scholarly journals Effect of glucocorticoids on bone metabolism in replacement therapy of adrenal insufficiency. Literature review

2021 ◽  
Vol 17 (4) ◽  
pp. 357-368
Author(s):  
M. Yu. Yukina ◽  
M. O. Chernova ◽  
N. F. Nuralieva ◽  
A. K. Eremkina ◽  
E. A. Troshina ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Bone Metabolism ◽  
Adrenal Cortex ◽  
Endocrine Disorders ◽  
Mineral Density ◽  
Adrenal Androgen ◽  
Water Salt ◽  
Bone Condition ◽  
Salt Homeostasis

Adrenal insufficiency (AI) is a syndrome caused by disturbance in the synthesis and secretion of hormones of the adrenal cortex, which ensure the vital activity, energy and water-salt homeostasis. The widest hormonal deficiency is observed in primary hypocorticism, when the synthesis of not only glucocorticoids (GC) and adrenal androgens, but also mineralocorticoids is disrupted. Lifelong replacement therapy with GCs for this pathology may be associated with a risk of bone loss and osteoporosis. However, at present, there are no clear guidelines for diagnosis of bone condition, including and bone mineral density (BMD) monitoring during treatment with GCs in patients with AI. This review summarizes collected data on the key pathogenetic links of glucocorticoid-induced osteoporosis, incidence of decreased BMD and fractures in patients with AI. In this review factors that influence bone metabolism in this cohort of patients are considered: the type and the dose of prescribed GCs, the type (primary, secondary, HH in congenital adrenal cortex dysfunction) and the duration of AI, age, gender, and the presence of concomitant endocrine disorders (hypogonadism, growth hormone (GH) deficiency). In addition, the review presents data on the effect of adrenal androgen replacement therapy and recombinant GH therapy on bone metabolism in secondary AI.

scholarly journals Prednisolone is associated with a worse bone mineral density in primary adrenal insufficiency

2018 ◽  
Vol 7 (6) ◽  
pp. 811-818 ◽  
Author(s):  
Kathrin R Frey ◽  
Tina Kienitz ◽  
Julia Schulz ◽  
Manfred Ventz ◽  
Kathrin Zopf ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Bone Mineral ◽  
Immediate Release ◽  
Modified Release ◽  
Mineral Density ◽  
Primary Adrenal Insufficiency ◽  
Z Scores

Context Patients with primary adrenal insufficiency (PAI) or congenital adrenal hyperplasia (CAH) receive life-long glucocorticoid (GC) therapy. Daily GC doses are often above the physiological cortisol production rate and can cause long-term morbidities such as osteoporosis. No prospective trial has investigated the long-term effect of different GC therapies on bone mineral density (BMD) in those patients. Objectives To determine if patients on hydrocortisone (HC) or prednisolone show changes in BMD after follow-up of 5.5 years. To investigate if BMD is altered after switching from immediate- to modified-release HC. Design and patients Prospective, observational, longitudinal study with evaluation of BMD by DXA at visit1, after 2.2 ± 0.4 (visit2) and after 5.5 ± 0.8 years (visit3) included 36 PAI and 8 CAH patients. Thirteen patients received prednisolone (age 52.5 ± 14.8 years; 8 women) and 31 patients received immediate-release HC (age 48.9 ± 15.8 years; 22 women). Twelve patients on immediate-release switched to modified-release HC at visit2. Results Prednisolone showed significantly lower Z-scores compared to HC at femoral neck (−0.85 ± 0.80 vs −0.25 ± 1.16, P < 0.05), trochanter (−0.96 ± 0.62 vs 0.51 ± 1.07, P < 0.05) and total hip (−0.78 ± 0.55 vs 0.36 ± 1.04, P < 0.05), but not at lumbar spine, throughout the study. Prednisolone dose decreased by 8% over study time, but no significant effect was seen on BMD. BMD did not change significantly after switching from immediate- to modified-release HC. Conclusions The use of prednisolone as hormone replacement therapy results in significantly lower BMD compared to HC. Patients on low-dose HC replacement therapy showed unchanged Z-scores within the normal reference range during the study period.

scholarly journals Growth Hormone Replacement Therapy Improves Body Composition and Increases Bone Metabolism in Elderly Patients with Pituitary Disease1

2000 ◽  
Vol 85 (11) ◽  
pp. 4104-4112 ◽  
Author(s):  
Rita Fernholm ◽  
Margareta Bramnert ◽  
Erik Hägg ◽  
Agneta Hilding ◽  
David J. Baylink ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Body Composition ◽  
Side Effects ◽  
Replacement Therapy ◽  
Bone Metabolism ◽  
Mineral Density ◽  
Normal Range ◽  
Gh Treatment ◽  
Gh Replacement ◽  
Igf I

Although a specific GH deficiency (GHD) syndrome in the adult and the response to GH replacement therapy are well recognized, there are few data available on the effect of GH replacement therapy in elderly GH-deficient patients. We studied the effect of GH therapy on body composition and bone mineral density measured by dual energy x-ray absorptiometry, markers for bone metabolism, insulin-like growth factors (IGFs), and IGF-binding proteins (IGFBPs) in 31 patients (6 women and 25 men; aged 60–79 yr; mean, 68 yr) with multiple pituitary hormone deficiencies. The GH response to arginine or insulin was below 3 μg/L (9 mU/L) in all subjects. They were randomized to GH (Humatrope, Eli Lilly & Co.) or placebo for 6 months, followed by 12 months of open treatment. The dose was 0.05 IU/kg·week for 1 month, and after that it was 0.1 IU/kg·week divided into daily sc injections (0.75–1.25 IU/day). There were no changes in any of the measured variables during placebo treatment. GH treatment normalized serum IGF-I in a majority of the patients and increased IGFBP-3 and -5 as well as IGFBP-4 and IGF-II to values within normal range. Lean body mass was increased, and the increase at 6 and 12 months correlated with the increase in IGF-I (r = 0.46; P = 0.010 and r = 0.54, respectively; P = 0.003). GH treatment caused a modest, but highly significant, reduction of total body fat. Mean bone mineral density was not different from that in healthy subjects of the same age and did not change during the observation period. Markers for bone formation (bone-specific alkaline phosphatase activity, osteocalcin, and procollagen I carboxyl-terminal peptide in serum) increased within the normal range, and levels were sustained throughout the study. The bone resorption marker (pyridinoline in urine) was significantly elevated for 12 months. Side-effects were mild, mostly attributed to fluid retention. In two patients with normal glucose tolerance at the start of the study, pathological glucose tolerance occurred in one patient and was impaired in one. In conclusion, elderly patients with GHD respond to replacement therapy in a similar manner as younger subjects, with an improvement in body composition and an increase in markers for bone metabolism. Side-effects are few, and elderly GHD patients can be offered treatment. As long-term risks are unknown, GH doses should be titrated to keep IGF-I within the age-related physiological range.

scholarly journals Primary adrenal insufficiency replacement therapy

2000 ◽  
Vol 46 (3) ◽  
pp. 31-45
Author(s):  
V. V. Fadeev ◽  
G. A. Melnichenko
Keyword(s):  
Heart Failure ◽  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Adrenal Cortex ◽  
Adrenal Glands ◽  
Pathological Process ◽  
Clinical Syndrome ◽  
Primary Adrenal Insufficiency ◽  
Adrenal System ◽  
System 2

Adrenal insufficiency is a clinical syndrome caused by insufficient secretion of hormones by the adrenal cortex, which is the result of a malfunction of one or more parts of the hypothalamic-pituitary-adrenal system [2]. Primary chronic adrenal insufficiency (1-CNI) develops as a result of the destruction of more than 90% of the cortex of both adrenal glands by a pathological process. The main causes of 1-CNN are currently autoimmune (80–85%) and tuberculosis (5–10%) destruction of the adrenal cortex [2, 3]. 1-CNN of the indicated etiology is better known as "Addison's disease." 1-CNN is a relatively rare disease (40-110 new cases per 1 million people per year) [2, 3], but it is of considerable importance in the practice of endocrinology. Without exception, all patients with a diagnosis of 1-chronic heart failure need lifelong replacement therapy with corticosteroids (CS), which will be discussed in this work.

scholarly journals Latent Adrenal Insufficiency: From Concept to Diagnosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Nada Younes ◽  
Isabelle Bourdeau ◽  
Andre Lacroix
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Standard Dose ◽  
Signs And Symptoms ◽  
Serum Cortisol ◽  
Zona Glomerulosa ◽  
Adrenocortical Function ◽  
Adrenal Crisis ◽  
Zona Fasciculata ◽  
Adrenal Androgen

Primary adrenal insufficiency (PAI) is a rare disease and potentially fatal if unrecognized. It is characterized by destruction of the adrenal cortex, most frequently of autoimmune origin, resulting in glucocorticoid, mineralocorticoid, and adrenal androgen deficiencies. Initial signs and symptoms can be nonspecific, contributing to late diagnosis. Loss of zona glomerulosa function may precede zona fasciculata and reticularis deficiencies. Patients present with hallmark manifestations including fatigue, weight loss, abdominal pain, melanoderma, hypotension, salt craving, hyponatremia, hyperkalemia, or acute adrenal crisis. Diagnosis is established by unequivocally low morning serum cortisol/aldosterone and elevated ACTH and renin concentrations. A standard dose (250 µg) Cosyntropin stimulation test may be needed to confirm adrenal insufficiency (AI) in partial deficiencies. Glucocorticoid and mineralocorticoid substitution is the hallmark of treatment, alongside patient education regarding dose adjustments in periods of stress and prevention of acute adrenal crisis. Recent studies identified partial residual adrenocortical function in patients with AI and rare cases have recuperated normal hormonal function. Modulating therapies using rituximab or ACTH injections are in early stages of investigation hoping it could maintain glucocorticoid residual function and delay complete destruction of adrenal cortex.

scholarly journals Adrenal Insufficiency

2016 ◽  
pp. 43-48
Author(s):  
SM Ashrafuzzaman ◽  
Muhammad Abdur Rahim
Keyword(s):  
Weight Loss ◽  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
High Index ◽  
Electrolyte Imbalance ◽  
Adrenal Crisis ◽  
Adrenal Androgen ◽  
Primary Adrenal Insufficiency ◽  
Short Acting ◽  
High Index Of Suspicion

Adrenal insufficiency means hypo-function of the adrenal cortex, usually glucocorticoid, may be associated with mineralocorticoid and rarely adrenal androgen. It can be categorized into two types: Primary adrenal insufficiency, or Addison’s disease (cortisol low and ACTH high) or secondary/ tertiary adrenal insufficiency due to pituitary or hypothalamic disorders (both cortisol and ACTH are low). Identification of etiology is very important for plan of treatment. The reported incidence of adrenal insufficiency varies greatly depending on the population studied, the test and cut off levels used, and the cause. Many patients may present with adrenal crisis, some of them have subtle symptoms, hyperpigmentation, hypotension, electrolyte imbalance, shock etc. Many of them have iatrogenic adrenal insufficiency with features of Cushing’s syndrome. So, the manifestations of adrenal insufficiency are numerous and nonspecific, and clinicians should have a high index of suspicion and be alert to see important diagnostic clues, such as hyponatremia, hyperkalemia, and hypotension (that are refractory to fluids and vasopressors), diarrhea, weight loss, vomiting, fever etc. without any clear causation. Treatment of adrenal insufficiency is usually life-long, of course based on etiology. Short acting glucocorticoid is better, like hydrocortisone. Patients may be treated with prednisolone. Patients should be provided a “steroid card”. Sometimes it is essential to take patients under “withdrawal protocol”.Birdem Med J 2015; 5(1) Supplement: 43-48

Concentration of selected micro-nutrients in saliva among women in menopausal period treated with hormone replacement therapy

2013 ◽  
Vol 22 (01) ◽  
pp. 46-51
Author(s):  
M. Rahnama ◽  
I. Jastrzêbska-Jamrogiewicz ◽  
R. Jamrogiewicz
Keyword(s):  
Bone Mineral Density ◽  
Hormone Replacement Therapy ◽  
Blood Serum ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Surgical Removal ◽  
Femoral Bone ◽  
Mineral Density ◽  
Natural Menopause ◽  
Copper Zinc

Summary Objective: The aim of this study was to observe the variability of the level of copper, zinc and manganese in saliva amongst women with hypoestrogenia, treated and untreated with hormone replacement therapy (HRT). Methods: The study was conducted on a group of 60 women treated and untreated with HRT. Half of the patients were after natural menopause and other half was after surgical removal of ovaries. Research on micronutrients in non-stimulated saliva and blood serum was carried out in 2005. Tests on saliva were repeated in 2010. Investigation of bone mineral density (BMD) of femoral bone was performed in year 2010. Results: Statistical analysis of concentration of copper and zinc revealed a linear correlation between the levels of these microelements in blood serum and saliva. The study revealed that HRT has a beneficial effect on BMD and the concentration of copper and manganese in saliva and blood serum of patients after the menopause. Patients treated with HRT showed higher BMD values than groups not treated with hormones. Conclusions: Saliva appears to be a promising diagnostic material which can be used to analyze the content of trace elements, but further research should be carried out on a broader research group.

Results of study of biochemical markers of bone metabolism in men with coronary heart disease

2020 ◽  
pp. 39-43
Author(s):  
A. V. Voronkina ◽  
T. A. Raskina ◽  
M. V. Letaeva ◽  
Yu. V. Averkieva ◽  
O. S. Malyshenko ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Bone Formation ◽  
Bone Metabolism ◽  
Biochemical Markers ◽  
Coronary Atherosclerosis ◽  
Cathepsin K ◽  
Arterial Calcification ◽  
Mineral Density ◽  
Bone Remodeling Markers

The development of atherosclerosis is closely related to the calcification of the vessel intima and fibrous plaques, being a complex and multifactorial process, in which the markers of bone formation and resorption play an important role. Objective. To study the biochemical markers of bone metabolism in men with stable coronary heart disease (CHD). Material and methods. The study included 102 men with verified CHD. Data were evaluated by densitometry, coronary angiography, multispiral computed tomography, color duplex scanning of brachiocephalic arteries, serum lipids (total cholesterol, triglycerides [TG], high-density [LHD] and low-density lipoprotein cholesterol), concentrationsin the blood of osteocalcin (OC), bone alkaline phosphatase (BAP), cathepsin K and C-telopeptides (CTx). Results. Concentrations of BAP, cathepsin K and CTx in patients with CHD were significantly higher than in men without CHD. The concentration of OC in men with normal bone mineral density was significantly lower than in patients with osteopenic syndrome. There was a direct correlation between OC and antiatherogenic HDL cholesterol and the inverse correlation between OC and TG, CTx and TG. There was no correlation between the level of bone remodeling markers and coronary artery (CA) lesion variant and the severity of coronary atherosclerosis on SYNTAX scale. The correlation analysis did not reveal the connection of biochemical markers of bone metabolism with the severity of coronary atherosclerosis and calcification and thickness of intima-media complex of carotid arteries. Absolute values of bone formation indices (BAP, OC) were significantly higher in patients with severe СA calcification than in patients without signs of calcification. Summary. Increased rates of osteogenesis and osteoresorption characterize the accelerated process of bone metabolism and indicate in favor of high rates of bone loss in men with CHD, which confirms the likelihood of common pathophysiological mechanisms of bone resorption and arterial calcification.

Adrenal insufficiency: review of clinical outcomes with current glucocorticoid replacement therapy

2016 ◽  
Author(s):  
Gudmundur Johannsson ◽  
Alberto Falorni ◽  
Stanko Skrtic ◽  
Hans Lennernas ◽  
Marcus Quinkler ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Clinical Outcomes ◽  
Glucocorticoid Replacement Therapy
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