Adrenal

Adrenal Involvement in Disseminated Histoplasmosis

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An 82-year-old man presented to the emergency department with a 3-year history of progressive generalized weakness. Four months before presentation, a left adrenal mass had been identified incidentally on computed tomography (CT) that had been performed to evaluate an episode of chest pain. During the month preceding presentation, he had lost 8 kg of weight and had become unable to sit up in bed. The physical examination was unremarkable. Laboratory studies were notable for a white-cell count of 2700 per cubic millimeter (reference range, 3700 to 10,500), a normal adrenal axis, and negative testing for human immunodeficiency virus. Owing to concern for cancer, positron-emission tomography–CT of the whole body was performed and showed an adrenal mass on each side with fluorodeoxyglucose (FDG) uptake (Panel A shows a coronal view), a 17-cm-long spleen without FDG uptake (asterisk in Panel A), and no other abnormal findings. A subsequent biopsy of the left adrenal mass showed necrotizing granulomatous inflammation with intracellular fungal organisms (Panel B, arrows; hematoxylin and eosin staining) that stained positive with Grocott’s methenamine silver (Panel C), a finding consistent with Histoplasma capsulatum. A diagnosis of chronic progressive disseminated histoplasmosis was made. Treatment with itraconazole was initiated. The patient died on hospital day 13 from hospital-acquired pneumonia

Noninvasive Skin Test May Aid in Cushing Diagnosis

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Tissue accumulation of advanced glycation end products (AGEs) is associated with the presence of hypercortisolism, suggesting a potential future noninvasive method to assist in the diagnosis of Cushing syndrome, new research suggests.

Tissue accumulation of AGEs — harmful compounds formed by glycation of macromolecules — has been implicated in aging, diabetes, and cardiovascular disease. Now, in a new single-center prospective study, a group of 208 patients with endogenous hypercortisolism was found to have significantly higher median tissue AGE levels than 103 reference subjects without hypercortisolism.

The findings were presented at the American Association of Clinical Endocrinology Annual Meeting 2023 by Rashi Sandooja, MD, an endocrinology fellow at the Mayo Clinic, Rochester, Minnesota.

“Diagnosis of endogenous hypercortisolism can be quite challenging. Often patients can have nonspecific symptoms with biochemical testing being equivocal. In these situations, new biomarkers of hypercortisolism such as AGE measurement could potentially be useful,” Sandooja told Medscape Medical News.

“After proper validation, it could help clinicians in cases which may not be straightforward and could serve as an additional” instrument in the toolkit to reach a conclusive diagnosis, she added.  

Asked to comment, session moderator Anupam Kotwal, MD, told Medscape Medical News: “I think it’s very exciting data…I envision its use in mild autonomous cortisol secretion, where there are not a lot of overt Cushing features but they may have a small adrenal mass…It might be used to guide care when there’s not a clear-cut answer.”

However, he cautioned that more validation is needed to determine the correlates of AGEs by different etiologies and magnitudes of cortisol excess.

Moreover, “Skin can become thin in hypercortisolism, so is [the reader device] just detecting it more with skin testing? I think a blood test for validation would be a very good next step,” added Kotwal, who is an assistant professor in the Division of Diabetes, Endocrinology and Metabolism at the University of Nebraska, Omaha.

Ipilimumab-induced autoimmune adrenalitis.

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A 56-year-old woman presented with fatigue and headache after receiving four doses of ipilimumab, a monoclonal antibody against cytotoxic T-lymphocyte antigen 4, for the treatment of metastatic melanoma. Low morning serum concentrations of corticotropin (<1·1 pmol/L [reference range 2·2—13·2 pmol/L]) and cortisol (41·4 nmol/L [reference range 165·5—662·2 nmol/L]), combined with pituitary enlargement, were consistent with hypophysitis-related secondary adrenal insufficiency.

adrenal

Treatment with a replacement dose of hydrocortisone was initiated. Before ipilimumab treatment, her adrenal glands (circled) were normal in size (figure A). A subsequent surveillance CT scan of the abdomen showed bilateral enlargement of adrenal glands (figure B). Her serum cortisol and aldosterone concentrations did not respond to cosyntropin stimulation, which indicated primary adrenal insufficiency. 6 weeks later, her adrenal glands normalised in size (figure C). The dynamic size change of the adrenal glands suggests ipilimumab-related autoimmune adrenalitis. Although secondary adrenal insufficiency is a fairly common endocrinopathy related to ipilimumab treatment, the identification of primary adrenal insufficiency that could coexist with secondary adrenal insufficiency is important.

Source: Lancet