Dehnlundberg3800

He was diagnosed with adrenal histoplasmosis because of the evidence of AI and bilateral adrenal enlargement in the setting of DH. He was started on glucocorticoid replacement for primary AI and continues to be on glucocorticoids even after 5 years of diagnosis. DH frequently involves the adrenal gland (80%) and can present as adrenal enlargement but does not always cause primary AI.

Our case demonstrates the importance of being vigilant about infections like histoplasmosis as a potential cause of AI. Delay in treatment in such cases could result in life-threatening consequences.

Our case demonstrates the importance of being vigilant about infections like histoplasmosis as a potential cause of AI. Delay in treatment in such cases could result in life-threatening consequences.

To evaluate a rare case of a postmenopausal woman with hirsutism and virilization due to Leydig cell tumors (LCTs) of both ovaries.

In this challenging case, the diagnostic studies included the detection of total/free testosterone, hemoglobin, and estradiol levels; adrenal computed tomography; and pelvic magnetic resonance imaging.

A 61-year-old woman presented for the evaluation of hirsutism. Physical examination revealed normal vital signs and evidence of virilization. The baseline laboratory findings were hemoglobin level of 16.2 g/dL (reference, 12.0-15.5 g/dL), total testosterone level of 803 ng/dL (reference, 3-41 ng/dL), and free testosterone level of 20.2 pg/mL (reference, 0.0-4.2 pg/mL). Pelvic magnetic resonance imaging showed bilateral homogeneous ovarian enhancement. Based on the magnetic resonance imaging findings and clinical presentation, the patient was diagnosed with ovarian hyperthecosis and underwent laparoscopic bilateral oophorectomy. Pathology confirmed LCTs in both ovaries. Six months later, testosterone levels normalized, with significant improvement in hirsutism and virilization.

Clinicians should be aware of androgen-secreting tumors, including rare bilateral LCTs in postmenopausal women presenting with progressing hirsutism and virilization. Marked hyperandrogenemia with total testosterone level of >150 ng/dL (5.2 nmol/L) or serum dehydroepiandrosterone sulfate level of >700 μg/dL (21.7 mmol/L) is typically found. It should be recognized that diffuse stromal Leydig cell hyperplasia and small LCTs may be missed on imaging, and in some cases only pathology can confirm the result.

700 μg/dL (21.7 mmol/L) is typically found. It should be recognized that diffuse stromal Leydig cell hyperplasia and small LCTs may be missed on imaging, and in some cases only pathology can confirm the result.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a novel group of oral hypoglycemic agents with multiple proven beneficial effects. However, their use has been associated with euglycemic diabetic ketoacidosis (DKA), typically triggered by risk factors such as acute illness, surgery, and decreased calorie intake. Therefore, it is recommended that patients discontinue SGLT2 inhibitors at least 24 hours before surgery to minimize this risk. We report a case of a postoperative euglycemic DKA in a patient who had discontinued SGLT2 inhibitor therapy 48 hours prior to surgery.

We describe the clinical course of a patient with type 2 diabetes mellitus on empagliflozin therapy who was referred for coronary artery bypass graft surgery.

A 60-year-old man with type 2 diabetes mellitus developed euglycemic DKA a few hours after coronary artery bypass graft surgery. Laboratory results showed acute postoperative elevated anion gap metabolic acidosis with normal glucose and elevated blood ketone levels. It was later revealed that the patient was treated as an outpatient with empagliflozin; the last dose was taken 48 hours prior to his procedure.

Euglycemic DKA can occur postoperatively in patients with a history of SGLT2 inhibitor use, even 48 hours after the discontinuation of therapy. This case highlights the need to revisit the recommended time to discontinue these agents, specifically prior to major surgery, because their pharmacokinetic effects may persist after 24 hours of discontinuation, putting patients at risk for postoperative euglycemic DKA.

Euglycemic DKA can occur postoperatively in patients with a history of SGLT2 inhibitor use, even 48 hours after the discontinuation of therapy. This case highlights the need to revisit the recommended time to discontinue these agents, specifically prior to major surgery, because their pharmacokinetic effects may persist after 24 hours of discontinuation, putting patients at risk for postoperative euglycemic DKA.

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are a relatively novel class of oral medications for the treatment of type 2 diabetes mellitus (T2DM). Their use has increased recently due to their beneficial renal and cardiovascular outcomes, but they come with the rare risk of diabetic ketoacidosis (DKA) at normal or slightly elevated glucose values, termed euglycemic DKA (euDKA). Recently, carbohydrate-deprived, ketogenic diets have gained popularity due to benefits of weight loss and improved control of T2DM. We describe 2 patients with T2DM who developed euDKA caused by SGLT2 inhibitor use while on a ketogenic diet and provide a review of the literature.

We describe the hospital course, laboratory data, and treatment of 2 patients and provide a literature review.

Both of our patients were found to have normal or mildly elevated serum glucose levels, with an elevated anion gap and ketosis, representative of euDKA. Selleckchem Siponimod The first patient developed euDKA after only 1 dose of empagliflozin, while the second patient developed euDKA after only 1 week of being on a ketogenic diet while on an SGLT2 inhibitor.

While there have been a few reports of euDKA with SGLT2 inhibitors and ketogenic diets, many physicians prescribing these medications may not be aware of this association. Therefore, they must inform their patients to avoid a ketogenic diet if on an SGLT2 inhibitor. If a patient presents with symptoms of DKA and is eating a carbohydrate-free diet while taking an SGLT2 inhibitor, there should be a low threshold to screen for DKA.

While there have been a few reports of euDKA with SGLT2 inhibitors and ketogenic diets, many physicians prescribing these medications may not be aware of this association. Therefore, they must inform their patients to avoid a ketogenic diet if on an SGLT2 inhibitor. If a patient presents with symptoms of DKA and is eating a carbohydrate-free diet while taking an SGLT2 inhibitor, there should be a low threshold to screen for DKA.