An adrenal incidentaloma can be either a nonfunctioning adrenocortical adenoma or may cause disease, such as adrenocortical carcinoma, pheochromocytoma, hormone-producing adenoma or metastasis. However, less commonly, it can be a manifestation of infection such as tuberculosis. The case is a 40-year-old male who emigrated from China two years ago, referred to the endocrine clinic after he was found to have a 3 cm right adrenal macroadenoma on MRCP after hospitalization for acute cholecystitis. The patient was also found to have positive Quantiferon, but CXR was clear. He was started on isoniazid therapy for latent tuberculosis and was later switched to rifampin postoperatively. One month after hospital discharge, he was evaluated by Endocrinology. Vital signs, including BP were normal with no symptoms of dizziness or orthostatic hypotension. He had no symptoms of adrenal insufficiency or excess. Electrolytes, renal, liver function tests, and CBC were within normal. Albumin was 4.3g/dL(RR 3.4-5). Fasting 8 AM labs: ACTH 9 pg/mL (RR 0-47), cortisol 10.10 ug/dL (RR 5.3-22.5), DHEA S 130 mcg/dL (RR 80-560), plasma metanephrines and normetanephrines and midnight salivary cortisol were normal, aldosterone 10 ng/dL, renin 1.49 ng/mL/h with ARR of 6.7. Adrenal CT w/wo contrast showed right adrenal mass with absolute washout 78% and relative washout 53% consistent with adenoma, as well as bilateral subcentimeter lipid rich adenomas and marked mesenteric lymphadenopathy. Mycobacterium tuberculosis complex spreads to the adrenal glands hematogenously. Clinical manifestations of adrenal insufficiency in tuberculosis may take years to take effect, after 90% of gland destruction occurs. The majority of patients with active or recently acquired disease (<2 years) have bilateral adrenal enlargement, while calcification and atrophy is found with remote infection or inactive disease. The adrenals can be enlarged in patients with pulmonary tuberculosis even without active involvement of the glands solely due to stress and inflammation. The hypothalamic-pituitary-adrenal (HPA) axis can be activated or even under-activated in active pulmonary tuberculosis. Cortisol levels return to baseline after anti-tuberculous treatment. Rarely tuberculosis can cause adrenal incidentaloma. Adrenal biopsy is not necessary for primary adrenal insufficiency with bilateral adrenal enlargement in a patient with proven extra-adrenal tuberculosis. However, about 12% of patients with adrenal tuberculosis have no evidence of active extra-adrenal tuberculosis. Adrenal biopsy was refused but is generally necessary in these patients to prove adrenal involvement by tuberculosis. Our case highlights the fact that tuberculosis should be considered in the differential of adrenal masses. Reference: Fassnacht M, Arlt W, Bancos I, et al. Management of adrenal incidentalomas: European Society of Endocrinology Clinical Practice Guideline in collaboration with the European Network for the Study of Adrenal Tumors. Eur J Endocrinol. 2016 Aug;175(2): G1-G34. doi: 10.1530/EJE-16-0467. PMID: 27390021. Presentation: No date and time listed
Background Hypogonadism in males results when there is either a failure of the testes to produce testosterone, hypothalamic or pituitary dysfunction. Although testosterone supplementation is used for documented hypogonadism, it has become widely abused, with a variety of false claims for promoting energy, virility, and muscular development, as well as enhanced athletic performance. We present a case of surreptitious abuse. Clinical Case A 63-year-old male with coronary artery disease, was initially consulted to endocrinology for evaluation of Graves’ disease with ophthalmopathy. He was treated with methimazole 5 mg daily. However, on subsequent visits, he requested measurement of testosterone levels. Laboratory tests showed FSH<0.2 mIU/ml (0.7-10.8); LH<0.2 mIU/ml; free testosterone 3050 pg/ml (35-155); total testosterone 7377 ng/DL (250-1100); prolactin 9.6 ng/ml; Hgb 14.7 g/dL (13. -17); HCT 45.5% (40-51); TSH 1.94 uIU/ml (0.358-3,74); Free T4 0.74 ng/dL (0.76-1.46); Free T3 2.60 pg/ml (2.82-3.98). When confronted with these values, he admitted that due to interest in building muscle mass and energy, for lifting weights, he was taking hormone and protein supplements ordered from an internet program. These therapies were claimed to enhance muscle mass and energy, increase testosterone and lower estrogen. He did not have blood tests for over 6 months, and it was not clear who monitored this plan. He was taking testosterone 400 mg injections of testosterone cypionate and proprionate twice weekly, as well as another form of oral testosterone, which amounted to more than double the total dose required to treat hypogonadism in 1 week. He was counseled about the risks of taking excess testosterone, for which he had no prior knowledge (including CAD, cardiomyopathy, erythrocytosis, coagulation abnormalities, major mood disorder, gynecomastia, increased risk for prostate cancer), and also that it is unclear whether he even had hypogonadism. He agreed to stop taking these supplements. Four months later, he reported slightly less energy, but he was not exercising due to back pain, and no other changes. Laboratory tests: Total testosterone 572 ng/dL, Free Testosterone 74.6, LH 3. 0 mIU/ml; FSH =3.4 mIu/ml (8-10.8). Discussion and Conclusion Although hyperthyroidism can cause an increase in total testosterone via an increase in hepatic synthesis of SHBG, the free level is normal. Abnormally high testosterone levels in men are most commonly due to anabolic steroids taken to increase muscle mass and enhance athletic performance. It is also important to evaluate for other causes, such as adrenal or testicular tumors. This case is an example of a patient innocently taking unregulated and hazardous hormonal supplements for false claims, which may result in abnormal hormonal laboratory results, and lead to unnecessary and expensive evaluations. Therefore, it is important to take a good medication history, and to query abnormal lab results at each outpatient visit. Presentation: No date and time listed
Hypothyroidism is a well-known cause of pericardial effusion with an incidence of about 3-27%. If not diagnosed in time it can lead to potentially serious complications, such as cardiac tamponade leading to hemodynamic instability. It should be considered as a causative or exacerbating agent in any patient presenting with pericardial effusion and known, suspected or laboratory evidence of hypothyroidism, e. g., elevated TSH or reduced serum free T4. We present a case of a 50-year-old woman with a Past Medical Hx of hypertension, intermittently insulin-treated type 2 diabetes for 20 years, coronary artery disease, and hypothyroidism with medical non-compliance, and s/p right BKA. She initially presented to an outside hospital for altered mental status (specifically, inability to follow simple commands and orientation only to self). She was transferred to this facility for evaluation of limb ischemia. She was agoitrous with no reported palpable thyroid abnormalities. Her admission chest x-ray exhibitedan enlarged cardiac silhouette. Her initial serology was significant for a serum TSH of 178 uIU/mL (NL: 0.45-5.33 uIU/mL), FreeT4 <0.25 ng/dl (NL: 0.58-1.64 ng/dl),Free T3 1.65 pg/mL (NL: 2.5-3.9 pg/mL), andhighly elevated anti-thyroglobulin and anti-peroxidase antibodies. She was diagnosed as having primary hypothyroidism secondary to Hashimoto's thyroiditis. She was re-started on levothyroxine (L-T4) at a dose of 150 mcg on day 1, which was reduced to 100 mcg daily on days 2-4 but readjusted to 125 mcg daily on days 5-8 and 150 mcg daily thereafter. During the 25 th day of admission in the Rehabilitation unither serum TSH showed a gradual decline from 178 to 22 prior to discharge. Her Free T4 increased to 1.18 and her Free T3 increased to 2.24 by discharge. Her pericardial effusion was managed by placement of a pericardial window. Pericardiocentesis yielded over 600 ml of clear serous fluid (protein content 5.1 gm/dl) without evidence of malignancy, infection or inflammation. This case highlights the importance of not only recognizing the diagnosis of hypothyroidism but of assessing the duration and adequacy of its management. Likewise, an enlarged cardiac silhouette in this setting should be considered as possibly representing a pericardial effusion and impending source of a cardiac tamponade. 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
The recently recognized 'long COVID' syndrome, encompasses symptoms of shortness of breath, chest pain, palpitations and orthostatic intolerance which can last for weeks or more following even mild illness. 'Long COVID' is postulated to be related to a virus- or immune-mediated disruption of the autonomic nervous system resulting in orthostatic intolerance syndromes. We report a 32-yr old female nurse who presented to the endocrinology clinic for symptoms of orthostatic hypotension following two COVID 19 infections. She had received 1 dose of Moderna vaccine in February and March of 2021 respectively. She was hospitalized for COVID June and September of 2021. Following the first hospitalization, she developed severe orthostatic hypotension, chest pain, shortness of breath, fatigue, anxiety, memory, concentration and word finding difficulty. Blood pressure ranged from 110/78 to 124/82 while lying and from 85/45 to 103/59 while standing. HR ranged from 88 to 96 while lying and from 130 to 42 while standing. She was started on midodrine 10 mg three times daily which was discontinued due to patient intolerance. She followed a regimen of adequate hydration, adequate salt intake, fall precautions, physical and speech therapy and high protein/low carb diet with frequent snacks, which improved her symptoms of dizziness and orthostasis, but without complete resolution. However, symptoms of anxiety, dizziness, chest pain and palpitations became even worse after the second hospitalization. She was started on Propranolol 20 mg 2-3 times daily depending on symptoms, and she felt better with this intervention. Evaluation for secondary causes of hypotension were all negative [Cortisol of 19 ug/dL (n=5.3-22.5); ACTH 20 pg/mL (n=0-47); TSH 2.36 uIU/mL (n=0.358 -3.74); Free T4 0.97 ng/dL (n=0.76-1.46); B12 480 pg/mL (n=193-986); Hba1c 4.9%; 25 OH Vitamin D 24.3 ng/mL; tryptase 3.7 mcg/L (n= <11); Sed rate 4 mm/HR (n=0-20). CBC, CMP, TPO and Tg abs, troponin levels, iron studies, ANA panel, Rheumatoid factor, anti-CCP abs, myasthenia gravis panel], CT head and MRI brain, EKG and QTc interval. Echocardiogram= small PFO. 'Post-acute COVID' refers to persistent symptoms 3 weeks after COVID-19 infection, while 'Chronic COVID' describes symptoms lasting more than 12 weeks. Symptoms include fatigue, dyspnea, chest pain, palpitations, dizziness, body aches, presyncope and orthostatic intolerance. Individuals may even develop post-traumatic stress disorder, panic attacks and irritable bowel syndrome. Orthostatic intolerance occurs due to release of epinephrine and norepinephrine leading to development of palpitations, breathlessness, and chest pain. It has been well described that orthostatic intolerance is preceded by viral infections and is associated with the development of autoantibodies α-/β-adrenoceptors and muscarinic receptors. COVID 19 itself can affect the autonomic nervous system through the release of a cytokine storm leading to sympathetic activation. It is crucial to consider the diagnosis of orthostatic intolerance syndromes post COVID infection. Presentation: No date and time listed
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