Objective: Posaconazole (PSO) is commonly used in the treatment of invasive fungal infections. PSO-induced primary adrenal insufficiency (PAI) is rare, and we present what we think to be the third case report of its incidence. We want to bring awareness to this rare but significant side effect that can impact management and monitoring of patients on this medication. Methods: After clinical assessment, the patient was evaluated with diagnostic studies including measurements of cortisol, adrenocorticotropic hormone, renin activity, and aldosterone levels. Imaging studies such as abdominal computed tomography were also performed. Results: A 65-year-old man with a history of hemophagocytic lymphohistiocytosis on a dexamethasone taper, complicated with mucormycosis on PSO presented to the emergency department with weakness, fatigue, decreased appetite, orthostatic hypotension, low morning cortisol (0.4 μg/dL), low adrenocorticotropic hormone (3.4 pg/mL), elevated plasma renin (16.7 ng/mL/hour), and low-normal aldosterone (1.7 ng/dL). Abdominal computed tomography imaging revealed bilaterally intact adrenal glands. A diagnosis of PSO-induced PAI was made. Fludrocortisone was initiated in addition to glucocorticoids with improvement of fatigue, appetite, blood pressure, and normalization of sodium and potassium. A month after discontinuing PSO, steroids and fludrocortisone were discontinued with measured morning cortisol of 13 μg/dL and an adrenocorticotropic hormone level of 53.9 pg/mL, both normal. Conclusion: Available data suggest that the adverse effect profile of PSO is more favorable than other triazoles. However, our case is the third report suggesting that PAI may be an underrecognized side effect. Awareness of this complication is particularly important in patients with severe or resistant fungal infections.
Background: Novel immune checkpoint proteins inhibitors, such cytotoxic T-lymphocyte antigen 4 (anti-CTLA-4) like ipilimumab could produce hypophysitis as a side effect with a prevalence between 0 to 10%. There are no guidelines in how to monitor patients receiving similar agents. We present a case that was follow up hormonally and developed hypophysitis. Clinical Case: A 63-year-old male presented in 2015 with severe frontal headache that lasted 4 days with no improvement with Ibuprofen and fatigue 5 days after receiving third dose of ipilimumab for metastatic malignant melanoma. He denied nausea, vomiting, visual symptoms. Magnetic resonance (MRI) demonstrated a diffuse pituitary enlargement. Laboratory results showed decreased hormones like: cortisol (0.5mcg/dl, n:4-22mcg/dl), freeT4 (0.36 ng/dl, n:0.8-1.8ng/dl), TSH (0.36 mIU/L, n:0.40-4.5mIU/L) prolactin (<1ng/ml, n 2-18 ng/ml), free testosterone (33.6 pg/ml, n:35-155pg/ml) and normal IGF-1 (62 ng/ml, n:41-279) consistent with panhypopituitarism in the setting of hypophysitis secondary to ipilimumab. Cortisol and thyroid hormones levels where checked before beginning ipilimumab and after receiving first dose and were within normal limits. After patient received the second dose, patient had an episode of colitis which lasted 10 days, which required prednisone 40 mg for 1 week and then it was tapered for another 2 weeks. At that point cortisol was checked which was normal (9.9 mcg/l n:4-22mcg/dl), however patient was on steroids. Patient received third dose of ipilimumab and then he developed severe headache and was diagnosed with hypophysitis. Patient was started on dexamethasone high doses, which was tapper down and switched to hydrocortisone 20 mg am and 10 at pm and was started on levothyroxine 137 mcg daily. Two months after diagnosis an MRI was repeat which did not show any pituitary enlargement, however patient had persistent panhypopituitarism on laboratory results. Four months after diagnosis was started on testosterone replacement therapy. Last visit was in 2018 patient was without fatigue, he is on hydrocortisone 15mg am, 10mg pm, levothyroxine 175 mcg, and testosterone gel every day. His cortisol is decreased (1 mcg/dl , n:4-22mcg/dl), IGF-1 now is low (37 ng/ml n:41-279), prolactin is decrease (1.3 ng/ml, n 2-18 ng/ml), free T4 normal on replacement (1.1 ng/dl, n:0.8-1.8ng/dl), normal free testosterone on replacement (57.6 pg/ml, n:35-155pg/ml). Conclusion: endocrinopathies are seen up to 10% in patients on CTLA-4 , therefore awareness of more serious deficits like hypophysitis should need to be promptly recognized and follow up is recommended, like we are implementing this approach in our institution.
Thyroid nodules are palpable on up to 7% of asymptomatic patients. Cancer is present in 8% to 16% of those patients with previously identified thyroid nodules. Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer, accounting for approximately 85% of thyroid cancers. Although most appear as solid nodules on ultrasound imaging, a subset of 2.5% to 6% has cystic components. The presence of cystic changes within thyroid nodules decreases the accuracy of fine needle aspiration (FNA) in the diagnosis of thyroid cancer, given the difficulty of obtaining appropriate cellular content. This becomes a diagnostic and therapeutic challenge. We present a case of a 31-year-old female with a 1-month history of palpitations, fatigue, and night sweats, who underwent evaluation, and was diagnosed with subclinical hyperthyroidism. She presented 4 years later with compressive symptoms leading to repeat FNA, showing Bethesda III-atypia of undetermined significance and negative molecular testing. Thyroid lobectomy revealed PTC with cystic changes. This case is a reminder that patients with hyperfunctioning thyroid nodule should have closer follow-up. It poses the diagnostic dilemma of how much is good enough in the evaluation and management of a thyroid nodule. Early detection and action should be the standard of care.
Background: Rhabdomyolysis is a potential life threatening condition defined as injury of the skeletal muscle, which results in the release of intracellular contents into the circulation. This muscle injury is often associated with the development of myoglobinuria, electrolyte abnormalities, and often ARF; it can be caused by diverse mechanisms including drugs and toxins. We present a case of rhabdomyolysis complicated by hypercalcemia and ARF in a patient with a history of polysubstance abuse after using intravenous heroin. Case: A 28 y/o male with h/o polysubstance comes to the ED with c/o fatigue, nausea, vomiting and decreased urine output for about 5 days; patient acknowledged using heroin and afterwards he developed weakness and tenderness in upper and lower extremities. Additionally he admitted cocaine and marijuana abuse. On physical exam vital signs were unremarkable and he had some mild tenderness to palpation mostly of the quadriceps bilaterally. Laboratory data was significant for acute kidney injury (cr 11.33 mg/dl, n: 0.7–1.5 mg/dl) and CPK 171920 u/l (n: 22–269 u/l). He received 2 L of NS in the ED and was started on NS at 100cc/hour. He underwent hemodialysis on day 2; initially he was treated for hypocalcemia with calcium and vitamin D supplementation until day 11 were hypercalcemia (calcium 12.7 mg/dl, n: 8.7–10.3 mg/dl; ionized calcium 1.7 mmol/l, n: 1.12–1.32) was noted; this was associated with concomitant suppression of PTH (5 pg/ml, n: 10–65 pg/ml). He remained asymptomatic from calcium abnormalities during his hospitalization, his urine output recovered progressively, hemodialysis was discontinued on day 13. Upon discharge was recommended to f/u with nephrology. Discussion: Various neurological and neuromuscular complications of heroin abuse have been described; one of these is rhabdomyolysis; its pathophysiology in heroin abuse is thought to be multifactorial; including acidosis, hypoxia, muscle compression and adulterants found in heroin. Narcotics may also have direct cell toxicity and alter membrane transport. Usually upon initial presentation hypocalcemia is one of the most common electrolyte imbalances seen with rhabdomyolysis. The proposed mechanism is precipitation of serum calcium salts in necrotic muscle. This may be followed by hypercalcemia during the diuretic phase of ARF which appears to be a relatively unusual complication associated with the presence of severe muscle damage due to metastatic calcium salts that are liberated from the necrotic muscle and the return to the serum. Conclusion: This case report highlights the importance of recognizing potential electrolyte imbalances in patients with rhabdomyolysis; it appears, that concomitant rhabdomyolysis and ARF are needed for a patient to develop hypercalcemia. Serum calcium should always be routinely measured and the appropriate treatment should be implemented to improve outcomes.
Introduction: CYP3A4 is the principal enzyme of cytochrome P450 and is the primary metabolic step for the degradation of corticosteroids. Cobicistat is a potent CYP3A4 inhibitor, it is used to increase the levels of antiretrovirals in the treatment of HIV. It is currently available as part of a fixed-dose combination, where it is used to enhance the integrase inhibitor elvitegravir. The interaction of CYP3A4 inhibitors and substrates can lead to numerous side effects. We present a case of drug-drug interaction resulting in adrenal insufficiency. Case: A 34 y/o male with PMH HIV and asthma comes to the office for evaluation of low cortisol noticed on an AM serum blood test, at the time of visit reported being evaluated by his HIV specialist for complaints of stretch marks and facial swelling; at the time of our evaluation these symptoms had resolved, but prompted further evaluation and a cortisol level 0.2 ug/dl was found. He was diagnosed with HIV in 2015 and since 2016 had been on HAART therapy with a combination of elvitegravir/cobicistat/emtricitabine/tenofovir (Genvoya); additionally, was recently started on a Breo-Ellipta inhaler which consists of fluticasone and vilanterol. During an initial assessment, the patient complained of fatigue and lightheadedness. He denied weakness, weight loss, nausea or vomiting. It was suspected that the etiology of these findings was due to a drug-drug interaction between cobicistat and the inhaled steroids, as this could be causing adrenal insufficiency secondary to the interference of steroid metabolism. On a follow-up visit, an ACTH stimulation test was scheduled, measures of serum cortisol remained at 0.2 ug/dl confirming the diagnosis. He was prescribed prednisone 5 mg daily. Patient was recommended to suspend his inhaler and follow up with a pulmonologist. After discontinuing inhaled steroids, initial symptoms gradually improved, repeat ACTH stimulation test a month later showed regain of adrenal function. He is currently asymptomatic. Conclusion: This case report highlights the importance of recognizing potential interactions between medications in patients with chronic diseases. Clinicians should continuously consider drug-drug interactions when prescribing enzyme inhibitors; currently, the majority of the literature available focuses on protease inhibitors and less on integrase inhibitors. The management of patients with HIV and asthma requires an interdisciplinary approach to improve outcomes.
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