Read this blog to learn what happens when you stop taking amlodipine, including the side effects of stopping, withdrawal, and alternatives.

Learning point for cliniciansPrimary aldosteronism is one of the few potentially curable causes of hypertension and it requires a high index of suspicion i

Low renin hypertension is a subtype of high blood pressure where a person has lower than typical renin levels. Learn more about this condition here.

Learning point for cliniciansPrimary aldosteronism is one of the few potentially curable causes of hypertension and it requires a high index of suspicion i

Patients with primary aldosteronism can lead healthy lives with some lifestyle adjustments to their regular diet and exercise.

Primary aldosteronism, the most common secondary form of hypertension, is thought to be present in ≈5% to 10% of hypertensive adults. However, recent studies indicate that its prevalence may be at least 3-fold higher based on the identification of renin-independent (autonomous) aldosterone production that is not suppressible with dietary sodium loading in a large fraction of adults with primary hypertension. Currently, the screening rate for primary aldosteronism in adults with primary hypertension is <1%. This review summarizes current thinking about primary aldosteronism from the standpoint of 3 key questions: Where are we now? Where to from here? So how do we get there?

Estradiol (E2) plays an underrecognized role in modulating body-wide systems, including important interactions with the renin-angiotensin-aldosterone system (RAAS). The RAAS is an immunomodulating system that is critical for maintaining homeostasis across multiple organ systems. The diverse interactions between E2 and the RAAS help maintain cardiometabolic homeostasis, including successful physiologic responses to trauma and infectious pathogens. Estradiol deficiency (ie, menopause) results in impaired responses and increased susceptibility to infectious pathogens.

Left untreated, hyperkalemia, or high levels of potassium in the blood, can be dangerous. Talk with your doctor if you experience any hyperkalemia symptoms.

Estradiol (E2) plays an underrecognized role in modulating body-wide systems, including important interactions with the renin-angiotensin-aldosterone system (RAAS). The RAAS is an immunomodulating system that is critical for maintaining homeostasis across multiple organ systems. The diverse interactions between E2 and the RAAS help maintain cardiometabolic homeostasis, including successful physiologic responses to trauma and infectious pathogens. Estradiol deficiency (ie, menopause) results in impaired responses and increased susceptibility to infectious pathogens.

One in four patients with resistant hypertension actually have primary aldosteronism, so it is quite reasonable to ask: “Do I have PA?”

Patients with primary aldosteronism can lead healthy lives with some lifestyle adjustments to their regular diet and exercise.

Potassium is an essential mineral. This article describes low potassium symptoms, causes, and possible treatment options.

Thyroid Antibodies testing can help determine if your immune system and thyroid are functioning properly. It’s often used to diagnose Graves’ disease or Hashimoto’s thyroiditis.

Primary aldosteronism (PA) is a disease characterized by high aldosterone levels caused by benign adrenal tumors being the most frequent cause of secondary hypertension. Aldosterone plays vital physiological roles through the mineralocorticoid receptor (MR) but in certain cell types, it can also activate the glucocorticoid (GC) receptor (GR). Both MR and GR are structurally and functionally related and belong to the same family of ligand-dependent transcription factors that recognize identical GC regulatory elements (GREs) on their target genes. GCs play key roles in skin pathophysiology acting through both GR and MR; however, the effects of aldosterone and the potential association of PA and skin disease were not previously addressed. Skin samples from PA revealed histopathological alterations relative to control subjects, featuring epidermal hyperplasia, impaired differentiation, and increased dermal infiltrates, correlating with increased NF-κB signaling and up-regulation of TNF-A and IL-6 cytokines. PA skin samples also showed significantly higher expression of MR, GR, and HSD11B2. In cultured keratinocytes, aldosterone treatment increased GRE transcriptional activity which was significantly inhibited by co-treatment with GR- and MR-antagonists. This study demonstrates that high levels of aldosterone in PA patients correlate with skin anomalies and inflammatory features associated with abnormal GR/MR activation in epidermal keratinocytes.

Primary aldosteronism (PA) is a disease characterized by high aldosterone levels caused by benign adrenal tumors being the most frequent cause of secondary hypertension. Aldosterone plays vital physiological roles through the mineralocorticoid receptor (MR) but in certain cell types, it can also activate the glucocorticoid (GC) receptor (GR). Both MR and GR are structurally and functionally related and belong to the same family of ligand-dependent transcription factors that recognize identical GC regulatory elements (GREs) on their target genes. GCs play key roles in skin pathophysiology acting through both GR and MR; however, the effects of aldosterone and the potential association of PA and skin disease were not previously addressed. Skin samples from PA revealed histopathological alterations relative to control subjects, featuring epidermal hyperplasia, impaired differentiation, and increased dermal infiltrates, correlating with increased NF-κB signaling and up-regulation of TNF-A and IL-6 cytokines. PA skin samples also showed significantly higher expression of MR, GR, and HSD11B2. In cultured keratinocytes, aldosterone treatment increased GRE transcriptional activity which was significantly inhibited by co-treatment with GR- and MR-antagonists. This study demonstrates that high levels of aldosterone in PA patients correlate with skin anomalies and inflammatory features associated with abnormal GR/MR activation in epidermal keratinocytes.

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Point of Care - Clinical decision support for Hyperaldosteronism. Treatment and management. Introduction, Etiology, Epidemiology, Pathophysiology, Histopathology, History and Physical, Evaluation, Treatment / Management, Differential Diagnosis, Surgical Oncology, Prognosis, Complications, Postoperative and Rehabilitation Care, Consultations, Deterrence and Patient Education, Pearls and Other Issues, Enhancing Healthcare Team Outcomes

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Hyperaldosteronism is when one or both of your adrenal glands creates too much aldosterone. This causes your body to lose too much potassium and retain too much sodium, increasing your water retention, blood volume, and blood pressure. Learn about both the primary and secondary types, as well as treatment options.