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Hypercalcemia can result from either hyperparathyroidism or non-parathyroid conditions. When hypercalcemia is accompanied by undetectable parathyroid hormone (PTH) levels, hyperparathyroidism is rarely considered the diagnosis. Herein, we report the case of a 65-year-old Caucasian woman referred to our hospital for further evaluation of hypercalcemia. Her symptoms included fatigue and brain fog, with undetectable PTH levels. A comprehensive workup, including a series of laboratory and imaging tests, excluded common non-parathyroid causes such as malignancy and familial hypocalciuric hypercalcemia. Ultrasound identified a likely enlarged parathyroid gland, which was further confirmed by a sestamibi scan. After 2 weeks of cinacalcet treatment, the patient's calcium levels decreased, indicating the parathyroid gland as the likely source of hypercalcemia. Parathyroidectomy was subsequently performed, revealing a 1927 mg adenoma. Postoperatively, the patient's calcium levels normalized, PTH levels became detectable within the normal range, and her symptoms resolved, with a marked improvement in energy. This case demonstrates that primary hyperparathyroidism can present with hypercalcemia and undetectable PTH. A genetic mutation in the PTH gene within the adenoma may explain the undetectable PTH levels preoperatively. Plain Language Summary: This case report discusses a 65-year-old woman who was found to have high calcium levels in her blood, a condition known as hypercalcemia. Typically, hypercalcemia can result from either a condition where the parathyroid glands produce too much parathyroid hormone (PTH) or from other non-parathyroid-related issues like cancer. However, when hypercalcemia occurs with undetectable levels of PTH, it is unusual for hyperparathyroidism to be the cause. In this patient's case, she experienced symptoms like fatigue and brain fog, but her initial tests showed undetectable PTH levels. Further tests ruled out other common causes of high calcium, such as cancer or a genetic condition called familial hypocalciuric hypercalcemia. An ultrasound and a special scan called a sestamibi scan revealed an enlarged parathyroid gland, suggesting the presence of a parathyroid adenoma, a non-cancerous tumor. To confirm this, the doctors gave the patient a medication called cinacalcet, which is known to lower calcium levels if the parathyroid glands are involved. After two weeks of treatment, her calcium levels dropped, indicating that the parathyroid gland was indeed the source of the problem. The patient underwent surgery to remove the adenoma, which weighed nearly two grams. Following the surgery, her calcium levels returned to normal, and her PTH levels became detectable again within the normal range. Her symptoms, including fatigue, improved significantly, and she reported feeling more energetic. This case is unusual because it demonstrates that primary hyperparathyroidism can still be the cause of hypercalcemia even when PTH levels are initially undetectable. The doctors suspect that a genetic mutation in the adenoma might explain why PTH levels were undetectable before surgery. This case emphasizes the importance of thorough clinical evaluation, even when initial test results are not typical. [ABSTRACT FROM AUTHOR]

Background: Stiff person syndrome spectrum disorders (SPSD) are rare, disabling disorders of the nervous system that are associated with risk factors for Coronavirus disease 2019 (COVID-19). However, limited data exist on the overall impact of COVID-19 on SPSD. Methods: Patients with SPSD and COVID-19 who are followed at Johns Hopkins SPS Center were included. Demographics and SPSD characteristics along with COVID-19-specific data were recorded. Results: Thirty-five cases of SPSD with COVID-19 cases were reported during the study time period. Mean age of the cohort was 56 (SD ± 10) and most were female (66.7%). Eighty percent of the COVID-19 cases were confirmed with testing, and the rest were highly suggestive of COVID-19. COVID-19 comorbidities among patients were hypertension (n = 6), diabetes (n = 6), obesity (n = 5), and cardiovascular disease (n = 4). The majority of participants were on immune therapies and/or benzodiazepines. Out of the cases reported, only 2 required hospitalization, both of whom had diabetes, and one was on immunosuppressive therapy. The majority of cases were post-full-vaccination cases. Fever was the most common COVID-19-associated symptom. Transient neurological symptoms were also reported. Conclusion: Risk factors for developing severe COVID-19 in SPSD appear to be the same as historical data in the general population. Importantly, COVID-19 did not appear to be associated with worsening SPSD post-COVID-19. Vaccination may have played a role in preventing severe cases of COVID-19. [ABSTRACT FROM AUTHOR]

Background: While males present with more adverse clinicopathologic features in papillary thyroid carcinoma (PTC), younger age has previously been shown to be a favorable prognostic factor. We examined the combined effect of male sex and young age on PTC outcomes. Methods: We conducted a retrospective analysis of a prospectively maintained database of thyroid cancer surgery patients (2000–2020) at a single quaternary care institution. We included papillary thyroid carcinoma cases and excluded those with prior cancer‐related thyroid surgery. We examined demographics, cancer stage, surgical outcomes, and complications by age and sex, analyzing groups below and above the age of 40 years. Results: A total of 680 patients with PTC were included. Females constituted 68% (age ≥40 years: 44% and <40 years: 24%) and males 32% (≥40 years: 24% and <40 years: 8%). A significant difference (p < 0.001) of N1 disease distribution was found between the groups. N1a metastasis was greater in patients younger than 40 regardless of sex ((M < 40 (15%), F < 40 (15%), M ≥ 40 (12%), and F ≥ 40 (9%)). While, M < 40 had greater N1b metastasis (36%) than all other groups (M ≥ 40 (28%), F < 40 (22%), and F ≥ 40 (10%)). There was no significant difference in the distribution of T stages between groups. Groups showed no differences in 30‐day outcomes, recurrence at 1 year, reoperation, mortality, nerve injury, or hypocalcemia. Conclusions: Young males with PTC face increased occurrence of nodal metastasis yet experience similar recurrence rates as their female and older counterparts. Subgroup analysis underscores the predictive role of sex and age in advanced PTC cases. [ABSTRACT FROM AUTHOR]

Context There are differences in diagnosis, treatment, and outcomes for thyroid between racial and ethnic groups that contribute to disparities. Identifying these differences and their causes are the key to understanding and reducing disparities in presentation and outcomes in endocrine disorders. Evidence Acquisition The present study reviews original studies identifying and exploring differences between benign and malignant thyroid diseases. A PubMed, Web of Science, and Scopus search was conducted for English-language studies using the terms " thyroid ," " thyroid disease ," " thyroid cancer ," " race ," " ethnicity ," and " disparities " from inception to December 31, 2022. Evidence Synthesis Many racial and ethnic disparities in the diagnosis, presentation, treatment, and outcomes of thyroid disease were found. Non-White patients are more likely to have a later time to referral, to present with more advanced disease, to have more aggressive forms of thyroid cancer, and are less likely to receive the appropriate treatment than White patients. Overall and disease-specific survival rates are lower in Black and Hispanic populations when compared to White patients. Conclusions Extensive disparities exist in thyroid disease diagnosis, treatment, and outcomes that may have been overlooked. Further work is needed to identify the causes of these disparities to begin to work toward equity in the care of thyroid disease. [ABSTRACT FROM AUTHOR]

Background Hyperparathyroidism (HPT) and malignancy are the most common causes of hypercalcemia. Among kidney transplant (KT) recipients, hypercalcemia is mostly caused by tertiary HPT. Persistent tertiary HPT after KT is associated with allograft failure. Previous studies on managing tHPT were subjected to survivor treatment selection bias; as such, the impact of tertiary HPT treatment on allograft function remained unclear. We aim to assess the association between hypercalcemic tertiary HPT treatment and kidney allograft survival. Materials and Methods We identified 280 KT recipients (2015-2019) with elevated post-KT adjusted serum calcium and parathyroid hormone (PTH). KT recipients were characterized by treatment: cinacalcet, parathyroidectomy, or no treatment. Time-varying Cox regression with delayed entry at the time of first elevated post-KT calcium was conducted, and death-censored and all-cause allograft failure were compared by treatment groups. Results Of the 280 recipients with tHPT, 49 underwent PTx, and 98 received cinacalcet. The median time from KT to first elevated calcium was 1 month (IQR: 0-4). The median time from first elevated calcium to receiving cinacalcet and parathyroidectomy was 0(IQR: 0-3) and 13(IQR: 8-23) months, respectively. KT recipients with no treatment had shorter dialysis vintage (P  = .017) and lower PTH at KT (P  = .002), later onset of hypercalcemia post-KT (P  < .001). Treatment with PTx (adjusted hazard ratio (aHR) = 0.18, 95%CI 0.04-0.76, P  = .02) or cinacalcet (aHR = 0.14, 95%CI 0.004-0.47, P  = .002) was associated with lower risk of death-censored allograft failure. Moreover, receipt of PTx (aHR = 0.28, 95%CI 0.12-0.66, P  < .001) or cinacalcet (aHR = 0.38, 95%CI 0.22-0.66, P  < .001) was associated with lower risk of all-cause allograft failure. Conclusions This study demonstrates that treatment of hypercalcemic tertiary HPT post-KT is associated with improved allograft survival. Although these findings are not specific to hypercalcemia of malignancy, they do demonstrate the negative impact of hypercalcemic tertiary HPT on kidney function. Hypercalcemic HPT should be screened and aggressively treated post-KT. [ABSTRACT FROM AUTHOR]