Birchfallesen4637
his setting.
Vitamin D deficiency is prevalent worldwide and is usually treated with oral supplementation. Bioavailability of vitamin D may differ among individuals due to variable absorption and metabolism in the body.
A 66-year-old woman presented for evaluation of low 25-hydroxyvitamin D (25[OH]D) level. She had no known prior history of gastric or intestinal surgeries or malabsorptive conditions. She had previously been treated with oral vitamin D
at 2,000 IU daily with poor response. She was then treated with oral vitamin D
at 50,000 IU weekly, with persistently low 25(OH)D level at 14 ng/mL after 8 weeks of treatment.
Celiac screen was negative and duodenal biopsy was normal. Due to demonstration of poor oral absorption, she was prescribed vitamin D
at 50,000 IU sublingually for 8 weeks and then changed to over-the-counter vitamin D
drops sublingually (1,000 IU/drop) at 4,000 IU twice daily due to suboptimal response with vitamin D
. 25(OH)D level improved gradually to 28 ng/mL after 12 weeks on this regimen and was at 37 ng/mL at 1 year.
Sublingual vitamin D
may be an effective alternative mode of vitamin D supplementation in patients who demonstrate poor oral vitamin D absorption despite adequate supplementation for various reasons.
Sublingual vitamin D3 may be an effective alternative mode of vitamin D supplementation in patients who demonstrate poor oral vitamin D absorption despite adequate supplementation for various reasons.
Isolated adrenocorticotropic hormone (ACTH) deficiency is characterized by loss of adrenocorticotropic hormone, resulting in adrenal insufficiency, which can lead to life threatening severe hypoglycemia. We report a case of isolated ACTH deficiency with emphases on presentation, common etiologies, diagnosis, and management.
The clinical course in addition to laboratory and imaging results are presented. These include cortisol level, ACTH, other pituitary hormones, insulin tolerance test, pituitary antibodies, and pituitary magnetic resonance imaging.
A 19-year-old male was brought by ambulance to the emergency department with loss of consciousness and a random blood sugar of 30 mg/dL. Our patient had a barely detectable level of plasma ACTH repeatedly and cortisol <1 μg/dL. There was no involvement of other pituitary hormones. Steroid replacement therapy led to resolution of all symptoms and prevented further episodes of hypoglycemia.
Isolated ACTH deficiency is a rare condition that is challenging to diagnose and can lead to serious life-threatening problems if unrecognized. Proper management can be achieved with appropriate hydrocortisone supplementation to mimic the normal secretion under both normal conditions and during a state of stress.
Isolated ACTH deficiency is a rare condition that is challenging to diagnose and can lead to serious life-threatening problems if unrecognized. Proper management can be achieved with appropriate hydrocortisone supplementation to mimic the normal secretion under both normal conditions and during a state of stress.
To discuss the diagnosis and management of paraprotein interference in the setting of multiple myeloma (MM).
We discuss the evaluation of hypophosphatemia in a patient with MM and present a review of the relevant literature.
Our patient, who had a history of MM, was found to have persistently undetectable serum phosphate which did not respond to aggressive phosphate replacement. His clinical condition was not consistent with severe phosphate depletion and hence paraprotein interference secondary to MM was suspected. Re-analyzation of samples on a different machine showed normal serum inorganic phosphate levels.
Paraprotein interference from MM causing pseudohypophosphatemia can be overlooked and lead to unnecessary treatment. Recognition of this phenomenon is important to all clinicians, especially in light of potential complications of unnecessary treatment.
Paraprotein interference from MM causing pseudohypophosphatemia can be overlooked and lead to unnecessary treatment. Recognition of this phenomenon is important to all clinicians, especially in light of potential complications of unnecessary treatment.
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. this website 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. 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. Nevertheless, our case, along with the limitations described, joins other reports, and raises questions about possible interaction between a convulsion disorder and a potent bone resorption inhibition administration, leading to a relative hypocalcemia and possible seizure threshold reduction. This question should be further explored by other studies.
Our interpretation of the scenario described is based on clinical judgment and not supported by ancillary studies. Nevertheless, our case, along with the limitations described, joins other reports, and raises questions about possible interaction between a convulsion disorder and a potent bone resorption inhibition administration, leading to a relative hypocalcemia and possible seizure threshold reduction. This question should be further explored by other studies.
