Introduction Calcium is a mineral that is required for nearly every cell in the human body to operate properly. Calcium homeostasis is mediated by active vitamin D (calcitriol) and parathyroid hormone (PTH) on calcium absorption in the GI tract, calcium excretion in the kidney, and osteoclast/osteoblast activity in the skeleton. Under normal settings, PTH promotes bone production and resorption by increasing the number of osteoblasts and, as a result, indirectly increasing the number of osteoclasts. Hypocalcemia, a decrease in extracellular calcium defined as serum total calcium < 8.5 mg/dl corrected for serum albumin. Hypocalcemia is caused by a lack of vitamin D (which can lead to secondary hyperparathyroidism), abnormal phosphate or magnesium levels, and partial or complete hypoparathyroidism. Hypocalcemia was found to be present in 1.6% of cases of cancer. We present a patient with prostate cancer and severe hypocalcemia, predominantly due to extensive osteoblastic metastases. Clinical case: A 42 y/o Male with prostate cancer metastases to bone and lymph Nodes developed severe hypocalcemia and hypophosphatemia during the course of treatment. Patient was treated aggressively with per oral (PO) and intravenous (IV) calcium and phosphorous supplementation with no significant improvement in the values. Vitals were stable except for a heart rate of 101 beats per minute. The physical exam was normal. Labs: Calcium-5.1 mg/dl(8.5-10.1), Ionized calcium-0.74 mmol/L(1.2-1.38), Albumin-4.2gm/dl(3.4-5. 0),Phosphorous - 0.6 mg/dl(2.5-4.9), Alkaline phosphatase- 1.573 units/l(45-117), Magnesium-1.8mg/dl(1.7-2.4), Vitamin D25 OH-17ng/ml(30-100), PTH-281 pg/ml(18.4-88), Ferritin-725ng/ml(30-300), TSH- 1.45 ulU/ml(0.36-3.74). Imaging: CT scan chest/abdomen/pelvis showed metastatic disease throughout sternum, lumbar spine, pelvis, and proximal femur. MRI thoracic spine showed extensive metastatic disease throughout the thoracic spine. The patient was diagnosed with hypocalcemia in the setting of metastatic prostate cancer due to avid calcium uptake by bone metastasis. The patient was treated with radiation therapy, high dose Vitamin D every week, calcitriol, phosphorous, and labs were closely monitored every month. His labs showed normalized calcium, phosphorous, alkaline phosphatase, and Vitamin D level after eleven months, and his symptoms improved. This improvement was paralleled by a significant improvement in PSA concentrations while on androgen deprivation therapy and chemotherapy for Prostate cancer. Conclusion Hypocalcemia in cancer patients is a rare event. However, it can be life-threatening, so it is essential to rule out other causes by measuring magnesium, creatinine, phosphate, vitamin D, and PTH levels to determine the treatment. Hypocalcemia can occur at any time during therapy, it is most frequently reported within six months of treatment initiation. For patients with a substantial burden in bone (=>three bone lesions), prophylactic calcium and vitamin D are associated with fewer hypocalcemia adverse effects. Patients should be informed about the risk of hypocalcemia and the significance of supplement adherence, serum calcium levels should be checked to assess adherence with close follow-up. Presentation: No date and time listed
Background: Pheochromocytoma is a rare catecholamine secreting neuroendocrine tumor. It arises from the chromaffin cells of adrenal medulla. It is diagnosed in 5–6.5% of adrenal incidentalomas which is not common. The usual clinical presentation includes the classic triad of sweating, headache and tachycardia. However, asymptomatic cases are seen in 8% of the patients with pheochromocytoma. We present a clinically asymptomatic patient diagnosed during work up of adrenal incidentaloma. The possible etiology for silent presentation includes one of the following:(i) Presence of a smaller functional tissue (ii)Accelerated turnover of the tumor causing release of the unmetabolized catecholamines in small amounts (iii) Pulsatile tumor secretion (iv)Tumors triggered by stress (v) Laboratory errors due to inappropriate handling of specimen at high-temperature (vi) False negative test results secondary to caffeine ingestion in the prior 24 hours. Clinical Case: 59 years old Caucasian female with past medical history of type 2 diabetes mellitus, obesity, essential hypertension, nonischemic cardiomyopathy, and asthma presented to the emergency room with complaints of worsening shortness of breath and pedal edema for 1 month. Physical exam: Blood pressure 146/78 mm of Hg and heart rate 82 beats/min, mild pedal edema, no pulmonary crackles. On imaging, CT angio chest showed irregularly enhancing right adrenal mass measuring 3.4 cm. This adrenal incidentaloma was not visualized on imaging done 5 years ago. Further, MRI abdomen revealed 4.1 cm right adrenal mass. Laboratory testing showed high total plasma metanephrines: 890 pg/ml (< or = 205), 24-hour urine metanephrines: 2337 (140–785), A1C: 10%. This confirmed the diagnosis of adrenal pheochromocytoma. Preoperatively, she was started on phenoxybenzamine 10 mg BID and encouraged on liberal salt intake. During the course, her blood pressure and heart rate were monitored daily. She underwent right adrenalectomy. Surgical pathology revealed 4.1 cm pheochromocytoma, negative margins with extension to the adipose tissues and vascular invasion, PASS score = 4. Post operatively, patient declined to get labs done. Due to high risk behavior of the tumor, patient needs to be monitored annually for lifelong. Conclusion: Pheochromocytoma is an uncommon tumor with varied clinical presentation. It can manifest itself widely from being silent to aggressive disease. This warrants high suspicion, early detection and management, thereby reducing the morbidity and mortality. Lately, there has been increased incidence of adrenal incidentalomas owing to widespread use of radiological investigations. We report a case of incidental pheochromocytoma which is biochemically active but clinically asymptomatic. This emphasizes the importance of being more vigilant during the evaluation of adrenal incidentalomas.
Background: Acromegaly is a rare clinical syndrome caused by excessive production of growth hormone. The incidence rate is 3 to 4 cases per million people per year. It is a sporadic disease seen in middle-aged adults. Anterior pituitary adenoma secreting the growth hormone (GH) is the most common etiology. Other rare causes include hypothalamic and neuroendocrine tumors. Treatment modalities include surgical, radiotherapeutic and pharmacological with a goal to reduce or remove the tumor, prevent recurrences, and improve comorbidities. The persistent hypersecretion of GH and insulin-like growth factor-1 (IGF-1) leads to an overgrowth in many tissues, including connective tissue, cartilage, bone, skin, and visceral organs. Cardiovascular disease is one of the critical systemic complications resulting in about 60% of the deaths. The cardiovascular manifestations include hypertension, cardiomyopathy (CMP), congestive heart failure, and arrhythmias. Our patient presented with congestive heart failure and dilated CMP in the setting of undiagnosed Acromegaly. Clinical Case: 45 -year old Caucasian lady presented with complaints of worsening shortness of breath, chest tightness, and palpitations for one month. Past medical history includes hypertension, type 2 diabetes mellitus, obesity, and hyperlipidemia. She was diagnosed with dilated CMP in her early 30s, AICD placement seven years ago and normal cardiac catheterization three years ago. On physical exam, she was found to have an enlarged nose and bibasilar crackles. Vitals were stable and proBNP: 4,699 (1-150 pg/ml). ECHO revealed EF of 30-35%, severely dilated left ventricle. Cardiac catheterization showed severely decreased left ventricular systolic dysfunction and elevated LVEDP. Further workup - GH: 16 (<10 ng/ml) and IGF-1: 637 (62 - 205 ng/ml), A1C 13.2%. Pituitary MRI showed a 1.6 cm macroadenoma, extending to the right cavernous sinus border with a deviation of the pituitary stalk to the left. On neurosurgical evaluation, she was considered to be a poor surgical candidate due to her underlying CMP. Currently, she is in the process of getting started on oral octreotide treatment. Conclusion: Cardiovascular disease is the most captious complication and a leading cause of mortality in Acromegaly patients. The subtle clinical presentation results in a diagnostic delay for 5-10 years. A careful review of history and physical examination is vital to identify acromegalic features in non-ischemic DCM. Early diagnosis with prompt treatment has shown improvement in cardiac function and reduced mortality. This case underscores the importance of considering Acromegaly as one of the differentials in patients with dilated cardiomyopathy.
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