Hypertension and severe hypokalaemia associated with ectopic ACTH production

Ferreira, T.; Silva, Tiago Nunes da; Canário, Dolores; Delerue, Maria Francisca

doi:10.1136/bcr-2017-223406

Cited by 8 publications

(13 citation statements)

References 15 publications

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“…Hypokalemia occurred if there was severe hypercortisolism in both CD and ectopic ACTH patients. 4,9,18,[25][26][27][28] Moreover, the UFF/UFE ratio in patients with hypokalemia was significantly higher than that in adrenal CS patients with normokalemia (P < 0.001), suggesting that 11β-HSD2 deficiency was ACTH independent. 29 Otherwise, we analyzed the incidence of hypokalemia in patients hospitalized in our department with ACTH-independent cortisol-secreting adrenal adenoma and carcinoma.…”

Section: Discussionmentioning

confidence: 92%

Association of hypokalemia with cortisol and ACTH levels in Cushing's disease

Fan

Zhuang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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Hypokalemia is a common feature in patients with Cushing's syndrome (CS). Whether the occurrence of hypokalemia is associated with cortisol and adrenocorticotropic hormone (ACTH) levels is still unclear. Approximately 80% of cases of endogenous CS are due to Cushing's disease (CD). The purpose of this study was to determine the association of hypokalemia with cortisol and ACTH levels in patients with CD. The retrospective study included 195 patients with CD referred to our medical center from January 2011 to December 2017. The results show that 25.64% (50/195) of the patients had hypokalemia. The 24‐h urinary free cortisol (UFC) and plasma cortisol levels were significantly higher in patients with hypokalemia than those with normokalemia (P < 0.05). Plasma ACTH levels were similar between the patients with hypokalemia and normokalemia (P > 0.05). Cortisol levels were negatively correlated with plasma potassium levels (08:00: r = −0.344 (P < 0.01), 00:00: r = −0.435 (P < 0.01); 24‐h UFC: r = −0.281 (P < 0.05)). There was no significant correlation between the plasma ACTH and potassium (08:00: r = −0.093 (P > 0.05), 00:00: r = −0.184 (P > 0.050)). Our current data suggest that cortisol level, instead of ACTH level, is correlated with plasma potassium level. A high cortisol level may be the principal cause of hypokalemia.

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Section: Discussionmentioning

confidence: 92%

Association of hypokalemia with cortisol and ACTH levels in Cushing's disease

Fan

Zhuang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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“…For example, it has been reported that among seven patients, conventional chemotherapy did not reduce plasma ACTH levels in two patients. Although five patients showed a transient reduction of ACTH levels reduced concomitantly with decreased tumour size and a duration of 1.5–3 months to reach normal ACTH levels, there have been no reports regarding adrenal insufficiency during chemotherapy to the best of our knowledge ( 1 , 4 , 5 , 6 , 7 , 8 ).…”

Section: Discussionmentioning

confidence: 90%

“…EAS represents between 5 and 10% of cases of ACTH-dependent Cushing’s syndrome ( 1 ). EAS results from unregulated ACTH expression by NETs, including SCLC, carcinoid, gut NET, and medullary thyroid carcinoma ( 7 , 8 ). Recently, ICIs have been approved for SCLC, and clinical trials of ICIs for NETs have been performed ( 10 ).…”

Section: Discussionmentioning

confidence: 99%

Adrenal insufficiency in immunochemotherapy for small-cell lung cancer with ectopic ACTH syndrome

Nakajima

Niida

Hamada

et al. 2021

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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Summary Ectopic ACTH (adrenocorticotrophic hormone) syndrome (EAS) is rarely associated with small-cell lung cancer (SCLC). Although chemotherapy is initially effective for SCLC, complicated EAS scarcely improves. Recently, immune checkpoint inhibitors have been used to treat SCLC. Atezolizumab plus chemotherapy for SCLC improved progression-free survival compared to conventional chemotherapy. However, little has been reported on the efficacy of the combination therapy for SCLC with EAS. We report a 72-year-old male who presented with 4-week history of leg oedema, proximal myopathy, weight loss, and worsened symptoms of diabetes and hypertension. Laboratory findings revealed hypokalaemia, increased plasma ACTH, and serum cortisol levels. Cortisol levels were not suppressed by the high-dose dexamethasone test. Chest and abdominal CT revealed a right lower lobe tumour with multiple metastases on the hilar lymph nodes, liver, lumbar spine, and bilateral enlarged adrenal glands. The patient was diagnosed with stage 4B SCLC with EAS. Hypercortisolaemia was then treated with metyrapone and atezolizumab plus chemotherapy, which was started for SCLC. After 10 days, the tumour shrank noticeably, and the ACTH level drastically decreased concomitantly with low cortisol levels with symptoms of fever, appetite loss, and general fatigue. Hydrocortisone treatment was initiated, and the symptoms resolved immediately. We describe a case of SCLC with EAS treated with atezolizumab plus chemotherapy, presenting with adrenal insufficiency. Close observation is required for patients with adrenal insufficiency receiving atezolizumab plus chemotherapy because of its stronger effect. Furthermore, advances in cancer therapy and care for endocrine paraneoplastic syndrome needs to be adapted. Learning points The immune checkpoint inhibitor atezolizumab has recently been approved for the treatment of small-cell lung cancer (SCLC). Approximately 1–6% of tumour ectopically produce ACTH and cause ectopic ACTH syndrome (EAS) as an endocrine paraneoplastic syndrome. The use of combined chemotherapy and atezolizumab in the ectopic ACTH syndrome secondary to small-cell lung cancer may cause a precipitous fall in circulating ACTH/cortisol, resulting in symptomatic adrenal insufficiency The advances in cancer therapy and treatment for endocrine paraneoplastic syndrome need to be adapted.

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“…193 The mechanism of paraneoplastic ACTH-induced hypokalemia is through excessive cortisol secretion by the adrenal gland, which produces a significant mineralocorticoid effect and can be treated with a mineralocorticoid receptor antagonist, such as spironolactone or eplerenone. 217,218 Another cancer-related cause of hypokalemia is through production of lysozyme by various leukemias, resulting in tubular injury and failure to reabsorb urinary potassium. 219,220 The mainstay of treatment involves intravenous or oral potassium, an increase in dietary potassium intake, avoidance of medications known to promote potassium loss (such as diuretics), and co-correction of concurrent hypomagnesemia.…”

Section: Hypokalemiamentioning

confidence: 99%

“…The causes of hypokalemia are grouped into cancer‐related or chemotherapy‐related hypokalemia and can be broadly categorized further into 4 categories: 1) inadequate dietary potassium intake (anorexia, nausea, mucositis, surgery, or tumor‐induced dysphagia/odynophagia), 2) increased extrarenal potassium losses (vomiting and diarrhea from chemotherapy use or gastrointestinal neuroendocrine tumors, 3) increased renal losses (diuretic use, Fanconi syndrome from chemotherapy use [cisplatin, ifosfamide, and lenalidomide], hypomagnesemia [cetuximab use or platinum compounds], or from excess ACTH production by tumor cells [squamous cell cancers, thyroid medullary cancer, neuroendocrine tumors]), and 4) redistribution of potassium into cells (high cell‐turnover states, such as with leukemia, certain lymphomas, and the use of hematopoietic growth factors) 193 . The mechanism of paraneoplastic ACTH‐induced hypokalemia is through excessive cortisol secretion by the adrenal gland, which produces a significant mineralocorticoid effect and can be treated with a mineralocorticoid receptor antagonist, such as spironolactone or eplerenone 217,218 . Another cancer‐related cause of hypokalemia is through production of lysozyme by various leukemias, resulting in tubular injury and failure to reabsorb urinary potassium 219,220 …”

Section: Electrolyte Disorders In Patients With Cancermentioning

confidence: 99%

Onconephrology: The intersections between the kidney and cancer

Rosner

Jhaveri

McMahon

et al. 2020

CA A Cancer J Clinicians

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Onconephrology is a new subspecialty of nephrology that recognizes the important intersections of kidney disease with cancer. This intersection takes many forms and includes drug-induced nephrotoxicity, electrolyte disorders, paraneoplastic glomerulonephritis, and the interactions of chronic kidney disease with cancer. Data clearly demonstrate that, when patients with cancer develop acute or chronic kidney disease, outcomes are inferior, and the promise of curative therapeutic regimens is lessened. This highlights the imperative for collaborative care between oncologists and nephrologists in recognizing and treating kidney disease in patients with cancer. In response to this need, specific training programs in onconephrology as well as dedicated onconephrology clinics have appeared. This comprehensive review covers many of the critical topics in onconephrology, with a focus on acute kidney injury, chronic kidney disease, drug-induced nephrotoxicity, kidney disease in stem cell transplantation, and electrolyte disorders in patients with cancer.

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Hypertension and severe hypokalaemia associated with ectopic ACTH production

Cited by 8 publications

References 15 publications

Association of hypokalemia with cortisol and ACTH levels in Cushing's disease

Association of hypokalemia with cortisol and ACTH levels in Cushing's disease

Adrenal insufficiency in immunochemotherapy for small-cell lung cancer with ectopic ACTH syndrome

Onconephrology: The intersections between the kidney and cancer

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