Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review

Joseph, Rebecca M.; Hunter, Louise; Ray, David; Dixon, William G

doi:10.1016/j.semarthrit.2016.03.001

Cited by 136 publications

(129 citation statements)

References 83 publications

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“…Adrenal gland recovery time can be short (few days) [ 15 ], or as long as several weeks [ 16 ] or even more. The results from a recent systematic review show that hypoadrenalism persists in 15% of patients retested three years after GC withdrawal [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Treatment with Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal Axis

Paragliola

Papi

Pontecorvi

et al. 2017

IJMS

130

104

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Chronic glucocorticoid (GC) treatment represents a widely-prescribed therapy for several diseases in consideration of both anti-inflammatory and immunosuppressive activity but, if used at high doses for prolonged periods, it can determine the systemic effects characteristic of Cushing’s syndrome. In addition to signs and symptoms of hypercortisolism, patients on chronic GC therapy are at risk to develop tertiary adrenal insufficiency after the reduction or the withdrawal of corticosteroids or during acute stress. This effect is mediated by the negative feedback loop on the hypothalamus-pituitary-adrenal (HPA) axis, which mainly involves corticotropin-release hormone (CRH), which represents the most important driver of adrenocorticotropic hormone (ACTH) release. In fact, after withdrawal of chronic GC treatment, reactivation of CRH secretion is a necessary prerequisite for the recovery of the HPA axis. In addition to the well-known factors which regulate the degree of inhibition of the HPA during synthetic GC therapy (type of compound, method of administration, cumulative dose, duration of the treatment, concomitant drugs which can increase the bioavailability of GCs), there is a considerable variation in individual physiology, probably related to different genetic profiles which regulate GC receptor activity. This may represent an interesting basis for possible future research fields.

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Section: Introductionmentioning

confidence: 99%

Treatment with Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal Axis

Paragliola

Papi

Pontecorvi

et al. 2017

IJMS

130

104

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“…However, the role of prednisone in causing adrenal suppression, even after a 4-week course, is well documented in literature. (50) In conclusion, the use of budesonide in place of prednisone for LT immune suppression appears to be safe and effective in our pilot study. It is associated with similar rates of ACR but lower rates of NODAT and infectious complications.…”

Section: Discussionmentioning

confidence: 53%

Safety and Efficacy of Budesonide for Liver Transplant Immune Suppression: Results of a Pilot Phase 2a Trial

et al. 2020

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Earn MOC for this article: www.wileyhealthlearning.com/aasld.aspx Despite adverse effects like hyperglycemia, new-onset diabetes after transplant (NODAT), and infectious complications, corticosteroid use remains an important part of liver transplantation (LT) immune suppression. Budesonide, a synthetic corticosteroid, undergoes extensive first-pass hepatic metabolism with only 10% systemic bioavailability, providing an opportunity for an improved toxicity-therapeutic ratio. Although effective in the treatment of autoimmune hepatitis, the effects of budesonide for LT immune suppression are unknown. We conducted a single-center phase 2a trial to study the safety and efficacy of budesonide immunosuppressive therapy. From July 2017 to November 2018, 20 patients undergoing a first LT received budesonide tapering doses (from 9 to 3 mg) for 12 weeks. Patients were compared with matched control patients who received prednisone from the same time period. Additionally, both groups received calcineurin inhibitors and mycophenolate mofetil. Outcome measures at week 24 included rates of biopsy-proven acute cellular rejection (ACR), NODAT (hemoglobin A1c >6.4%), and infectious complications. In the budesonide arm, 1 patient developed ACR at week 5 and was removed from the study. Another patient stopped the study drug at week 8 due to persistent nausea. Rates of ACR were similar between the budesonide and control groups (5% versus 5%, P = 1.00). Three patients in the control group developed NODAT versus none in the budesonide group (15% versus 0%; P = 0.23). There were 6 infections in the control group compared with none in the budesonide group (30% versus 0; P = 0.02). These pilot data suggest that budesonide has the potential to be a safe and effective alternative to prednisone for LT immune suppression while reducing steroid-induced infections and NODAT. Randomized controlled trials are required to validate these findings.

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“…Kortikosteroidlerin adrenal yetmezlik riski nedeni ile uzun süreli ve yüksek dozlarda kullanımları sonrasında aniden kesilmemesi ve doz azaltılarak kesilmesi gerektiği unutulmamalıdır. Özellikle prednizolonun 5 mg/gün üzerindeki dozlarda 4 haftadan uzun süreli kullanımı sonrası adrenal yetmezlik riski artar (38).…”

Section: Kortikosteroidlerunclassified

Oncologic Approaches for Bone Metastasis Related Pain

Yekedüz¹,

Utkan²,

Ürün³

2020

nts

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Ağrı, kanser hastalarında palyasyon gerektiren semptomların başında gelmektedir. Ağrı sıklığı hastalık evresine göre değişmekle birlikte erken evre ve aktif kanser tedavisi alan hastalarda %25-50 civarında iken, metastatik hastalarda bu oran %70-80'e kadar yükselmektedir (1). Ağrı kanser hastalarında sadece fiziksel olumsuz etkiler yaratmakla kalmayıp, hastalarda ciddi psikososyal etkilere de neden olmaktadır. Ağrı nedeni ile hastalarda iştah kaybı, uyku bozuklukları, depresyon, anksiyete bozukluğu ve sonuç olarak ciddi yaşam kalitesi bozukluğu görülmektedir (2). Yeterli tedavi edilememiş ağrı varlığında hastaların kanser tedavisine uyumları ve kendi öz bakımları bozulabilmektedir (3). Kanser hastalarında ağrı sadece tümörün kendisinden kaynaklanmamaktadır. Özellikle kemoterapötik ajanlar ile akut dönemde ortaya çıkan oral mukozit, ekstravazasyon gibi etkilere bağlı ağrı, platin ve taksan Bone is the third most common metastatic site after lungs and liver in advanced stages of cancer. Bone pain may be caused by local compression and/or invasion of the tumor or a pathological fracture due to bone metastasis. The mainstay of pain management is the treatment of underlying cancer. Furthermore, in case of pathologic fracture, surgery and/or radiotherapy may be considered. Besides, analgesics might be needed in most of the cases. Opioid analgesics are the backbone for the management of cancer pain. Nevertheless, paracetamol and nonsteroidal anti-inflammatory agents may be combined with opioid analgesics for the control of cancer pain. Adjuvant analgesics which are used as an analgesic due to their secondary effects are another option for the management of bone-related pain. Bisphosphonates and denosumab which are osteoclast inhibitors are used as an adjuvant analgesics, too. Furthermore, steroids are used as an adjuvant analgesic due to their anti-inflammatory effects.

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Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review

Cited by 136 publications

References 83 publications

Treatment with Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal Axis

Treatment with Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal Axis

Safety and Efficacy of Budesonide for Liver Transplant Immune Suppression: Results of a Pilot Phase 2a Trial

Oncologic Approaches for Bone Metastasis Related Pain

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