Global Longitudinal Strain Reduction With Apical Sparing in Cushing Syndrome-Related Heart Failure With Preserved Ejection Fraction (HFpEF): A Case Report

Posted on December 5, 2025 by MaryO

Abstract

We describe a case of a 56-year-old woman with a history of recurrent pituitary adenoma, not well followed, and known comorbidities of coronary artery disease, hypertension, and type 2 diabetes mellitus. She arrived with severely high blood pressure and signs pointing to hypercortisolism. Further evaluation revealed left ventricular hypertrophy, reduced global longitudinal strain, and preserved left ventricular ejection fraction, consistent with heart failure with preserved ejection fraction (HFpEF). Workup for amyloidosis was negative. This case highlights that chronic hypercortisolism may cause pathophysiological changes in the heart, leading to HFpEF, and may induce myocardial fibrosis and impaired myocardial mechanics, producing an echocardiographic pattern that can mimic infiltrative cardiomyopathy. Recognition of this overlap is crucial to avoid misdiagnosis and to ensure timely endocrine and cardiovascular management.

Introduction

Hypercortisolism is defined as a clinical condition resulting from excessive tissue exposure to cortisol or other glucocorticoids. Sustained exposure ultimately leads to Cushing syndrome (CS), a well-established constellation of clinical manifestations arising from chronic endogenous or exogenous cortisol excess [1]. CS is associated with profound metabolic derangements that significantly increase cardiovascular risk, not only during the active phase of the disease but also persisting long after biochemical remission [2,3]. Cardiovascular complications, including premature atherosclerosis, coronary artery disease (CAD), heart failure, and cerebrovascular events, are major contributors to the excess mortality observed in CS compared with the general population [1,3]. Among these complications, arterial hypertension remains the most frequent cardiovascular disorder in patients with Cushing disease (CD) [4].

Although left ventricular (LV) systolic function is generally preserved in patients with CS, several studies have demonstrated that chronic cortisol excess induces structural and functional cardiac alterations, predisposing to major adverse cardiac events and the development of heart failure [5] In the broader context of chronic congestive heart failure, disease progression is tightly coupled with activation of neuroendocrine stress pathways, most notably the hypothalamic-pituitary-adrenal axis, which governs cortisol secretion [6]. Cortisol, a pivotal stress hormone, increases in response to physiological strain, and its sustained elevation contributes to adverse myocardial remodeling.

Heart failure with preserved ejection fraction (HFpEF), a chronic and progressive syndrome, exemplifies the deleterious effects of persistent myocardial stress. While overt heart failure is an uncommon complication of CS, when it does occur, it most often presents with preserved LV ejection fraction (LVEF) or with subclinical LV dysfunction [7]. Prior evidence has also linked CS to LV hypertrophy, diastolic dysfunction, and subtle systolic impairment, with many of these changes demonstrating reversibility upon normalization of cortisol levels [8].

This case is unique as it highlights the interplay between CS and cardiac amyloidosis, emphasizing their overlapping yet distinct echocardiographic features. Global longitudinal strain (GLS), a measure of myocardial deformation, is particularly useful for differentiating these conditions and reveals subtle differences in strain patterns between the two.

Case Presentation

A 56-year-old woman with a significant past medical history of recurrent pituitary macroadenoma, treated with two prior surgical resections, the most recent five years earlier without subsequent follow-up, CAD, long-standing hypertension, and type 2 diabetes mellitus, presented to the emergency department with hypertensive urgency.

On arrival, she presented with a hypertensive crisis, with blood pressure measured at 200/110 mmHg, associated with severe cephalalgia, without syncope, visual changes, or focal neurological deficits. An MRI Brain demonstrated no evidence of acute intracranial hemorrhage or mass effect (Video 1). Initial laboratory testing showed normal complete blood count, renal function, and serum electrolytes. On physical examination, she exhibited characteristic Cushingoid stigmata, including rounded moon facies, central adiposity, and bilateral lower-extremity pitting edema.

She was commenced on intensive antihypertensive therapy, including spironolactone, clonidine, telmisartan, carvedilol, amlodipine, and intravenous furosemide (20 mg, subsequently escalated to 40 mg). Given her clinical appearance and history of pituitary disease, an endocrine evaluation was undertaken. An overnight dexamethasone suppression test revealed an unsuppressed morning cortisol of 360 nmol/L, consistent with hypercortisolism.

Cardiac assessment supported a diagnosis of HFpEF. Transthoracic echocardiography demonstrated preserved left ventricular ejection fraction (60%), impaired GLS (-10%), and mild concentric left ventricular hypertrophy (Figure 1; Video 2).

Transthoracic-echocardiography-demonstrating-reduced-global-longitudinal-strain-(-10%)-consistent-with-preserved-EF-(60%)
Figure 1: Transthoracic echocardiography demonstrating reduced global longitudinal strain (-10%) consistent with preserved EF (60%)

EF: Ejection Fraction

Workup for alternative causes of HFpEF, including renal impairment and infiltrative cardiomyopathy, was unremarkable; both serum and urine protein electrophoresis with immunofixation excluded amyloidosis.

Magnetic resonance imaging of the pituitary revealed recurrence of the macroadenoma. The patient was referred to neurosurgery for consideration of repeat resection, and glucocorticoid-sparing medical therapy was initiated. During hospitalization, her blood pressure was gradually stabilized, diuretic therapy improved signs of congestion, and her functional status returned to near baseline with restored mobility (Video 3).

Discussion

Epidemiology and clinical significance

CD is a severe endocrine disorder characterized by chronic exposure to excess glucocorticoids. Patients with CD have a two- to fivefold higher mortality compared with the general population, predominantly due to cardiovascular complications [4]. Chronic hypercortisolism is associated with systemic hypertension, left ventricular hypertrophy (LVH), diastolic dysfunction, and accelerated atherosclerosis, increasing the risk of myocardial ischemia and heart failure. While these cardiovascular manifestations are common, the development of isolated dilated cardiomyopathy (DCM) in the absence of other major comorbidities is rare but clinically noteworthy [9].

Pathophysiology of cardiac involvement

Chronic glucocorticoid excess contributes to cardiovascular remodeling via multiple mechanisms. Persistent hypertension and metabolic disturbances promote LVH and diastolic dysfunction. Additionally, glucocorticoid excess induces endothelial dysfunction, insulin resistance, and myocardial fibrosis, impairing ventricular compliance and predisposing to HFpEF [1,6]. Advanced echocardiographic techniques, such as GLS, can detect subclinical systolic dysfunction before overt reductions in LVEF [6]. In our patient, preserved LVEF (60%) coupled with markedly reduced GLS (-10%) and concentric LVH was consistent with HFpEF secondary to chronic cortisol excess, further supported by clinical signs of volume overload such as edema and severe hypertension [7].

Apical sparing and mimicking amyloidosis

An important observation in this case was relative apical sparing despite markedly reduced GLS, a strain pattern classically associated with cardiac amyloidosis [10]. Although infiltrative disease was excluded (negative serum and urine protein electrophoresis with immunofixation), this overlap illustrates how hypercortisolism-induced remodeling can phenocopy amyloidosis on imaging. Recent work has shown that hypercortisolism, beyond metabolic derangements, impairs myocardial mechanics and contractile efficiency [11]. Thus, patients with atypical strain findings should undergo careful endocrine evaluation to avoid misdiagnosis. Ultimately, the recognition that hypercortisolism may produce amyloid-like echocardiographic signatures has both diagnostic and management implications. It broadens the differential diagnosis of HFpEF and stresses the need for a multidisciplinary approach involving endocrinology and cardiology to prevent misdiagnosis and ensure tailored therapy.

Dilated cardiomyopathy in CS

Although uncommon, DCM with severe LV systolic dysfunction has been described in CS. Frustaci et al. reported eight cases of hypercortisolism due to adrenal adenoma among 473 patients with DCM (1.7%), all presenting with LVEF <30% and symptomatic heart failure. Endomyocardial biopsy revealed cardiomyocyte hypertrophy, interstitial fibrosis, and myofibrillolysis, distinct from idiopathic DCM and valvular disease controls. Follow-up biopsies in three patients one year post-adrenalectomy demonstrated substantial regression of these changes, highlighting the reversibility of glucocorticoid-induced myocardial injury [12].

Although not assessed in our patient, prior studies have implicated atrogin-1 in CS-related myocardial remodeling. At the molecular level, upregulation of atrogin-1, an E3 ubiquitin ligase expressed in skeletal, smooth, and cardiac muscle, was observed in CS-associated DCM compared with idiopathic DCM and controls [13]. Atrogin-1, implicated in skeletal muscle atrophy and sarcopenia, facilitates proteasomal degradation of intracellular proteins. Its overexpression in cardiomyocytes contributes to glucocorticoid-mediated myocardial remodeling. Importantly, atrogin-1 expression declined significantly following surgical correction of cortisol excess, paralleling improvements in cardiac structure and function. This reversibility mirrors recovery seen in glucocorticoid-induced skeletal myopathy and underscores the unique potential for cardiac recovery in CS-related DCM [9].

Clinical implications and differential diagnosis

This case underscores the multisystem burden of endogenous hypercortisolism, with particular cardiovascular susceptibility [1,6]. Chronic cortisol excess should be considered in the differential diagnosis of HFpEF, particularly when conventional risk factors coexist with systemic features such as central obesity, moon facies, and proximal myopathy [8]. Secondary causes of HFpEF, including cardiac amyloidosis, were excluded, supporting hypercortisolism as the primary etiology. Recognizing CS as a reversible contributor to myocardial dysfunction has important clinical implications, as timely endocrine intervention can improve cardiac function, lower blood pressure, and potentially prevent progression to irreversible myocardial remodeling.

Left ventricular hypertrophy and structural remodeling

Electrocardiographic and echocardiographic studies have characterized the cardiac phenotype in patients with CS. In a cohort of 12 consecutive patients, most had concomitant hypertension (11/12) and diabetes mellitus (7/12). Preoperative ECGs commonly demonstrated high-voltage QRS complexes (10 patients) and T-wave inversions (7 patients), indicative of LV strain. Echocardiography revealed LVH in nine patients, all exhibiting asymmetric septal hypertrophy. Interventricular septal thickness ranged from 16 to 32 mm, with septal-to-posterior wall ratios from 1.33 to 2.67. Compared with essential hypertension or primary aldosteronism, CS patients exhibited more pronounced LVH and a higher prevalence of asymmetric septal hypertrophy, suggesting a unique glucocorticoid-mediated remodeling pattern [13].

Postoperative follow-up in nine patients demonstrated normalization of ECG abnormalities, decreased septal thickness, and resolution of asymmetric septal hypertrophy in all but one patient, highlighting the partial reversibility of LVH following correction of hypercortisolism. The pronounced septal thickening relative to the posterior wall implies that excessive cortisol exposure, beyond hemodynamic effects of hypertension, contributes significantly to myocardial remodeling [13].

Impact of disease duration on concentric remodeling

Fallo et al. evaluated 18 patients with CS compared with 18 matched controls, adjusting for sex, age, body size, blood pressure, and duration of hypertension. Eleven participants in each group were hypertensive. Echocardiography revealed elevated relative wall thickness (RWT >0.45) in 11 patients with CS (five normotensive, six hypertensive) versus two hypertensive controls. Left ventricular mass index was abnormal in three CS patients and in four hypertensive controls, while systolic function was preserved in all participants [14].

No correlation was observed between RWT and either blood pressure or urinary cortisol levels in patients with CS. Instead, RWT correlated significantly with disease duration, indicating that prolonged exposure to glucocorticoid excess, rather than hormone levels or hemodynamic load, is the primary determinant of concentric LV remodeling. Postoperative echocardiography showed normalization of RWT in five of six patients previously affected, reinforcing the concept of reversible myocardial structural changes following correction of hypercortisolism [14].

Conclusions

CS represents a rare but clinically important etiology of heart failure with preserved ejection fraction and, less commonly, dilated cardiomyopathy. Chronic hypercortisolism promotes systemic hypertension, LVH, diastolic dysfunction, myocardial fibrosis, and remodeling that may mimic infiltrative cardiomyopathies such as amyloidosis on echocardiography. GLS with apical sparing, although typically associated with amyloidosis, may also occur in cortisol-induced cardiomyopathy. Advanced imaging, including GLS, can detect subclinical myocardial impairment before overt systolic dysfunction develops. Notably, cardiac structural and functional abnormalities may partially or completely reverse following normalization of cortisol levels, highlighting the importance of early recognition and timely endocrine intervention. Clinicians should maintain a high index of suspicion for hypercortisolism in patients presenting with unexplained LVH, HFpEF, or atypical DCM, particularly when systemic features of CS are present. Future studies are needed to better characterize strain patterns in endocrine cardiomyopathies and to refine imaging-based algorithms for early detection.

References

  1. Uwaifo GI, Hura DE: Hypercortisolism. StatPearls [Internet]. StatPearls Publishing, Treasure Island (FL); 2024.
  2. De Leo M, Pivonello R, Auriemma RS, et al.: Cardiovascular disease in Cushing’s syndrome: heart versus vasculature. Neuroendocrinology. 2010, 92 Suppl 1:50-4. 10.1159/000318566
  3. Graversen D, Vestergaard P, Stochholm K, Gravholt CH, Jørgensen JO: Mortality in Cushing’s syndrome: a systematic review and meta-analysis. Eur J Intern Med. 2012, 23:278-82. 10.1016/j.ejim.2011.10.013
  4. Uzie Bło-Życzkowska B, Krzesinński P, Witek P, Zielinński G, Jurek A, Gielerak G, Skrobowski A: Cushing’s disease: subclinical left ventricular systolic and diastolic dysfunction revealed by speckle tracking echocardiography and tissue Doppler imaging. Front Endocrinol (Lausanne). 2017, 8:222. 10.3389/fendo.2017.00222
  5. Brosolo G, Catena C, Da Porto A, Bulfone L, Vacca A, Verheyen ND, Sechi LA: Differences in regulation of cortisol secretion contribute to left ventricular abnormalities in patients with essential hypertension. Hypertension. 2022, 79:1435-44. 10.1161/HYPERTENSIONAHA.122.19472
  6. Gladden JD, Linke WA, Redfield MM: Heart failure with preserved ejection fraction. Pflugers Arch. 2014, 466:1037-53. 10.1007/s00424-014-1480-8
  7. Owan TE, Redfield MM: Epidemiology of diastolic heart failure. Prog Cardiovasc Dis. 2005, 47:320-32. 10.1016/j.pcad.2005.02.010
  8. Pereira AM, Delgado V, Romijn JA, Smit JW, Bax JJ, Feelders RA: Cardiac dysfunction is reversed upon successful treatment of Cushing’s syndrome. Eur J Endocrinol. 2010, 162:331-40. 10.1530/EJE-09-0621
  9. Gill A, Dean N, Al-Agha R: Cushing’s, dilated cardiomyopathy and stroke: case report and literature review. Can J Gen Intern Med. 2016, 11:46-9.
  10. Klein AL, Oh J, Miller FA, Seward JB, Tajik AJ: Two-dimensional and Doppler echocardiographic assessment of infiltrative cardiomyopathy. J Am Soc Echocardiogr. 1988, 1:48-59. 10.1016/s0894-7317(88)80063-4
  11. Sahiti F, Detomas M, Cejka V, et al.: The impact of hypercortisolism beyond metabolic syndrome on left ventricular performance: a myocardial work analysis. Cardiovasc Diabetol. 2025, 24:132. 10.1186/s12933-025-02680-1
  12. Frustaci A, Letizia C, Verardo R, Grande C, Calvieri C, Russo MA, Chimenti C: Atrogin-1 pathway activation in Cushing syndrome cardiomyopathy. J Am Coll Cardiol. 2016, 67:116-7. 10.1016/j.jacc.2015.10.040
  13. Sugihara N, Shimizu M, Kita Y, et al.: Cardiac characteristics and postoperative courses in Cushing’s syndrome. Am J Cardiol. 1992, 1:1475-80.
  14. Fallo F, Budano S, Sonino N, Muiesan ML, Agabiti-Rosei E, Boscaro M: Left ventricular structural characteristics in Cushing’s syndrome. J Hum Hypertens. 1994, 8:509-13.

From https://www.cureus.com/articles/413845-global-longitudinal-strain-reduction-with-apical-sparing-in-cushing-syndrome-related-heart-failure-with-preserved-ejection-fraction-hfpef-a-case-report?score_article=true#!/

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Graphic Era Hospital’s Milestone Treatment of Two Complex Cases

Posted on August 26, 2025 by MaryO
DEHRADUN, 23 August: Graphic Era Hospital has achieved a remarkable mileston by successfully treating two complex cases of the rare hormonal disorder Cushing’s Disease in Dehradun. The hospital’s experts used advanced technology and surgical skills to give the patients a new lease on life, marking this significant achievement.
In the first case, a 27-year-old woman was brought to the Endocrinology Department at Graphic Era Hospital after long-term weight gain, facial puffiness, irregular menstrual cycles, high blood pressure, and kidney stones. Tests and lab reports confirmed that the patient was suffering from ACTH-dependent Cushing’s Syndrome – Pituitary Microadenoma. A 3-Tesla Dynamic Pituitary MRI revealed a 6 mm tumor, while other organs were normal.
The specialists performed surgery using endoscopic trans-nasal neuro-navigation technology, completing it successfully without opening the brain. After the operation, the patient experienced significant weight loss, normalized blood pressure, regular menstrual cycles, and all hormone levels returned to normal.
In the second case, a 24-year-old woman came to Graphic Era Hospital with extremely high blood pressure (200/100), headache, weight gain, and irregular menstrual cycles. MRI revealed a 7–9 mm tumor in an unusual location in the pituitary gland, which was also affecting the pituitary fossa bone. Despite multiple medications, her blood pressure remained uncontrolled, and CT scans showed an impact on her heart.
The multi-specialty team performed surgery using endoscopic trans-nasal neuro-navigation technology, again without opening the brain. After surgery, her blood pressure normalized and her menstrual cycles became regular.
In both cases, pituitary microadenomas were diagnosed. The surgeries were done through the nasal route using microscopes and endoscopes, with neuro-navigation helping to accurately locate the tumors while protecting the pituitary gland. The multi-specialty team included Head of Neurosciences and HOD Neurosurgery Partha P Bishnu, Senior Consultant Neurosurgery Ankur Kapoor, Senior Neurosurgeon and Neurointervention Specialist Payoz Pandey, Senior Consultant ENT Parvendra Singh, Director Endocrinology, Obesity and Diabetes Sunil Kumar Mishra, and the Neuro-Anesthesia Team.
With the latest technology and expert doctors at Graphic Era Institute of Medical Sciences, new milestones continue to be achieved. Previously, the hospital’s expert doctors had successfully implanted pacemakers in the brain, placed a third pacemaker in complex pediatric cases, replaced two heart valves without open-heart surgery, unblocked the esophagus without surgery, and performed open-heart surgery through a small 2.5-inch facial incision without cutting bones. Director of Graphic Era Hospital, Puneet Tyagi,  Mefical Superintendent, Gurdeep Singh Jheetay, Dean SL Jethani and COO Atul Bahl were present at the press conference.

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Connecting Canine and Human Health to Fight Cushing’s Disease

Posted on May 5, 2025 by MaryO

Cushing’s Disease is common in dogs but rare and hard to diagnose in people. That’s why University of Georgia researchers are leveraging canine treatments to find new solutions to battle the condition in humans. This collaboration between veterinary medicine and human health care is just one example of how UGA uses a Precision One Health approach to find and tailor new medical treatments for people and animals.

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Imagine your body as a well-run newsroom. Each day, the editor-in-chief—in this case, the pituitary gland—provides assignments, keeping everything running smoothly. One day, however, the editor’s role is usurped by a rogue reporter who declares breaking news nonstop, flooding the newsroom with bulletins and sending everyone into overdrive.

This is a bit like Cushing’s Disease. The rogue reporter is a tiny, usually benign tumor, the stress bulletins cortisol. The newsroom—your body—responds with metabolic fluctuations, burnt out muscles, emotional distress, and more. Over the long haul, Cushing’s Disease can cause lasting deterioration of the body: osteoporosis, muscle weakness, high blood pressure and heart disease, diabetes, memory and mood issues, fatigue, and more.

It’s a common disease and easier to detect in canines. In people, however, it is rare and difficult to diagnose. University of Georgia researchers are leveraging canine treatments to find new solutions to battle the condition in humans.

This collaboration between veterinary medicine and human health is just one example of how UGA uses a Precision One Health approach to find and tailor new medical treatments for people and animals.

From https://research.uga.edu/news/connecting-canine-human-health-to-fight-cushings-disease/

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7 Things Your Hair Reveals About Your Health

Posted on January 20, 2022 by MaryO

Your hair can tell you and your doctor if you are stressed, have a nutritional deficiency, thyroid problem, or other health issues. Here are seven key things to look for in your hair.

You probably think about your hair every day: worrying about a bad day, enjoying a good blow-dry, or wondering if you have to try the new style you noticed in your favorite celebrity. But you may be missing the clues your hair reveals about your health. Research shows that changes in the look, texture, or thickness of your hair can be signs of underlying health issues. Here’s how to tell if your hair changes are due to a health condition, genetics, stress, or a nutritional deficiency.

1 Stress (and genes) can cause you to turn gray

Anyone who has observed the hairstyle changes of a President of the Republic from one campaign to another has noticed that stress seems to cause hair to turn white. A mouse study published in the journal Nature suggests that chronic stress may actually contribute to white hair by causing DNA damage and reducing the number of pigment-producing cells in hair follicles. Stress can also lead to hair loss.

Another type of stress, known as oxidative stress, can also play a role in white hair. Oxidative stress can affect pigment-producing cells. Turning gray is actually a completely natural part of aging because hair follicles produce less color as you age. Your genes also play a role in when your hair turns gray. Ask your parents how old they were when they first saw the signs of silvering, and you might do the same. In fact, a study published in March 2016 in the journal Nature Communications was the first to identify the gene responsible for white hair.

2 brittle hair could be a sign of Cushing’s syndrome

Brittle hair is one of the symptoms of Cushing’s syndrome, which is a rare condition caused by excess cortisol, the main hormone body stress. But, there are many other, more obvious symptoms of Cushing’s syndrome, including high blood pressure, fatigue, and back pain. Treatment for Cushing’s syndrome may involve changing the dose of medication that may be causing the condition, such as glucocorticoids, which are steroids used to treat inflammation caused by various diseases.

3 Thinning hair may be a sign of thyroid disease

People with hypothyroidism, a condition that occurs when the thyroid gland does not produce enough thyroid hormones, may notice increased hair loss and change in hair appearance. About 4.6% of the population aged 12 years and older have hypothyroidism, although most cases are mild. Hypothyroidism can lead to thinning hair and other symptoms, such as fatigue, intolerance to cold, joint pain, muscle aches, puffy face and weight gain. A thyroid stimulating hormone (TSH) test can diagnose the condition, and treatment involves taking thyroid medication.

In addition to thinning hair, some thyroid disorders put you at risk for risk of autoimmune hair loss called alopecia areata. This type of hair loss causes round patches of sudden hair loss and is caused by the immune system attacking the hair follicles.

4 Hair loss can be a sign of anemia

If you suddenly notice a lot more hair in your hairbrush or on the floor of your shower, it may be a sign that your body has low iron stores, or anemia , and may warrant testing. This is another blood test we do when you complain of hair changes. Vegetarians or women with heavy periods increase their risk that hair changes are due to iron deficiency.

It is unclear why iron deficiency can lead to hair loss. hair, but iron is essential for many biological and chemical reactions, perhaps including hair growth. Hair loss can also occur (temporarily) with sudden changes in estrogen levels and is often noticed after pregnancy or stopping birth control pills.

5 The loss of hair could indicate protein deficiency

Protein is essential for hair health and growth (a lack of protein has been linked to hair thinning and hair loss ). Protein deficiency is not a problem for most people. Most adults need 0.8 grams of protein per kilogram of body weight. Good sources of protein include low-fat Greek yogurt, chickpeas, and chicken breast. People who have gastrointestinal difficulties or who have just had gastric bypass surgery may have problems digesting protein. These special situations will need to be managed with the help of your doctor. But most cases of thinning hair, even in women, are probably due to genetics.

6 White or yellow flakes can mean you have dandruff

Yellow or white flakes in your hair, on your shoulders and even in your eyebrows are a sign of dandruff, a chronic scalp condition. Dandruff is usually not a sign of a health problem and can be treated with specialized over-the-counter or prescription shampoos.

One of the most common causes of dandruff is a medical condition called seborrheic dermatitis. People with seborrheic dermatitis have red, oily skin covered in white or yellow scales. A yeast-like fungus called malassezia can also irritate the scalp. Insufficient shampoo, sensitivity to hair care products, and dry skin can also cause dandruff. (Dandruff is usually more severe in the winter, when indoor heating can make skin drier).

7 Damaged hair can mask other health issues

Although hair can reveal your condition, women more often complain about the damage caused by hair coloring and heat treatment. Excessive heat, from daily use of a flat iron or blow-drying, can certainly damage your hair, making it dry, brittle and difficult to maintain. Best not to use more than one hot tool per day (occasional double heat treatment is okay, but not daily). When applying heat to your hair, always use products with protective ingredients. Serums and shine drops tend to have hair-preserving qualities when using direct and indirect heat.

From https://www.mvdemocrat.com/appearance-texture-thickness-7-things-your-hair-reveals-about-your-health/

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‘Benign’ Adrenal Gland Tumors Might Cause Harm to Millions

Posted on January 8, 2022 by MaryO

Millions of people are at increased risk of type 2 diabetes and high blood pressure and don’t even know it, due to a hidden hormone problem in their bodies.

As many as 1 in 10 people have a non-cancerous tumor on one or both of their adrenal glands that could cause the gland to produce excess amounts of the stress hormone cortisol.

Up to now, doctors have thought that these tumors had little impact on your health.

But a new study out of Britain has found that up to half of people with these adrenal tumors are secreting enough excess cortisol to raise their risk of diabetes and high blood pressure.

Nearly 1.3 million adults in the United Kingdom alone could suffer from this disorder, which is called Mild Autonomous Cortisol Secretion (MACS), the researchers said.

Anyone found with one of these adrenal tumors should be screened to see if their health is at risk, said senior researcher Dr. Wiebke Arlt, director of the University of Birmingham Institute of Metabolism and Systems Research in England.

“People who are found to have an adrenal tumor should undergo assessment for cortisol excess and if they are found to suffer from cortisol overproduction they should be regularly screened for type 2 diabetes and hypertension and receive treatment if appropriate,” Arlt said.

These tumors are usually discovered during imaging scans of the abdomen to treat other illnesses, said Dr. André Lacroix, an endocrinologist at the University of Montreal Hospital Center, who wrote an editorial accompanying the study. Both were published Jan. 4 in the Annals of Internal Medicine.

Adrenal glands primarily produce the hormone adrenaline, but they are also responsible for the production of a number of other hormones, including cortisol, Lacroix said.

Cortisol is called the “fight-or-flight” hormone, and can cause blood sugar levels to rise and blood pressure to surge — usually in response to some perceived bodily threat.

Previous studies had indicated that about 1 in 3 adrenal tumors secrete excess cortisol, and an even lower number caused cortisol levels to rise so high that they affected health, researchers said in background notes.

But this new study of more than 1,300 people with adrenal tumors found that previous estimates were wrong.

About half of these patients had excess cortisol due to their adrenal tumors. Further, more than 15% had levels high enough to impact their health, compared to those with truly benign tumors.

MACS patients were more likely to be diagnosed with high blood pressure, and were as much as twice as likely to be on three or more blood pressure medications.

They also were more likely to have type 2 diabetes, and were twice as likely to require insulin to manage their blood sugar, the study found.

“This study clearly shows that mild cortisol production is more frequent than we thought before, and that the more cortisol you produce, the more likely to you are to have consequences such as diabetes and hypertension,” Lacroix said.

About 70% of people with MACS were women, and most were of postmenopausal age, the researchers said.

“Adrenal tumor-related cortisol excess is an important previously overlooked health issue that particularly affects women after the menopause,” Arlt said.

Lacroix agreed that guidelines should be changed so that people with adrenal tumors are regularly screened.

“Everybody who is found to have an adrenal nodule larger than 1 centimeter needs to be screened to see if they’re producing excess hormone or not,” he said. “That’s very clear.”

A number of medications can reduce cortisol overproduction or block cortisol action, if an adrenal tumor is found to be causing an excess of hormone.

People with severe cortisol excess can even have one of their two adrenal glands removed if necessary, Lacroix said.

“It is quite possible to live completely normally with one adrenal gland,” he said.

More information

The Cleveland Clinic has more about adrenal tumors.

SOURCES: Wiebke Arlt, MD, DSc, director, Institute of Metabolism and Systems Research, University of Birmingham, U.K.; André Lacroix, MD, endocrinologist, University of Montreal Hospital Center; Annals of Internal Medicine, Jan. 4, 2022

From https://consumer.healthday.com/1-4-benign-adrenal-gland-tumors-might-cause-harm-to-millions-2656172346.html

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