Case Reports in Endocrinology最新文献

Neonatal diabetes mellitus (NDM) is a monogenic form of diabetes. Management of hyperglycemia in neonates with subcutaneous insulin is challenging because of frequent feeding, variable quantity of milk intake with each feed, low insulin dose requirements, and high risk for hypoglycemia and associated complications in this population. We present a case of NDM in a proband initially presenting with focal seizures and diabetic ketoacidosis due to a pathologic mutation in the beta cell potassium ATP channel gene KCNJ11 c.679G > A (p.E227K). We describe the use of continuous glucose monitoring (CGM), insulin pump, automated insulin delivery system, and remote patient monitoring technologies to facilitate rapid and safe outpatient cross-titration from insulin to oral sulfonylurea. Our case highlights the safety and efficacy of these technologies for infants with diabetes, including improvements in glycemia, quality of life, and cost-effectiveness by shortening hospital stay.

Background: Acute Sheehan's syndrome is rare, as well as hyponatremia as its initial manifestation. In addition, spontaneous pregnancy in patients after Sheehan's syndrome is unusual. To our knowledge, no cases of spontaneous pregnancy after acute Sheehan's syndrome have been reported. We describe a case of Sheehan's syndrome that presented with acute hyponatremia and a spontaneous pregnancy.

Case: A 34-year-old female developed blood loss during delivery, which required a blood transfusion. On day seven postpartum, she presented with headaches, lethargy, and difficulty in breastfeeding. The workup showed hyponatremia (118 mEq/l), secondary hypothyroidism, and low prolactin levels. Magnetic resonance imaging showed pituitary necrosis. She was treated with NaCl, hydrocortisone (cortisol results were not available), and levothyroxine. Laboratory tests six weeks after discharge showed low IGF-1 and 8 AM cortisol and normal FT4, LH, FSH, and PRL levels. She was able to partially breastfeed until 4 months postpartum. Regular menstrual cycles started three months later. She became spontaneously pregnant one year later.

Conclusion: Acute Sheehan's syndrome should be considered in the evaluation of postpartum patients with suggestive symptoms. Physicians should be aware that hyponatremia could be an initial manifestation of Sheehan's syndrome, which requires a high index of suspicion for diagnosis. Spontaneous pregnancy can occur after acute Sheehan's syndrome.

Background: SARS-CoV-2 has been known to cause multisystemic involvement, gaining entry through ACE-2 and TMPRSS2 receptors. COVID-19 vaccine-associated thyroiditis cases are now being reported. Case Report. Case 1. A 36-year-old woman with a history of right hemithyroidectomy for a benign thyroid nodule, on a stable dose of levothyroxine with euthyroid labs, presented with progressively worsening left neck pain, episodic palpitations, and heat intolerance after the second dose of mRNA1273 (Moderna) vaccine. Examination revealed an enlarged and tender left lobe of the thyroid with suppressed TSH but normal free T4 and ESR, signifying subacute thyroiditis. She was managed conservatively without corticosteroids or beta-blockers, and her symptoms resolved. A follow-up revealed increasing TSH, and levothyroxine was restarted. Case 2. A 33-year-old man with a history of anxiety disorder on Sertraline, presented with a two-week history of palpitations, heat intolerance, and 10-pound weight loss after the second dose of BNT162b2 (Pfizer-BioNTech) vaccine. Examination revealed a normal thyroid gland with no tenderness with elevated thyroid peroxidase and thyroglobulin antibodies. Ultrasound showed a diffusely heterogeneous thyroid with increased vascularity, suggesting silent thyroiditis. Follow-up revealed a hypothyroid phase with high TSH for which levothyroxine supplementation was started. Discussion. COVID-19 vaccine-associated subacute and silent thyroiditis have occurred following all three kinds of available vaccines, characterized by an initial thyrotoxic phase, followed by a hypothyroid phase and a recovery phase. Hypotheses include an immune response triggering thyroid inflammation or cross-reactivity with viral proteins.

Conclusions: COVID-19 vaccine-associated thyroiditis is rare, but long-term monitoring of these patients is essential to ensure appropriate diagnosis and management of the potential hypothyroid phase.

Acquired hypothyroidism due to iodine deficiency is extremely rare in the United States due to the introduction of table salt iodization in the 1920s (Leung et al., 2012). We present the case of an adolescent male with a history of mild autism spectrum disorder and an extremely restrictive diet who was found to have iodine deficiency as the etiology for his rapidly enlarging goiter and antibody-negative hypothyroidism. Thyroid-stimulating hormone (TSH) was 416 μIU/mL (0.350-5.500 μIU/mL), free thyroxine (T4) was <0.1 ng/dL (0.80-1.80 ng/dL), and triiodothyronine (T3) was 41 ng/dL (82-213 mg/dL) at diagnosis. The patient's 24-hour urinary iodine was undetectable. He was started on iodine supplementation with rapid visible improvement of goiter within two weeks and normalization of thyroid function tests within four weeks. Thorough dietary history and nutritional screening are important in cases of acquired hypothyroidism and/or goiter. Alternatively, diets that are low in iodized salt, dairy, bread, and seafood should raise concern for iodine deficiency, and patients with suspected or proven iodine deficiency should be screened for hypothyroidism.

Parathyroid adenoma is the most common cause of primary hyperparathyroidism (PHPT). We present the preoperative detection of a giant parathyroid adenoma (GPA) using (^99mTc)-sestamibi parathyroid scintigraphy in a patient presenting with severely elevated parathyroid hormone, hypercalcemia, hypophosphatemia, and vitamin D insufficiency. The patient complained of cerebral symptoms and intermittent abdominal discomfort without constipation. After surgical removal of the hyperactive parathyroid gland and D vitamin supplementation, all blood tests were normalized. The clinical and paraclinical characteristics of GPA may raise the suspicion of parathyroid carcinoma, but not absolutely in this case.

Hypophosphatemia is a less known complication of parenteral iron use, particularly after the use of certain iron formulations. We report the case of a young male with inflammatory bowel disease and iron deficiency anemia, who developed severe symptomatic hypophosphatemia after his third exposure to iron carboxymaltose with no evidence of the same occurring upon prior exposures to the compound. Investigations revealed serum phosphorous levels of 0.7 mg/dl, corrected serum calcium of 8-9.5 mg/dl, alkaline phosphatase of 50 U/L (38-126), 25 hydroxy vitamin D level of 40.2 ng/ml, and intact PTH elevated to 207 pg/ml. Urine studies indicated renal phosphate wasting. Presentation was not in keeping with refeeding syndrome. Intact fibroblast growth factor 23 level, measured after the initiation of treatment was within the normal range at 179 RU/mL (44-215). 1,25 dihydroxy vitamin D level, also measured after the initiation of treatment, was normal at 26.3 pg/ml (19.9-79.3). The patient was treated with calcitriol and aggressive oral and intravenous phosphorous repletion. Symptoms then resolved and the patient was discharged on an oral regimen. This phenomenon is postulated to occur due to an increase in the level and activity of FGF23 and decreased cleavage of the same, due to anemia as well as use of specific iron formulations. This is the first instance, in our literature review, of this complication known to occur, not after initial exposure to an implicated iron formulation but occurring on subsequent exposure.

Nesidioblastosis is a rare pancreatic disorder involving enlarged beta cells throughout the pancreas, causing elevated insulin production. We present the case of a 53-year-old woman with the initial symptom of fasting hypoglycemia. No pancreatic lesions were indicated on computed tomography and magnetic resonance imaging scans, and an octreotide scan was negative for insulinoma. Selective arterial calcium stimulation (SACST) showed increased insulin production from the stimulation of 3 out of 5 arteries. The SACST results suggested a diagnosis of nesidioblastosis, which was confirmed by histopathology after a subtotal distal pancreatectomy. The patient has normal glucose tolerance after surgery with no further problems of hypoglycemia, indicating that this is a rare case of nesidioblastosis extending only partially through the pancreas.

Thyrotoxic periodic paralysis (TPP) is an entity that has been described in the literature as a transient, symmetrical, flaccid paralysis, mainly affecting the lower limbs of patients with a current or previous history of hyperthyroidism. In most cases, Graves' disease is the cause of hyperthyroidism. Contrast and iodine-induced TPP have been described in the literature, but only one case of intravenous contrast induced TPP has been reported. We report a case of TPP following administration of intravenous contrast for a computed tomography scan of the neck prior to lymph node excision. A 35-year-old Kuwaiti male with known Graves' disease in remission until two months of his presentation, reported to the emergency room one early morning in December 2020. He sustained a fall from the stairs due to bilateral lower limb weakness, mostly proximal. The upper limbs were spared, and the patient did not experience any numbness or headache. His potassium was found to be 2.1 mmol/L and an electrocardiogram showed U waves and ST segment changes. He was initiated on 20 mEq of intravenous potassium chloride in 500 mL sodium chloride over one hour, following which his potassium approached normal and his weakness resolved. He was last known to be euthyroid in November 2019 but noted in October 2020 to be in the hyperthyroid state when thyroid function testing showed a thyroid-stimulating hormone of <0.005 (0.27-4.2 uIu/mL) and free thyroxine (T4) of 27.6 (7.8- pmol/L). In patients with known hyperthyroidism, more caution is required when iodine-containing substances are administered without proper evaluation of thyroid function.

A 23-year-old African American male with a medical history significant for poorly controlled type 1 diabetes mellitus (T1DM) presented with abdominal pain and vomiting. His laboratory workup was consistent with diabetic ketoacidosis (DKA). An acute elevation of liver enzymes was noted as the DKA resolved, with the alanine transferase and aspartate transferase levels elevated to more than 50 times the normal limit within the next 24 hours. Because abnormal liver function tests are found frequently in patients with type 1 diabetes mellitus, it is important to have a broad differential diagnosis. Furthermore, a low threshold of suspicion is required to identify a relatively underdiagnosed etiology like glycogenic hepatopathy (GH). This case report describes how patterns and trends of liver function tests provide important clues to the diagnosis of GH; how imaging modalities like ultrasonography, computerized tomography (CT) scan, and magnetic resonance imaging (MRI) scan could be used to differentiate GH from nonalcoholic fatty liver disease (NAFLD); and how the diagnosis of GH can be made without the need for invasive liver biopsy. The knowledge about GH should prevent its delayed diagnosis and improve the outcomes by appropriately managing uncontrolled type 1 DM.