No abstract

Introduction Primary aldosteronism (PA) demonstrates an increased risk of atherosclerotic heart disease. A less commonly known fact is that PA is often associated with increased risks of malignancy, especially renal cell carcinoma (RCC) and sleep apnea. We are reporting a 51-year-old male with a long history of untreated PA caused by an adenoma (APA) who developed coronary artery disease (CAD), RCC, and sleep apnea during the course of his illness. Case presentation A 51-year-old male was evaluated in the endocrine clinic for secondary hypertension. Patient developed hypertension and hypokalemia at the age of 39 years and laboratory tests showed plasma renin activity PRA 0.06 ng/mL/hr, aldosterone 6 ng/dL, plasma metanephrines 79 pg/mL (ref 0–145), normetanephrine 22 pg/mL (ref 0-62), a serum cortisol value of 0.8 mcg/dL after 1 mg dexamethasone suppression. Despite using several anti-hypertensive medications, including quinapril, amlodipine, and potassium chloride, both his hypertension and hypokalemia remained poorly controlled. He also was diagnosed with sleep apnea at the age of 44 years, treated with CPAP. Abdominal CT showed normal adrenals and angiomyolipoma involving the right interior pole of the kidney. At the age of 47 years, a diagnosis of Liddle syndrome was considered, and the patient was placed on amiloride. At the age of 48 years, the patient developed chest pain and further diagnostic tests confirmed coronary artery disease, and a stent was placed in the left anterior descending artery. Due to the poor control of hypertension, carvedilol and eplerenone were also added to the regimen. Another abdominal CT done at the age of 50 years showed a left adrenal adenoma 1.2 cm, left kidney lower pole cyst 2.9 cm, and atherosclerotic calcification of aorta. Family history was negative for endocrine diseases. Physical examination: HR 62/min, BP 160/90 mmHg, normal examination of the heart, lungs, and abdomen. No clinical features of Cushing syndrome was observed. Repeat laboratory evaluations showed plasma renin activity < 0.167 ng/ml/hr, plasma aldosterone 111.4 ng/dL, concerning for PA. A follow-up CT of the abdomen confirmed left adrenal adenoma and a 1.8 cm left renal lesion suggestive of RCC. The patient underwent an adrenal venous sampling, which localized the left adrenal adenoma as the cause of PA. The patient underwent left adrenalectomy and left partial nephrectomy and pathology confirmed left adrenal adenoma and RCC. One week after surgery plasma aldosterone was 1.9 ng/dL and his hypertension was controlled with fewer medications and he did not require potassium supplements. Conclusion Our case illustrates that delayed diagnosis of PA (poorly treated PA) may be associated with an increased risk of CAD, malignancy and sleep apnea. Early diagnosis and surgical intervention are recommended for PA, especially caused by an adenoma. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Introduction Periodic paralysis (PP) is a disorder of muscle ion channels. It is clinically manifested by episodes of painless muscle weakness and often precipitated by heavy exercise, fasting, or high-carbohydrate meals. Although first described in 1951, there is limited information for its long term course. We describe long term follow up of 3 cases of PP. Case 1 A 28-year-old male presented to the emergency room for abnormal sensations of lower extremities and inability to move his legs. Symptoms progressed to upper extremities with serum potassium of 1.7 mmol/L. He was treated with potassium chloride and discharged the next day with diagnosis of PP. He reported high intensity exercise precipitating these episodes and milder symptoms two years previously. Patient also had symptoms of hyperthyroidism, confirmed by thyroid functions tests. Physical examination showed normal vitals, small but palpable thyroid, and no neurological deficit. He was treated with methimazole, propranolol and KCl 20meq. Serum potassium normalized in 4 weeks and KCl was stopped. Following 3 months of treatment, patient developed hypothyroidism and was prescribed levothyroxine. Patient is currently euthyroid and able to perform daily activities without episodes of PP for the next 6 years of follow up. Case 2 A 29-year-old male presented with severe exertional muscle weakness for 1.5 years. Symptoms worsened with exercise. He had no family history of any neurologic diseases. Physical examination: normal vitals, thyroid, muscle, and neurologic exam. Laboratory values: normal thyroid function, serum potassium, liver function, and creatine kinase. EMG showed decreased amplitude of the compound muscle action potential (CMAP), with reduced motor unit recruitment or electrical silence. Patient was prescribed propranolol 20mg. Genetic testing revealed CACNA1S mutation consistent with hypokalemic periodic paralysis. He was prescribed eplerenone and acetazolamide. He has displayed no new symptoms from exertion and continues to perform normal daily activities on the current regimen. Case 3 A 72-year-old male presented with episodes of flaccid paralysis that lasted several minutes. Patient reported each episode started about an hour after eating dinner. During one episode serum potassium was 3.2 mmol/L and his symptoms slowly resolved after receiving potassium. His medical history was notable for hyperlipidemia, hypertension and pre-diabetes. Vital signs revealed stage-1 hypertension. Physical examination during the episode was notable for weakness greater in the proximal muscles and hyporeflexia. Laboratory values with TSH 2.03 mcIU/mL and follow-up potassium level 4.3 mmol/L. He continues to perform normal daily activities without any PP symptoms for the next 9 years following the initial episode. Conclusion Limited information is available regarding the long-term follow up of patients diagnosed with PP. Our 3 patients illustrate a relatively benign long-term course with appropriate treatment. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Incited by the tempestuous political histories that engender the repressive conditions of the country’s social reality, South African artists often conspire toward activism. For Cameron Platter, who lives in the urbanized province of KwaZulu-Natal near the former battlefield of Rorkes Drift, mining the country’s past has vitalized his historical imagination. Platter’s “expanded collage” reflects the explanatory narrative of the country’s industrial economy and it’s capitalistic dimensions of desire and consumption, and therefore a deviant contemporaneity: large-scale linocuts, mural paintings, and public installations co-opt the linguistic forms and pictorial metaphors of poster-strewn urban sidewalks. Deriving from the noble visions of John Muafangejo’s politically charged linocuts, Platter’s satirical drawings make textual references to familiar street advertisements bearing straplines and slogans promising services from reincarnation to sexual longevity. These universally resonant signs indexing the unity of cross-cultural depravity open a transcendental void and thus exist as chronicles of apparently self-destructive times in which mass consumption serves to palliate a darker reality.