SERUM CORTISOL APPEARANCE-DISAPPEARANCE IN ADRENAL INSUFFICIENCY AFTER ORAL CORTISONE ACETATE

1977 ◽  
Vol 84 (3) ◽  
pp. 600-604 ◽  
Author(s):  
Anthony L. Barbato ◽  
Richard L. Landau
Keyword(s):  
Oral Dose ◽  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Cortisone Acetate ◽  
Specific Information ◽  
Primary Adrenal Insufficiency ◽  
Hormone Levels ◽  
Cortisol Levels

ABSTRACT Six patients with long-standing idiopathic primary adrenal insufficiency were given 25 mg of cortisone acetate orally on two occasions. Circulating serum cortisol levels were determined hourly for five hours after ingestion. Two patients were additionally studied with an oral dose of 20 mg of cortisol. Marked patient to patient variation in peak hormone and in fifth hour hormone levels was observed. Both values were lowest in the two chronically symptomatic patients who had been maintained on empiric glucocorticoid replacement. Specific information on blood cortisol levels in treated Addisonian individuals has not been previously reported.

A case of cancer-associated hyponatraemia: primary adrenal insufficiency secondary to nivolumab

2021 ◽  
Vol 21 ◽  
Author(s):  
Silvia Galliazzo ◽  
Filippo Morando ◽  
Paola Sartorato ◽  
Michela Bortolin ◽  
Ernesto De Menis
Keyword(s):  
Adverse Events ◽  
Adrenal Insufficiency ◽  
Immune Checkpoint ◽  
Checkpoint Inhibitors ◽  
Serum Cortisol ◽  
Sodium Concentration ◽  
Primary Hypothyroidism ◽  
Biochemical Tests ◽  
Primary Adrenal Insufficiency ◽  
Replacement Treatment

Background: Immunotherapy with immune checkpoint inhibitors is a new frontier for cancer treatment. On the safety profile, this drug class is associated with a new spectrum of side effects, the so-called immune-related adverse events that can potentially affect any organs, mainly endocrine glands. Scant data are available to inform the appropriate strategy of their management and treatment. Case Presentation: A 74-years man with squamous non-small cell lung cancer on nivolumab was hospitalized for fatigue, nausea, vomiting and severe hyponatremia. Biochemical tests were significant for hypotonic hyponatremia with a high urine sodium concentration. Endocrine tests showed overt primary hypothyroidism and low serum cortisol and aldosterone levels associated with an elevated circulating level of adrenocorticotrophic hormone. Adrenal antibody screening and the search of adrenal lesion on CT abdomen were negative. Thus, a nivolumab-induced primary adrenal insufficiency was diagnosed. Nivolumab withdrawal and replacement treatment with glucocorticoid and mineralocorticoid allowed clinical and biochemical recovery. Conclusion: Physicians need to be aware of potential immune-related adverse events in all patients treated with an immune checkpoint inhibitor. Their timely recognition is essential to carry out the proper treatment.

scholarly journals Primary adrenal insufficiency due to bilateral adrenal infarction in COVID-19: a case report

2021 ◽  
Author(s):  
Iza F R Machado ◽  
Isabel Q Menezes ◽  
Sabrina R Figueiredo ◽  
Fernando Morbeck Almeida Coelho ◽  
Debora R B Terrabuio ◽  
...  
Keyword(s):  
Case Report ◽  
Adrenal Insufficiency ◽  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Case Reports ◽  
Serum Cortisol ◽  
Primary Adrenal Insufficiency ◽  
Acute Adrenal Insufficiency ◽  
Adrenal Infarction ◽  
New Onset

Abstract Context Coronavirus disease 2019 (COVID-19) is a proinflammatory and prothrombotic condition, but its impact on adrenal function has not been adequately evaluated. Case report A 46-year-old woman presented with abdominal pain, hypotension, skin hyperpigmentation after COVID-19 infection. The patient had hyponatremia, serum cortisol <1.0 ug/dL, ACTH of 807 pg/mL and aldosterone <3 ng/dL. Computed tomography (CT) findings of adrenal enlargement with no parenchymal and minimal peripheral capsular enhancement after contrast were consistent with bilateral adrenal infarction. The patient had autoimmune hepatitis and positive antiphospholipid antibodies, but no previous thrombotic events. The patient was treated with intravenous hydrocortisone, followed by oral hydrocortisone and fludrocortisone. Discussion Among 115 articles, we identified nine articles, including case reports, of new-onset adrenal insufficiency and/or adrenal hemorrhage/infarction on CT in COVID-19. Adrenal insufficiency was hormonally diagnosed in five cases, but ACTH levels were measured in only three cases (high in one case and normal/low in other two cases). Bilateral adrenal non- or hemorrhagic infarction was identified in five reports (two had adrenal insufficiency, two had normal cortisol levels and one case had no data). Interestingly, the only case with well-characterized new-onset acute primary adrenal insufficiency after COVID-19 had a previous diagnosis of antiphospholipid syndrome. In our case, antiphospholipid syndrome diagnosis was established only after the adrenal infarction triggered by COVID-19. Conclusions Our findings support the association between bilateral adrenal infarction and antiphospholipid syndrome triggered by COVID-19. Therefore, patients with positive antiphospholipid antibodies should be closely monitored for symptoms or signs of acute adrenal insufficiency during COVID-19.

An unusual presentation of primary adrenal insufficiency with new onset type 1 diabetes: case report and review of the literature

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Shelby Graf ◽  
Rachel Stork Poeppelman ◽  
Jennifer McVean ◽  
Arpana Rayannavar ◽  
Muna Sunni
Keyword(s):  
Type 1 Diabetes ◽  
Adrenal Insufficiency ◽  
Diabetic Ketoacidosis ◽  
Serum Cortisol ◽  
Unusual Presentation ◽  
Primary Adrenal Insufficiency ◽  
Onset Type ◽  
Autoimmune Conditions ◽  
New Onset

Abstract Objectives To describe an atypical presentation of primary adrenal insufficiency in conjunction with new onset type 1 diabetes. Case presentation Here, we describe a case of new-onset type 1 diabetes (T1D) presenting simultaneously with an unusual presentation of primary adrenal insufficiency in a previously healthy 16-year-old. He was admitted for a typical presentation of diabetic ketoacidosis, but with extreme hyponatremia. An extensive workup revealed a low aldosterone level, appropriate cortisol level, and positive 21-hydroxylase antibodies. While the phenomenon of multiple autoimmune conditions developing in the same patient is well-described, this particular case has several atypical aspects. Our patient’s case highlights the danger of relying on random serum cortisol in the setting of acute illness to rule out adrenal insufficiency. Conclusions Adrenal insufficiency can present as isolated hypoaldosteronism without hypocortisolemia and can manifest as severe hyponatremia in the context of diabetic ketoacidosis. Workup for an unusual presentation of T1D should include a 21-hydroxylase antibody, as well as thyroid and celiac disease studies.

Corticosteroid replacement: getting it right

1990 ◽  
Vol 28 (18) ◽  
pp. 71-72
Keyword(s):  
Adrenal Insufficiency ◽  
Cortisone Acetate ◽  
Adrenal Failure ◽  
Secondary Adrenal Insufficiency ◽  
Primary Adrenal Insufficiency ◽  
Acth Deficiency ◽  
Mineralocorticoid Activity

Glucocorticoid replacement is needed in primary and secondary adrenal insufficiency. Cortisol (hydrocortisone) is the most physiologically appropriate drug; prednisolone has little mineralocorticoid activity, and cortisone acetate suffers variable absorption and hepatic conversion to cortisol.1 Patients with primary adrenal insufficiency usually need additional mineralocorticoid replacement with fludrocortisone once a day. Patients with secondary adrenal failure (ACTH deficiency due to pituitary/hypothalamic disease) still produce aldosterone and so do not need fludrocortisone.

scholarly journals Primary Adrenal Insufficiency due to Multidrug-Resistant Tuberculosis: A Case Report

2017 ◽  
Vol 7 (3) ◽  
pp. 235-237
Author(s):  
Sultana Marufa Shefin ◽  
Kazi Nazmul Hossain ◽  
Jamal Uddin Ahmed ◽  
Mohammad Mostafizur Rahman
Keyword(s):  
Adrenal Gland ◽  
Adrenal Insufficiency ◽  
Adrenal Glands ◽  
Serum Cortisol ◽  
Needle Aspiration ◽  
Multidrug Resistant ◽  
Primary Adrenal Insufficiency ◽  
Resistant Tuberculosis ◽  
Multidrug Resistant Tuberculosis ◽  
Mdr Tb

Tuberculosis (TB) is a common infectious disease in developing countries like Bangladesh. Drug-resistant tuberculosis (DR-TB) poses a significant threat to the population. A relatively uncommon site of involvement of TB is adrenal gland, which is an important cause of chronic adrenal insufficiency. Here we present a case of a 40-year-old male with multidrug-resistant tuberculosis (MDR-TB) involving the adrenal glands. He was previously diagnosed as a case of disseminated TB involving lungs, right knee joint and lumbar spine and received anti-TB chemotherapy for several occasions and in different categories in last 12 years before this presentation. He presented with 4-month history of vomiting, diarrhea, generalized weakness, generalized pigmentation and postural hypotension. Investigations revealed hyponatremia with hyperkalemia. Adrenal insufficiency was suspected and serum cortisol was found to be low and serum adreno corticotropic hormone (ACTH) was high. On imaging there was bilateral adrenal enlargement. Fine needle aspiration cytology (FNAC) was done from adrenal gland which revealed granulomatous lesion suggestive of TB. Gene Xpert and culture-sensitivity of aspirated material for Mycobacterium tuberculosis revealed MDR-TB. Patient was finally diagnosed as a case of primary adrenal insufficiency due to MDR-TB of the adrenal glands and was treated with regime for MDR-TB for 20 months.Birdem Med J 2017; 7(3): 235-237

scholarly journals Primary Adrenal Insufficiency During Lenvatinib or Vandetanib and Improvement of Fatigue After Cortisone Acetate Therapy

2018 ◽  
Vol 104 (3) ◽  
pp. 779-784 ◽  
Author(s):  
Carla Colombo ◽  
Simone De Leo ◽  
Marta Di Stefano ◽  
Guia Vannucchi ◽  
Luca Persani ◽  
...  
Keyword(s):  
Adverse Event ◽  
Thyroid Cancer ◽  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Dosage Reduction ◽  
Adrenal Function ◽  
Cortisone Acetate ◽  
Drug Discontinuation ◽  
Primary Adrenal Insufficiency ◽  
Common Cause

Abstract Context Two tyrosine kinase inhibitors (TKIs), lenvatinib and vandetanib, are often used to treat advanced radioiodine-refractory differentiated thyroid cancer (RAI-R DTC) and medullary thyroid cancer (MTC), respectively. Fatigue is a common adverse event during treatment with these and other TKIs and a common cause of drug discontinuation or dosage reduction. Cases Description We evaluated the basal and stimulated adrenal function in 12 patients with advanced RAI-R DTC and MTC treated with lenvatinib or vandetanib, respectively. Ten patients complaining of fatigue showed a progressive ACTH increase with normal cortisol levels. Moreover, six of 10 patients had a blunted cortisol response after ACTH stimulation, thus confirming the diagnosis of primary adrenal insufficiency (PAI). The causal relationship between TKIs and PAI onset was also demonstrated by the repeated testing of adrenal function before and during treatment. Patients with PAI received cortisone acetate replacement therapy, with a substantial and prompt improvement in the degree of fatigue, as assessed by the Common Terminology Criteria for Adverse Events version 4.03, thus supporting the major impact of impaired adrenal function in the genesis of this adverse event. Conclusions We show that the occurrence of PAI may be a common cause of fatigue during lenvatinib and vandetanib treatment, and we therefore recommend testing adrenal function for a prompt start of replacement therapy to avoid treatment discontinuation, dosage reduction, and potentially severe PAI complications.

scholarly journals Treatment of gynecomastia with prednisone: case report and literature review

2019 ◽  
Vol 47 (5) ◽  
pp. 2288-2295 ◽  
Author(s):  
Yansheng Jin ◽  
Maoxiao Fan
Keyword(s):  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Underlying Disease ◽  
Left Breast ◽  
Serum Cortisol Level ◽  
Unique Case ◽  
Primary Adrenal Insufficiency ◽  
Adrenal Deficiency ◽  
Laboratory Investigations ◽  
The Brain

This study aimed to report a unique case of primary adrenal insufficiency that was accompanied by painful gynecomastia, which was resolved by treatment with prednisone. Enlargement of the left breast with continuous weakness and generalized nausea in a male was discovered 3 months before admission. Magnetic resonance imaging of the brain was normal 1 month before presentation. A physical examination revealed that the diameter of the left breast was 5 cm and the height was 3 cm. Laboratory investigations revealed hyponatremia, with a low serum cortisol level and an elevated prolactin level. Hyperprolactinemia was suspected because of adrenal deficiency that was directly or indirectly associated with increased prolactin levels. Thus, a diagnosis of hyperprolactinemia was confirmed. Ultrasonography of the left breast showed glandular tissue hyperplasia. In the present study, treating adrenal insufficiency with prednisone relieved both gynecomastia and hyponatremia. However, gynecomastia regression and hyponatremia resolution were observed when prednisone was stopped. Gynecomastia completely resolved by re-administering prednisone. Therefore, treating the underlying disease is essential so that prednisone can be given in a timely manner.

scholarly journals Assessment of Adrenal Function in Women Heterozygous for Adrenoleukodystrophy1

1997 ◽  
Vol 82 (3) ◽  
pp. 856-860
Author(s):  
Samer S. El-Deiry ◽  
Sakkubai Naidu ◽  
Lewis S. Blevins ◽  
Paul W. Ladenson
Keyword(s):  
Fatty Acid ◽  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Chain Fatty Acid ◽  
Acth Stimulation ◽  
Long Chain Fatty Acid ◽  
Increased Risk ◽  
The Mean ◽  
Cortisol Levels ◽  
Long Chain

Abstract Adrenoleukodystrophy (ALD) is an X-linked recessive disorder that destroys the white matter of the brain and is associated with adrenal insufficiency. The prevalence of adrenal dysfunction in 71 women carriers of the X-linked ALD gene was studied. These subjects were identified initially on the basis of being obligate carriers of the X-linked trait by pedigree analysis and were confirmed by plasma very long chain fatty acid levels consistent with a heterozygote status. One subject had well documented overt adrenal insufficiency, diagnosed and treated since age 9 yr. Among the remaining women, the mean serum 0800 h and 1 h post-ACTH cortisol concentrations [16 ± 7 (±sd) and 34 ± 8 μg/dL, respectively] were normal. All subjects had normal ACTH-stimulated serum cortisol levels, i.e. more than 20 μg/dL. However, 4 subjects (6%) had subnormal ACTH-stimulated aldosterone concentrations (mean, 9 ± 6 vs. 42 ± 16 ng/dL for other subjects; P = 0.001, by Mann Whitney rank sum test). Three of these women (75%) were taking nonsteroidal antiinflammatory agents (NSAIDs), whereas only 4 of 67 (6%) subjects with normal aldosterone responsiveness were NSAIDs users (P < 0.01, by Fisher’s exact test). Thus, NSAIDs use was associated with increased risk of hypoaldosteronism (odds ratio, 50.2; 95% confidence interval, 3.3–266; P < 0.002). Three of these four women had symptoms consistent with mineralocorticoid deficiency. Serum sodium and potassium concentrations were normal in all subjects. Basal and metyrapone-stimulated plasma ACTH concentrations were also normal in adequately tested subjects with and without mineralocorticoid insufficiency. Five of eight subjects (63%) who underwent testing with synthetic ovine CRH (oCRH) had abnormalities. Three did not meet the criteria for adequate cortisol stimulation (i.e. >20 μg/dL) and had peak ACTH levels greater than 30 pg/mL. Two other subjects had exaggerated ACTH responses with normal cortisol levels. There were no significant differences in the mean or median levels of very long chain fatty acid, C26:0, C24/22 ratios, or C26/22 ratios among the entire subject group, the subgroup with blunted aldosterone responses to ACTH, and the subgroup with blunted responses to oCRH (P > 0.05, by ANOVA and Kruskall-Wallis test for C26, C24/22 ratio, and C26/22 ratio). We conclude that 1) adrenal cortical insufficiency rarely develops in ALD heterozygotes; 2) isolated mineralocorticoid insufficiency can occur in ALD heterozygotes, as has been previously reported to occur with autoimmune and acquired immunodeficiency syndrome-related adrenal dysfunction; 3) ALD heterozygosity may predispose these individuals to NSAID-related hypoaldosteronism; and 4) a subclinical decrease in glucocorticoid reserve, as measured by oCRH testing, may be present in a majority of these women. Aldosterone levels should be included in the ACTH stimulation testing when seeking evidence of adrenal insufficiency in affected women. NSAIDs should be considered a risk factor for the development of hypoaldosteronism in women heterozygous for ALD.

scholarly journals Effects of Variations in Physiological Cortisol Levels on Thyrotropin Secretion in Subjects with Adrenal Insufficiency: A Clinical Research Center Study1

2000 ◽  
Vol 85 (4) ◽  
pp. 1388-1393
Author(s):  
M. H. Samuels
Keyword(s):  
Total Dose ◽  
Adrenal Insufficiency ◽  
Circadian Variation ◽  
Serum Cortisol ◽  
Physiological Study ◽  
Diurnal Pattern ◽  
Baseline Study ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
Tsh Levels

Although pharmacological doses of glucocorticoids suppress TSH secretion, less is known regarding the effects of physiological variations in cortisol levels on TSH. To study this issue, seven subjects with primary adrenal insufficiency each underwent four studies. In the first study subjects received infusions of saline for 48 h (baseline study). In the second study subjects received infusions of hydrocortisone for 48 h in a pulsatile and diurnal pattern that replicated serum cortisol levels in healthy subjects (physiological study). In most cases, the dose of hydrocortisone was 19 mg/24 h, but this was adjusted as necessary until the resulting serum cortisol levels reproduced those seen in healthy, nonstressed control subjects. In the third study subjects received the same total dose of hydrocortisone as in the physiological study, but with pulses of equal magnitude spaced evenly throughout the time period (constant study). In the fourth study subjects received the same total dose of hydrocortisone, but with the diurnal pattern shifted 12 h from the physiological infusion (reversed study). TSH levels were measured every 15 min during the final 24 h of each study. During the baseline study, the 24-h mean TSH level was 2.87 ± 0.56 mU/L and did not exhibit any diurnal variation. During the physiological study, daytime TSH levels decreased 39% compared to those during the baseline study due to decreased TSH pulse amplitude, and the normal TSH diurnal rhythm was reestablished. The constant and reversed studies did not lead to significant changes in serum TSH levels compared to baseline. These results suggest that the normal circadian variation in endogenous cortisol levels may control TSH secretion, with maximal TSH suppression seen during the time when cortisol levels are highest. However, changing the diurnal pattern of hydrocortisone infusion did not lead to reciprocal changes in TSH levels, and the specific nature of the interactions between cortisol and TSH within the physiological range remains to be fully elucidated.

scholarly journals Severe Psychotic Disorder as the Main Manifestation of Adrenal Insufficiency

2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Julia de Lima Farah ◽  
Carolina Villar Lauand ◽  
Lucas Chequi ◽  
Enrico Fortunato ◽  
Felipe Pasqualino ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Psychotic Disorder ◽  
Clinical Presentation ◽  
Neuropsychiatric Symptoms ◽  
Clinical Signs ◽  
Brain Magnetic Resonance Imaging ◽  
Serum Cortisol ◽  
Psychotic Symptoms ◽  
Primary Adrenal Insufficiency ◽  
Very High

We describe a case of severe psychotic disorder as the only manifestation of primary adrenal insufficiency. A 63-year-old man presented with psychotic symptoms without any prior psychiatric history. During the clinical and laboratorial investigation, exams revealed a normovolemic hyponatremia. The patient showed no other clinical signs or symptoms compatible with adrenal insufficiency but displayed very high ACTH and low serum cortisol concentrations. Brain magnetic resonance imaging showed no significant changes, including the pituitary gland. The patient was initially treated with intravenous corticosteroids, resulting in rapid remission of the psychotic symptoms. The association between adrenal insufficiency and neuropsychiatric symptoms is rare but these symptoms can often be the first clinical presentation of the disease.

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