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Diagnosis and Treatment > Medication

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Yasufumi Seki Departments of Endocrinology and Hypertension, Tokyo, Japan

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Satoshi Morimoto Departments of Endocrinology and Hypertension, Tokyo, Japan

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Naohiro Yoshida Departments of Endocrinology and Hypertension, Tokyo, Japan

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Kanako Bokuda Departments of Endocrinology and Hypertension, Tokyo, Japan

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Nobukazu Sasaki Departments of Endocrinology and Hypertension, Tokyo, Japan

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Midori Yatabe Departments of Endocrinology and Hypertension, Tokyo, Japan

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Junichi Yatabe Departments of Endocrinology and Hypertension, Tokyo, Japan

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Daisuke Watanabe Departments of Endocrinology and Hypertension, Tokyo, Japan

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Satoru Morita Departments of Diagnostic Imaging and Nuclear Medicine, Tokyo, Japan

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Keisuke Hata Departments of Urology, Kidney Center, Tokyo, Japan

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Tomoko Yamamoto Departments of Surgical Pathology, Tokyo Women’s Medical University, Tokyo, Japan

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Yoji Nagashima Departments of Surgical Pathology, Tokyo Women’s Medical University, Tokyo, Japan

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Atsuhiro Ichihara Departments of Endocrinology and Hypertension, Tokyo, Japan

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Summary

Primary aldosteronism (PA) is more common than expected. Aberrant adrenal expression of luteinizing hormone (LH) receptor in patients with PA has been reported; however, its physiological role on the development of PA is still unknown. Herein, we report two unique cases of PA in patients with untreated Klinefelter’s syndrome, characterized as increased serum LH, suggesting a possible contribution of the syndrome to PA development. Case 1 was a 39-year-old man with obesity and hypertension since his 20s. His plasma aldosterone concentration (PAC) and renin activity (PRA) were 220 pg/mL and 0.4 ng/mL/h, respectively. He was diagnosed as having bilateral PA by confirmatory tests and adrenal venous sampling (AVS). Klinefelter’s syndrome was suspected as he showed gynecomastia and small testes, and it was confirmed on the basis of a low serum total testosterone level (57.3 ng/dL), high serum LH level (50.9 mIU/mL), and chromosome analysis. Case 2 was a 28-year-old man who had untreated Klinefelter’s syndrome diagnosed in his childhood and a 2-year history of hypertension and hypokalemia. PAC and PRA were 247 pg/mL and 0.3 ng/mL/h, respectively. He was diagnosed as having a 10 mm-sized aldosterone-producing adenoma (APA) by AVS. In the APA, immunohistochemical analysis showed co-expression of LH receptor and CYP11B2. Our cases of untreated Klinefelter’s syndrome complicated with PA suggest that increased serum LH levels and adipose tissues, caused by primary hypogonadism, could contribute to PA development. The possible complication of PA in hypertensive patients with Klinefelter’s syndrome should be carefully considered.

Learning points:

  • The pathogenesis of primary aldosteronism is still unclear.

  • Expression of luteinizing hormone receptor has been reported in aldosterone-producing adenoma.

  • Serum luteinizing hormone, which is increased in patients with Klinefelter’s syndrome, might contribute to the development of primary aldosteronism.

Taxonomy:
Clinical Overview, Gland/Organ, Adrenal, Topic, Adrenal, Hormone, Aldosterone, Cortisol, FSH, LH, Testosterone, Condition/ Syndrome, Adrenocortical adenoma, Hyperaldosteronism, Hypertension, Hypogonadism, Hypokalaemia, Incidentaloma, Klinefelter syndrome, Patient Demographics, Age, Adult, Gender, Male, Ethnicity, Asian - Japanese, Country of Treatment, Japan, Diagnosis and Treatment, Signs and Symptoms, Gynaecomastia, Hypertension, Hypogonadism, Hypokalaemia, Obesity, Investigation, Adrenal venous sampling, Aldosterone (plasma), Aldosterone to renin ratio, Blood pressure, BMI, Chromosomal analysis, Cortisol (plasma), CT scan, Dexamethasone suppression, FSH, Haematoxylin and eosin staining, Immunohistochemistry, LH, Potassium, Renin plasma activity, Testosterone, Intervention, Laparoscopic adrenalectomy, Medication, Alpha-blockers, Amlodipine, Doxazosin, Eplerenone, Furosemide, Nifedipine, Testosterone enanthate esters, Publication Details, Case Report Type, Insight into disease pathogenesis or mechanism of therapy
DOI:
https://doi.org/10.1530/EDM-19-0126
Volume/Issue:
Volume 2019: Issue 1
Open access
Diana Oliveira Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitario de Coimbra EPE, Coimbra, Portugal

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Mara Ventura Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitario de Coimbra EPE, Coimbra, Portugal

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Miguel Melo Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitario de Coimbra EPE, Coimbra, Portugal

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Sandra Paiva Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitario de Coimbra EPE, Coimbra, Portugal

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Francisco Carrilho Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitario de Coimbra EPE, Coimbra, Portugal

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Summary

Addison’s disease (AD) is the most common endocrine manifestation of antiphospholipid syndrome (APS), but it remains a very rare complication of the syndrome. It is caused by adrenal venous thrombosis and consequent hemorrhagic infarction or by spontaneous (without thrombosis) adrenal hemorrhage, usually occurring after surgery or anticoagulant therapy. We present a clinical case of a 36-year-old female patient with a previous diagnosis of APS. She presented with multiple thrombotic events, including spontaneous abortions. During evaluation by the third episode of abortion, a CT imaging revealed an adrenal hematoma, but the patient was discharged without further investigation. A few weeks later, she presented in the emergency department with manifestations suggestive of adrenal insufficiency. Based on that assumption, she started therapy with glucocorticoids, with significant clinical improvement. After stabilization, additional investigation confirmed AD and excluded other etiologies; she also started mineralocorticoid replacement. This case illustrates a rare complication of APS that, if misdiagnosed, may be life threatening. A high index of suspicion is necessary for its diagnosis, and prompt treatment is crucial to reduce the morbidity and mortality potentially associated.

Learning points:

  • AD is a rare but life-threatening complication of APS.

  • It is important to look for AD in patients with APS and a suggestive clinical scenario.

  • APS must be excluded in patients with primary adrenal insufficiency and adrenal imaging revealing thrombosis/hemorrhage.

  • Glucocorticoid therapy should be promptly initiated when AD is suspected.

  • Mineralocorticoid replacement must be started when there is confirmed aldosterone deficiency.

  • Hypertension is a common feature of APS; in patients with APS and AD, replacement therapy with glucocorticoids and mineralocorticoids may jeopardize hypertension management.

Taxonomy:
Clinical Overview, Gland/Organ, Adrenal, Topic, Adrenal, Hormone, ACTH, Aldosterone, Androgens, Androstenedione, Cortisol, DHEA, Glucocorticoids, Mineralocorticoids, Thyroxine (T4), Condition/ Syndrome, Addison's disease, Adrenal insufficiency, Anti-phospholipid antibody syndrome, Patient Demographics, Age, Adult, Gender, Female, Ethnicity, White, Country of Treatment, Portugal, Diagnosis and Treatment, Signs and Symptoms, Asthenia, Deep vein thrombosis, Haematoma, Hyperkalaemia, Hypertension, Hyponatraemia, Miscarriage, Nausea, Renal failure, Splenomegaly, Thrombocytopenia, Vomiting, Investigation, ACTH, Aldosterone (serum), Androstenedione, Blood pressure, Cortisol (serum), Creatinine (serum), CT scan, DHEA Sulphate, FT4, Potassium, Sodium, Intervention, Dialysis, Medication, Fludrocortisone, Furosemide, Glucocorticoids, Hydrocortisone, Mineralocorticoids, Nifedipine, Pantoprazole, Warfarin, Related Disciplines, General practice, Radiology/Rheumatology, Publication Details, Case Report Type, Unique/unexpected symptoms or presentations of a disease
DOI:
https://doi.org/10.1530/EDM-18-0118
Volume/Issue:
Volume 2018: Issue 1
Open access