL (n=30-100). IVFs were started and the cause of hypercalcemia was thought to be calcium release from recovering muscles. Notably, patient had bilateral foot drop from rhabdomyolysis-associated muscle edema and mobility was limited. Due to prolonged hypercalcemia of >30 days. which became worse after IVFs were discontinued (peaked to 12.9 mg/dL corrected calcium), endocrinology was reconsulted: A whole body bone scan showed stress-related bone changes but no pockets of calcium deposit in muscle. C-telopeptide was 1603 pg/mL (n=87-1200). Immobilization-related hypercalcemia was then considered, and IVFs were restarted. As calcium remained <12 after discontinuing IVFs for one week and as patient was participating in frequent physical therapy, it was decided to hold off on bisphosphonate therapy. Rare causes of hypercalcemia were also excluded [IGF-1 240 ng/mL(n=10-548), AM-cortisol 12.92 ug/dL (n=5.3-22.5), ACTH 42 pg/mL (n=0-47), PTHrP 13 pg/mL (n=11-20)]. In rhabdomyolysis, cell death due to various stress insults (eg crush injury, ischemia, infection) causes release of phosphorus contributing to initial hypocalcemia from formation of calcium phosphate deposits. In the recovery phase of AKI, these deposits mobilize from muscle causing hypercalcemia. The average duration of hypercalcemia phase is 10 days. However, in our case the patient had prolonged hypercalcemia of more than one month, which caused concern for immobilization hypercalcemia. A bone scan was helpful in differentiating between the two entities as rhabdomyolysis-related hypercalcemia may have revealed calcium pockets in muscle. The elevated C-telopeptide also reinforced this diagnosis. Presentation: No date and time listed
Background: Prolactinomas are a common cause of hyperprolactinemia. Prolactin (PRL) level higher than 250 mcg/L is associated with a prolactinoma and serum prolactin levels generally correlate with tumor size. It is unusual to find a PRL level that is markedly elevated out of proportion to prolactinoma size. We present the case of a 32-year-old man who was referred to Endocrinology Clinic with fatigue and low testosterone, found to have a PRL level of 1302 mcg/L with a 9 x 8 x 9 mm microprolactinoma. Clinical Case: A 32-year-old man with past medical history of migraines reported fatigue, weight gain, low libido and erectile dysfunction and was referred to Endocrinology Clinic due to PRL elevation. His medications included a multivitamin and chasteberry herbal supplement. Physical exam was unremarkable and no visual field abnormalities were detected. Baseline lab results showed PRL: >1000 mcg/L and 1302 mcg/L after serial dilutions, FSH: 1.8 mIU/mL [0.7- 10.8 mIU/ml], LH:0.9 L [1.2- 10.6 mIU/ml], total testosterone 136 ng/dL [250-1100 ng/dl], free testosterone: 32 [35- 155 pg/ml], with normal cortisol, ACTH, IGF-1, TSH and Free T4 levels. MRI pituitary revealed a 9 mm x 8 mm x 9 mm microadenoma on the right side of the pituitary gland without optic chiasm compression. He was diagnosed with microprolactinoma, with very high PRL level causing secondary hypogonadism. Cabergoline 0.25 mg twice weekly resulted in significant improvement in PRL level. With dose increment to 0.5 mg twice weekly, PRL level improved further along with improvement in symptoms related to hypogonadism. Five months after initiation of treatment, total PRL was 58 ng/mL with monomeric PRL of 41 mcg/L, indicating only trace contribution of macroprolactin to the total PRL level. Review of the Literature: In a retrospective study by Colao et al. (2003), men with hyperprolactinemia due to micro-prolactinoma had average pre-treatment PRL levels of 187.7 mcg/L (SD 51.8 mcg/L) and average pre-treatment diameter of 8.0 mm (SD 1.4 mm). A retrospective study of 1234 patients by Vilar et al. (2008) reported similar findings: microprolactinomas had average baseline PRL of 165.6 mcg/L (SD 255.1 mcg/L) and the highest reported level of PRL due to microprolactinoma was 525 mcg/L. Conclusion: Our case illustrates that assumptions about prolactinoma size should not be made based on laboratory findings alone. References: Melmed S. et al, Diagnosis and Treatment of Hyperprolactinemia: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 96: 273-288, 2011.Colao A. et al. Gender differences in the prevalence, clinical features and response to cabergoline in hyperprolactinemia. European Journal of Endocrinology 148: 325-331.Vilar L. et al. Diagnosis and Management of Hyperprolactinemia: Results of a Brazilian Multicenter Study with 1234 Patients. J Endocrinol Invest 31:436-444.
Background Lithium is a drug used in the management of psychiatric condition such as acute mania and bipolar disorder. Lithium is generally known to decrease thyroid hormone synthesis and release, causing hypothyroidism and thyromegaly. Much less commonly, lithium can cause elevated thyroid function tests; we describe such a case. Clinical Case A 21-year-old man with bipolar disorder and polysubstance abuse, presented with acute mania and was started on Lithium. Baseline TSH was 1.42 [0.358-3.74 µIU/mL], but one week after starting Lithium, TSH was 0.1 uIU/mL [0.358 - 3.74 µIU/mL] with free T4 of 0.95 [0.76-1.46 ng/dL]. Three weeks later, TSH was 0. 01 µIU/mL [0.358 - 3.74 µIU/mL], FT4 1.52 ng/dL [0.76 - 1.46 ng/dL], FT3 6.16 pg/mL [ 2.18 - 3.98 pg/mL], total T3 221 ng/dL [76–181 ng/dL]. Six weeks after starting Lithium, TSH remained suppressed at <0. 005 µIU/mL [0.358 - 3.74 µIU/mL], FT4 1.66 ng/dL [0.76 - 1.46 ng/dL], FT3 6.21 pg/mL [ 2.18 - 3.98 pg/mL]. During this time the patient's only complaint was tremor, with no other symptoms of hyperthyroidism. Physical exam showed mild tachycardia, with no evidence of thyroid eye disease, and the thyroid gland was normal size and nontender. TSI was negative with normal thyroglobulin and iodine levels, negative thyroglobulin and peroxidase antibodies. Lithium was in the therapeutic range. Thyroid US was normal without thyromegaly, normal echogenicity and color flow and without nodules or masses. I-123 thyroid uptake and scan showed low uptake and no nodules. The patient was diagnosed with Lithium-induced silent thyroiditis. He was treated with propranolol 10 mg PO BID for tremors, which was stopped later, due to bradycardia and dizziness. Due to persistent suppression of TSH and elevated FT4 and FT3 eight weeks after initiation of Lithium, this was discontinued, and Depakote was started. Conclusion Prior studies have shown that Lithium-induced thyrotoxicosis occurs in 2.7 cases/per 1000 person-years, with Lithium-associated Graves’ disease in 1.4 cases/1000 person-years, and silent thyroiditis only in 1.3 cases/per 1000 person-years. Although rare, our case highlights the importance of considering silent thyroiditis in patients treated with lithium and hyperthyroidism. References: K. K. Miller and G. H. Daniels, Association between lithium use and thyrotoxicosis caused by silent thyroiditis. Clinical Endocrinology 2001; 55, 501-508Kibirige et al. Spectrum of lithium induced thyroid abnormalities: a current perspective. Thyroid Research 2013; 6: 3 Presentation: No date and time listed
Case 1 74-year-old Caucasian male with dysphagia, s/p laryngeal carcinoma, partial laryngectomy and past radiotherapy, was referred for breast enlargement with some increase over the last few years. He denied tenderness or breast discharge, but reported bilateral testicular atrophy, which he attributed to agent orange red exposure. Although married for 53 years, he did not have biological children. He had decreased libido, and denied testicular trauma, urinary symptoms, or history of infections, opiate, steroids abuse, or OTC herbal supplements. Pituitary MRI for head injury was normal. Physical exam-HT= 180.3 cm; 172 cm arm span, bilateral testicular atrophy. Laboratory findings: [PO4= 3.2mg/dL (2.5-4.9); Calcium=9.2 mg/dl(8.5-10.1);Magnesium =2.1 mg/dl(1.7-2.4); Vit D,25 OH=52.9 ng/mL (30–100); PTH =54.9 pg/ml (18.4-80.1),;FSH =41.7 mIU/mL(0 .7-10.8); LH=27.5 mIU/mL (1.2-10.6);Prolactin=4.5 ng/mL(2.5 -7.4); total Testosterone 81 ng/dL (250–1100); free testosterone 4.5pg/mL (30. 0-135. 0); Sex HBG 63 nmol/L (10–57); Estradiol <11.80 pg/mL(<11-39.8); Tumor marker BHCG <2mIU/mL (<5 mIU/ml; Cortisol, am=15.5 ug/dl (5.3-22.5);PSA=.260 ng/mL (0. 0- 4. 0)]. Karyotype analysis=47, XXY [15]/46, XX[5]. With supernumerary X chromosome, consistent with KS. DXA= osteopenia in AP spine and severe osteoporosis in other areas: femur neck left T-Score of -3.1. Right femur neck T-Score=-3. 0, total left femur T-Score= -2.9, right total femur T-Score of -2.9, left forearm radius 33% T-Score=-2.8. Mammogram: mild bilateral gynecomastia, L>R, Testosterone supplementation and intravenous zoledronic acid therapy were started. Case 2 74-year-old Caucasian male referred for low energy, generalized weakness, decreased libido and gynecomastia, long thin arms/legs and "difficulty building muscle". He was taking OTC "testosterone enhancers" herbals only. He reported no biological children. Physical exam: height 187.3 cm, with sparse body hair, absent facial hair, gynecomastia, small testes. Laboratory: [total testosterone=40 ng/dl; free testosterone=5.2 pg/ml; SHBG=40 nmol/L;LH=16.1 mIU/ml; FSH=31.8 mIU/ml; Prolactin=4.3 ng/ml; BHCG <3 mIU/ml; Estradiol=33.60 pg/m] Karyotype: mosaic KS 47, XXY[16]/46,XY[4] with additional X chromosome in 16/20 metaphase cells. DXA =normal bone density. Clinical symptoms and testosterone levels improved after starting testosterone supplementation. Discussion Hypogonadism is an important cause of male osteoporosis. Testosterone is known to regulate male bone metabolism both indirectly by aromatization to estrogens and directly through the androgen receptor on osteoblasts, promoting periosteal bone formation during puberty and reducing bone resorption during adult life. Early onset testosterone deficiency, as in KS, is an important risk factor for osteoporosis, although it is seen in only 40% of patients. Aromatization of testosterone into estradiol from adiposity, may also contribute to normal BMD in some patients. Therefore, it is important to recognize that osteoporosis is not always present in all Klinefelter's patients, even without testosterone therapy and that various phenotypes may account for discrepant conditions, as in these cases. Presentation: No date and time listed
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