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We report a case of a successful reimplementation of a very low carbohydrate ketogenic diet (VLCKD) after a case of euglycemic diabetic ketoacidosis (euDKA).

A 42-year-old female with a history of type 2 diabetes mellitus on a self-administered VLCKD was prescribed a sodium-glucose co-transporter 2 (SGLT2) inhibitor. Two weeks after initiation, she presented with nausea and vomiting and was found to be in euDKA which was treated with fluid resuscitation, insulin infusion, and cessation of the SGLT2 inhibitor. She was discharged on insulin and instructed not to resume a VLCKD.

After discharge, the patient experienced rapid weight gain and deteriorating glycemic control and desired to resume a VLCKD. She was referred to a university-based medical weight loss clinic that specializes in a VLCKD. The patient was monitored with daily contact via the electronic health record's patient portal and serial laboratory testing while her carbohydrate intake was slowly reduced and her insulin titrated off. She has safely remained in ketosis for 2 years without a further episode of euDKA.

As the clinical use of SGLT2 inhibitors and the VLCKD both become increasingly common, it is vital for practitioners to be aware that the combination can lead to euDKA. We present a case of successfully resuming a VLCKD after recovering from euDKA and cessation of SGLT2 inhibitor therapy.
As the clinical use of SGLT2 inhibitors and the VLCKD both become increasingly common, it is vital for practitioners to be aware that the combination can lead to euDKA. We present a case of successfully resuming a VLCKD after recovering from euDKA and cessation of SGLT2 inhibitor therapy.
Acrodysostosis is a rare skeletal dysplasia with one gene mutation associated with pseudohypoparathyroidism. We describe a 15-year-old male patient with genetic acrodysostosis who presented with hyperparathyroidism.

Laboratory testing, including genetic testing for acrodysostosis and biochemical evaluation for hypercalcemia, were obtained. SR18292 For evaluation of the source of hyperparathyroidism, parathyroid imaging including technetium (99mTc) sestamibi (MIBI) scan, ultrasound, and 4-dimensional computed tomography scans were performed.

The initial calcium level of 11.7 mg/dL (reference range is 8.4 to 10.2 mg/dL), phosphorus of 2.6 mg/dL (reference range is 2.9 to 5.0 mg/dL), and parathyroid hormone (PTH) of 177 pg/mL (reference range is 15 to 65 pg/mL) were suspicious for hyperparathyroidism. Magnesium, albumin, creatinine, and PTH-related peptide levels were normal. His calcium/creatinine ratio was 0.15, calcium/creatinine clearance ratio was 0.008, and the fractional excretion of phosphorus was 34%. Ourcemia are well reported in acrodysostosis. To the best of our knowledge, this is the first reported case of hypercalcemia caused by hyperparathyroidism in a patient with acrodysostosis.
The objective of this report was to describe an unusual case of emerging primary hyperparathyroidism (PHPT) accompanied by recovery of parathyroid blood flow 3 months after spontaneous parathyroid hemorrhage.

Neck images and laboratory tests including serum calcium and parathyroid hormone (PTH) were performed to evaluate parathyroid hemorrhage. Pathologic findings after parathyroidectomy are also presented.

A 58-year-old woman developed acute onset of neck pain and swelling with ecchymosis. Computed tomography showed a right paratracheal hematoma-like lesion behind the thyroid. Ultrasound (US) of the neck revealed a round, hypoechoic nodule measuring 27 × 25 × 18 mm in the right lower thyroid pole without vascular flow. Blood tests showed a corrected calcium of 9.3 mg/dL (normal, 8.7 to 10.3 mg/dL), and intact PTH of 68 pg/mL (normal, 10 to 65 pg/mL). Intact PTH measurement in fine-needle aspirate of the lesion was 339 pg/mL, confirming parathyroid origin. Repeat US after 3 months showed a remarkable defter parathyroid hemorrhage, and so follow-up blood biochemistry surveillance is necessary. Also, evaluating parathyroid blood flow using color Doppler US might be useful in verifying the recurrence of PHPT.
Hypercalcemia associated with the use of sodium-glucose transporter-2 (SGLT-2) inhibitors is very rare. Only 2 cases have been reported in the current literature. In these cases hypercalcemia occurred with the use of SGLT-2 inhibitors taken with thiazides and excessive calcium salts. We present a case of hypercalcemia and primary hyperparathyroidism diagnosed after dapagliflozin treatment.

We describe the medical history, laboratory test results, parathyroid ultrasound, 4-dimensional computed tomography-magnetic resonance imaging, and histopathology findings of the patient.

A 49-year-old man with 5-year history of type 2 diabetes mellitus was found to have hypercalcemia with corrected calcium of 11.28 mg/dL (reference range [RR] is 8.8 to 10.6 mg/dL) 6 months after starting dapagliflozin. Previous records showed normocalcemia for many years. Parathyroid hormone level was 70.8 pg/mL (RR is 15 to 65 pg/mL) and 24-hour urinary calcium excretion level was 492 mg/day (RR is 100 to 300 mg/day). On parathyroidlume depletion caused by SGLT-2 inhibitors may also contribute to hypercalcemia. For these reasons, calcium levels should be monitored in patients taking SGLT-2 inhibitors.
Seizures following administration of potent bisphosphonates have been reported only sporadically in the medical literature. The rare cases described were often attributed to other precipitating factors such as hypoglycemia, acute infection, or predisposition to post-bisphosphonate hypocalcemia. We review the previous cases and present a new case of suspected seizure episode following zoledronic acid therapy.

We describe a case of a 63-year-old woman with a history of well-controlled epileptic disorder with no seizure activity in recent years. She was treated with intravenous zoledronic acid due to osteoporosis. Twelve hours after treatment, she suffered an episode of loss of consciousness with urinary incontinence suspected to be seizure-related.

Unlike previously reported cases, our patient had a low risk for postinfusion hypocalcemia as her creati-nine, calcium, parathyroid hormone, and vitamin D were all within normal limits prior to the infusion.

Our interpretation of the scenario described is based on clinical judgment and not supported by ancillary studies.
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