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We present a possible explanation for why there is an increased risk for the development of Charcot neuroarthropathy in pregnancy.
Bilateral concurrent Charcot neuroarthropathic foot is uncommon, and to our knowledge, this is the first reported case in pregnancy. We present a possible explanation for why there is an increased risk for the development of Charcot neuroarthropathy in pregnancy.
To evaluate the case of a woman who presented with central hypogonadism and diabetes insipidus and further developed a persistent cough leading to an unexpected diagnosis of burnt-out Langerhans cell histiocytosis (LCH).
Clinical and laboratory endocrine evaluation, magnetic resonance imaging, high-resolution computed tomography, and open-lung biopsy results are discussed.
A 28-year-old woman presented at 10 months postpartum with polydipsia, polyuria, and amenorrhea for 3 months. Her results showed a prolactin level of 25 μg/L (reference,<23.5 μg/L), estrogen level of 91 pmol/L (reference, 110-180 pmol/L), follicle-stimulating hormone level of 6 IU/L (reference, 2-20 IU/L), and luteinizing hormone level of 6 IU/L (reference, 2-70 IU/L). A water-deprivation test found a sodium concentration of 148 mmol/L (reference, 135-145 mmol/L), serum osmolality of 310 mmol/kg (reference, 275-295 mmol/kg), and urine osmolality of 107 mmol/kg (reference, 50-1450 mmol/kg) that improved to 142 mEq/L, 295 mmol/kg, anesolution computed tomography led to a unifying definitive diagnosis of burnt-out LCH. This case highlights the importance of investigating for uncommon secondary causes of hypophysitis.
Many tumors can metastasize to the adrenal glands, making the diagnosis of adrenal masses challenging. Awareness that rare primary tumors can metastasize to the adrenals and consideration of biopsy for their diagnosis, sometimes at extra-adrenal sites, is essential to prevent unnecessary adrenalectomies and facilitate the right treatment. We report a rare case of bilateral adrenal masses due to metastasis from a nonseminomatous germ-cell tumor of a retroperitoneal lymph node origin.
The diagnosis of the adrenal masses from the nonseminomatous germ-cell tumor of a retroperitoneal lymph node origin was based on a retroperitoneal lymph node core biopsy. An initial core biopsy of the adrenal gland revealed necrotic tissue and inflammatory cells without evidence of malignancy. Due to nondiagnostic findings, the core biopsy was repeated, which showed degenerating cells with a high mitotic index and immunohistochemical staining positive for vimentin, suggesting the possibility of a high-grade sarcoma. A retropers in a young man, found to have metastasized from nonseminomatous germ-cell tumors. Histopathologic confirmation of the metastatic tumor was done, which prevented unnecessary adrenalectomy. The patient received appropriate chemotherapy.
We report a rare case of rapidly progressing adrenal masses in a young man, found to have metastasized from nonseminomatous germ-cell tumors. Histopathologic confirmation of the metastatic tumor was done, which prevented unnecessary adrenalectomy. The patient received appropriate chemotherapy.
To describe the rare occurrence of pediatric Hashimoto encephalopathy in 3 patients.
The patients, 9 to 13 years of age, presented with new-onset seizures and other neurologic symptoms, including hemiplegia, aphasia, and memory loss. Thyroid function tests and thyroid antibodies were measured. Magnetic resonance imaging (MRI) of the brain, cerebrospinal fluid analysis, and electroencephalography were also performed.
The first patient had a thyroid-stimulating hormone (TSH) level of 60 μIU/mL (range, 0.4-4.5), free T4 of 0.28 ng/dL (range, 0.7-1.6), and thyroid peroxidase antibody (TPO Ab) of 1243 IU/mL (range<9). The MRI results indicated a hyperintense signal along the gyri and sulci with diffuse leptomeningeal enhancement bilaterally. The second patient had a TSH level of 25 μIU/mL, free T4 level of 0.7 ng/dL, and TPO Ab level of 3340 IU/mL. The MRI result was normal. Epacadostat The third patient, who was already on levothyroxine, had a TSH level of 17 μIU/mL, free T4 level of 0.81 ng/dL, and TPO Ab level of 1200 IU/mL. The MRI result was normal. All patients had significant elevation of protein in the cerebrospinal fluid and background slowing on electroencephalography. All patients were treated with high doses of intravenous methylprednisolone followed by oral prednisone and thyroid hormone replacement.
These cases underscore the importance of thyroid function tests with antibodies in children presenting with acute neuropsychiatric manifestations, especially new-onset seizures without any identifiable cause. We believe that this condition is underdiagnosed in children, and a high index of suspicion is recommended.
These cases underscore the importance of thyroid function tests with antibodies in children presenting with acute neuropsychiatric manifestations, especially new-onset seizures without any identifiable cause. We believe that this condition is underdiagnosed in children, and a high index of suspicion is recommended.
Concurrent autoimmune disorders, including autoimmune hepatitis (AIH), with Graves disease have been reported. Glucocorticoids can simultaneously lower thyroid hormone levels and treat AIH. Recurrence of hyperthyroidism is associated with recurrence of hepatitis. We present a case of coexisting AIH and Graves thyrotoxicosis, which improved with prednisone, but the thyrotoxicosis recurred during a prednisone taper while the hepatitis stayed in remission.
Evaluation included measurements of liver enzyme levels, thyroid function tests, and thyroid-stimulating antibodies as well as abdominal ultrasound, magnetic resonance imaging, and liver biopsy.
A 47-year-old woman presented with nausea and jaundice. Workup showed an aspartate aminotransferase level of 1956 (reference, 10-42) U/L and alanine aminotransferase level of 1634 (reference, 14-54) IU/L. The liver biopsy was consistent with AIH. Nine months later, she reported palpitations, heat intolerance, and weight loss and was diagnosed with Graves disease. The patient received prednisone at 60 mg daily, and the liver and thyroid functions normalized after 1 month. Prednisone was tapered to 5 mg daily. Seven months later, she presented with a thyroid-stimulating hormone level of 0.049 (reference, 0.340-5.6) μIU/mL) and free thyroxine level of 3.96 (reference, 0.58-1.64) ng/dL. Liver enzymes remained at normal levels. Prednisone was increased from 5 to 20 mg to treat hyperthyroidism. The patient was referred for thyroidectomy for a diagnosis of Graves disease with thyrotoxicosis.
This case is an example of coexisting autoimmune diseases, Graves disease and AIH, with different clinical courses. Despite initial resolution with glucocorticoid therapy, Graves disease recurred, while AIH stayed in remission.
This case is an example of coexisting autoimmune diseases, Graves disease and AIH, with different clinical courses. Despite initial resolution with glucocorticoid therapy, Graves disease recurred, while AIH stayed in remission.
Adrenal insufficiency (AI), if not diagnosed in a timely manner, can lead to fatal outcomes. Here we describe an unusual case of AI secondary to disseminated histoplasmosis (DH) and the importance of being aware of the association of infections and AI.
A 56-year-old Hispanic man with untreated HIV infection presented for the evaluation of left upper jaw swelling and pain. A brain magnetic resonance imaging scan revealed a 4-cm soft-tissue mass in the left maxilla. Biopsy of the mass was consistent with histoplasmosis. He was also noted to have hyponatremia and hyperkalemia, which raised the suspicion of AI. Laboratory investigation showed a baseline cortisol level of 7 μg/dL (normal, 7-23 μg/dL) and adrenocorticotropic hormone level of 86 pg/mL (normal, 7-69 pg/mL). His 60-minute cortisol level after a 250-μg cosyntropin stimulation test was 9μg/dL (normal, 7-23 μg/dL). Computed tomography of the chest incidentally noted bilateral adrenal enlargement. An adrenal biopsy was not pursued due to the high index of clinical suspicion of DH as the etiology of AI.
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.
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