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The development of an iatrogenic Cushing's syndrome (ICS) followed by secondary adrenal failure remains an exceptional event after a single dose administration of a synthetic glucocorticoid. Medical attention has been drawn recently on the possible impact of ritonavir-based antiretroviral regimens
BACKGROUND
Highly effective antiretroviral treatment has improved the life expectancy of human immunodeficiency virus (HIV) infected patients, but has led to an increase in the comorbidities related to aging, such as the chronic obstructive pulmonary disease (COPD). All this implies the need for a
BACKGROUND
The frequency of hypothalamic-pituitary-adrenal axis dysfunction among HIV-infected patients receiving steroid injections has not been reported, and the risk factors for this adverse event are poorly characterized.
METHODS
We conducted a retrospective analysis of data from HIV-infected
A 14-year-old female with perinatally acquired HIV on boosted protease inhibitor (PI) therapy with atazanavir and ritonavir rapidly developed cushingoid features with excessive weight gain and moon facies within 2 weeks of receiving inhaled fluticasone/salmeterol for asthma treatment. Soon after
Triamcinolone is a long-acting glucocorticoid medication that can be responsible for transient suppression of the hypothalamic–pituitary–adrenal (HPA) axis. This physiologic alteration may persist for weeks after repeated or even single localized injection of this agent. However, when this
Triamcinolone is a long-acting glucocorticoid medication that can be responsible for transient suppression of the hypothalamic–pituitary–adrenal (HPA) axis. This physiologic alteration may persist for weeks after repeated or even single localized injection of this agent. However, when this
Cortisol is a hydrophobic molecule that is largely bound to corticosteroid-binding globulin (CBG) in the circulation. In the assessment of adrenal insufficiency, many clinicians measure a total serum cortisol level, which assumes that CBG is present in normal concentrations and with a normal binding
BACKGROUND
We have recently reported somatic mutations in the ubiquitin-specific protease USP8 gene in a small series of adenomas of patients with Cushing's disease.
OBJECTIVE
To determine the prevalence of USP8 mutations and the genotype-phenotype correlation in a large series of patients diagnosed
Strong cytochrome P450 (CYP) 3A4 inhibitors may induce Cushing syndrome and subsequent adrenal insufficiency when administered concurrently with corticosteroids. This drug-drug interaction has been well described with HIV protease inhibitors. A similar drug-drug interaction with corticosteroids and
As a consequence of inhibition of the hepatic cytochrome P450 3A4 isozyme, treatment with HIV protease inhibitors can result in significant drug-drug interactions. One noteworthy interaction is between protease inhibitors and inhaled or intranasal corticosteroids. This interaction can result in
OBJECTIVE
To investigate the relationship of cortisol concentrations during the first week of life to patent ductus arteriosus (PDA), markers of lung inflammation, and respiratory outcome in very low birth weight infants.
METHODS
Newborns <1,500 g birth weight were prospectively enrolled at 2
Ritonavir is commonly used in low doses to boost plasma levels of protease inhibitors in patients with human immunodeficiency virus (HIV) infections. It is also a potent inhibitor of cytochrome P450. We present a 50-year-old African American male with past medical history of HIV on highly active
Ritonavir is a protease inhibitor (PI) frequently prescribed with highly active antiretroviral therapy. It functions to boost the effectiveness of other PIs as a result of blocking their breakdown by the cytochrome P450 (3A4) pathway. Through this same mechanism, ritonavir has been shown to cause
BACKGROUND
Many reports have described endocrine and metabolic disorders in the human immunodeficiency virus (HIV) infection. This article reviewed various reports in the literature in order to increase the awareness and thus the need for early intervention when necessary.
METHODS
Data were obtained
Angiotensinogen is a glycoprotein synthesized mainly in hepatocytes and secreted into the circulation. Angiotensinogen is cleaved by the enzyme renin to produce angiotensin I, which is further converted into a vasoconstricting peptide, angiotensin II, the biologically active peptide of the renin