UNASSIGNED: Primary hyperparathyroidism is a commonly occurring endocrine disorder that is characterized by elevated calcium levels, decreased phosphate levels, and high levels of parathyroid hormone (PTH). The condition can lead to significant bone resorption and pathological fractures.
UNASSIGNED: We report a case of a 44-year-old female who presented with bilateral thigh pain after a trivial fall at home. Radiological investigations revealed a subtrochanteric fracture of the bilateral femur that was deemed pathological. Biochemical testing indicated severe hypercalcemia and hypophosphatemia with elevated levels of serum PTH and an increased alkaline phosphatase level. Ultrasound and computed tomography scans confirmed a parathyroid adenoma, which was treated through excision and histopathological examination. The patient underwent orthopedic intervention for bilateral subtrochanteric femur fracture, and follow-up investigations showed normal biochemical markers and fracture union within 6 months.
UNASSIGNED: Primary hyperparathyroidism should be kept in mind when dealing with bone lesions connected to hypercalcemia, even in asymptomatic individuals and individuals presenting with a trivial mode of trauma. The diagnosis of parathyroid adenoma requires a combination of radiological and biochemical investigations, and a multidisciplinary approach is recommended for the best possible outcome.

Primary Hyperparathyroidism (PHPT) is characterized by excessive parathormone (PTH) secretion and disrupted calcium homeostasis. Untargeted metabolomics offers a valuable approach to understanding the complex metabolic alterations associated with different diseases, including PHPT. Plasma untargeted metabolomics was applied to investigate the metabolic profiles of PHPT patients compared to a control group. Two complementary liquid-phase separation techniques were employed to comprehensively explore the metabolic landscape in this retrospective, single-center study. The study comprised 28 female patients diagnosed following the current guidelines of PHPT diagnosis and a group of 30 healthy females as a control group. To evaluate their association with PHPT, we identified changes in plasma metabolic profiles in patients with PHPT compared to the control group. The primary outcome measure included detecting plasma metabolites and discriminating PHPT patients from controls. The study unveiled specific metabolic imbalances that may link L-amino acids with peptic ulcer disease, gamma-glutamyls with oxidative stress, and asymmetric dimethylarginine (ADMA) with cardiovascular complications. Several metabolites, such as gamma-glutamyls, caffeine, sex hormones, carnitine, sphingosine-1-phosphate (S-1-P), and steroids, were connected with reduced bone mineral density (BMD). Metabolic profiling identified distinct metabolic patterns between patients with PHPT and healthy controls. These findings provided valuable insights into the pathophysiology of PHPT.

Primary hyperparathyroidism (PHPT) is the leading cause of hypercalcemia. It is secondary to hypersecretion of parathyroid hormone (PTH) by the parathyroid glands. Today, PHTP is asymptomatic in 80-90% of cases. Its repercussions are mainly renal (nephrolithiasis, nephrocalcinosis, decline in renal function) and skeletal (osteoporosis, fractures), and should be systematically investigated. Diagnosis is only biological, and in its classic form relies on the association of hypercalcemia, inappropriate PTH (normal or elevated) and hypercalciuria. Diagnosis of normocalcemic forms, where only PTH is elevated, requires elimination of secondary hyperparathyroidism and confirmation of elevated PTH on two consecutive samples, over a 3 to 6 months period. Imaging evaluation, which combines neck ultrasound with scintigraphy or 18F-choline PET/CT, is of interest only if surgery is indicated. Surgical management of the hyperfunctioning parathyroid gland(s) is the only curative treatment for HPTP. Medical management concerns patients for whom surgery is not indicated, who present a surgical contraindication or who refuse surgery. The diagnosis of HPTP warrants contact with an endocrinologist to ensure its management.

BACKGROUND: Primary hyperparathyroidism (PHPT) patients commonly report weakness and fatigue, though the underlying mechanisms are uncertain. Our purpose is to determine whether CT-derived muscle and adipose tissue metrics are associated with weakness and fatigue in PHPT patients.
METHODS: For this retrospective study, cross-sectional muscle and adipose tissue metrics were derived from CTs in PHPT patients undergoing preoperative imaging within 1 year of parathyroid surgery. Skeletal muscle index (SMI) and visceral adipose tissue (VAT)/subcutaneous adipose tissue (SAT) ratio were calculated based on a single CT image at the level of the L3 vertebra. Established sex-specific SMI thresholds were used to define sarcopenia. Demographic and clinical data were collected from the electronic health record. When available, postoperative CT images were analyzed to assess for changes in body composition pre- and post-parathyroidectomy.
RESULTS: The cohort comprised 53 PHPT patients (38 females, 15 males, mean age 61.4 years), of whom 24 (45%) reported weakness, 43 (81%) reported fatigue, and 31 (58%) met CT-based criteria for sarcopenia. Lower SMI was significantly associated with preoperative weakness in females but not males. For both weakness and fatigue, VAT/SAT ratios were higher in symptomatic females and lower in symptomatic males than their asymptomatic counterparts, though these differences were not statistically significant. In patients with postoperative CTs (n = 23), no significant changes in CT metrics were observed after parathyroidectomy.
CONCLUSIONS: In females but not males with PHPT, subjective preoperative weakness was significantly associated with lower SMI. Effects of parathyroid hormone on skeletal muscle and visceral adiposity may differ by sex.

Diagnosing primary hyperparathyroidism in pregnancy is difficult due to pregnancy-related changes in parathyroid hormone (PTH); calcium; 1,25 vitamin D; and renal calcium excretion. Parathyroid hormone-related peptide (PTHrP) produced by the placenta adds additional complexity. Our case is the first to demonstrate an increased rate of PTH degradation within a pregnant individual who returned unexpectedly low PTH levels. We describe a 27-year-old female patient who presented at 25 weeks gestation with pancreatitis and hypercalcemia. Primary hyperparathyroidism was suspected but variable PTH results led to uncertainty and an assay error was considered. PTH samples were collected in both serum-separating tubes (SST) and EDTA tubes and compared to controls (5 nonpregnant and 5 pregnant individuals). Samples were retested every 2 hours for a period of 10 hours. A rapid decline in the measured PTH was noted in the index case, an observation which differed from controls. We postulated that internal and/or external factors influenced the PTH measurement obtained from our patient. From our observations, rapid PTH degradation in pregnancy, and individual variation in PTH stability and laboratory processes, can influence PTH results and impact on interpreting hypercalcemia in pregnancy.

BACKGROUND: Primary hyperparathyroidism (PHPT)-induced acute pancreatitis (AP) during pregnancy has rarely been described. Due to this rarity, there are no diagnostic or treatment algorithms for pregnant patients.
OBJECTIVE: To determine appropriate diagnostic methods, therapeutic options, and factors related to maternal and fetal outcomes for PHPT-induced AP in pregnancy.
METHODS: A literature search of articles in English, Japanese, German, Spanish, and Italian was performed using PubMed (1946-2023), PubMed Central (1900-2023), and Google Scholar. The Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) protocol was followed. The search terms included \"pancreatite acuta,\" \"iperparatiroidismo primario,\" \"gravidanza,\" \"travaglio,\" \"puerperio,\" \"postpartum,\" \"akute pankreatitis,\" \"primärer hyperparathyreoidismus,\" \"Schwangerschaft,\" \"Wehen,\" \"Wochenbett,\" \"pancreatitis aguda,\" \"hiperparatiroidismo primario,\" \"embarazo,\" \"parto,\" \"puerperio,\" \"posparto,\" \"acute pancreatitis,\" \"primary hyperparathyroidism,\" \"pregnancy,\" \"labor,\" \"puerperium,\" and \"postpartum.\" Additional studies were identified by reviewing the reference lists of retrieved studies. Demographic, imaging, surgical, obstetric, and outcome data were obtained.
RESULTS: Fifty-four cases were collected from the 51 studies. The median maternal age was 29 years. PHPT-induced AP starts at the 20th gestational week; higher gestational weeks were seen in mothers who died (mean gestational week 28). Median values of amylase (1399, Q1-Q3 = 519-2072), lipase (2072, Q1-Q3 = 893-2804), serum calcium (3.5, Q1-Q3 = 3.1-3.9), and parathormone (PTH) (384, Q1-Q3 = 123-910) were reported. In 46 cases, adenoma was the cause of PHPT, followed by 2 cases of carcinoma and 1 case of hyperplasia. In the remaining 5 cases, the diagnosis was not reported. Neck ultrasound was positive in 34 cases, whereas sestamibi was performed in 3 cases, and neck computed tomography or magnetic resonance imaging was performed in 9 cases (the enlarged parathyroid gland was not localized in 3 cases). Surgery was the preferred treatment during pregnancy in 33 cases (median week of gestation 25, Q1-Q3 = 20-30) and postpartum in 12 cases. The timing was not reported in the remaining 9 cases, or surgery was not performed. AP was managed surgically in 11 cases and conservatively in 43 (79.6%) cases. Maternal and fetal mortality was 9.3% (5 cases). Surgery was more common in deceased mothers (60.0% vs 16.3%; P = 0.052), and PTH values tended to be higher in this group (910 pg/mL vs 302 pg/mL; P = 0.059). Maternal mortality was higher with higher serum lipase levels and earlier delivery week. Higher calcium (4.1 mmol/L vs 3.3 mmol/L; P = 0.009) and PTH (1914 pg/mL vs 302 pg/mL; P = 0.003) values increased fetal/child mortality, as well as abortions (40.0% vs 0.0%; P = 0.007) and complex deliveries (60.0% vs 8.2%; P = 0.01).
CONCLUSIONS: If serum calcium is not tested during admission, definitive diagnosis of PHPT-induced AP in pregnancy is delayed, while early diagnosis and immediate intervention lead to excellent maternal and fetal outcomes.

BACKGROUND: Primary hyperparathyroidism is regarded as a common endocrine disorder that is biochemically identified and could be symptomatic or asymptomatic. A detailed history and a thorough evaluation with regular follow-ups are required until a definite diagnosis is made. The study aims to evaluate the characteristics of patients and the performance of a tertiary endocrine center in managing the disease in Basrah, Iraq.
METHODS: A retrospective study was conducted at the Faiha Specialized Diabetes, Endocrine, and Metabolism Center in Basrah, southern Iraq, on 106 patients diagnosed with primary hyperparathyroidism between 2012 and 2023. The patients\' general characteristics were assessed, and those who underwent parathyroidectomy were evaluated post-surgery, and the cure rate was determined.
RESULTS: The mean age of presentation was 47.5 ± 14.6 years, with a median of 50 years. The highest occurrence is in the sixth decade. Females comprised 79 (75%) of the patients, and the female-to-male ratio was 3:1. Symptomatic patients were 84 (90%), 30 (70%) of the patients had nephrolithiasis, and 52 (68%) had osteoporosis. The cure rate was 15 (83%).
CONCLUSIONS: In our single-center study, the frequency of primary hyperparathyroidism has increased with time. The disease\'s highest occurrence was seen in the sixth decade. Females were substantially higher than males. Most patients were symptomatic. The cure rate was 83%.

OBJECTIVE: Renal function and the skeleton are classic target organs in primary hyperparathyroidism (PHPT), affected by the chronic course of the disease. Most patients diagnosed today exhibit mild PHPT, characterized by slight hypercalcemia and no or unspecific symptoms. Concerns have been raised that PHPT could promote deteriorating kidney function and increase cardiovascular risk directly. To examine the effect of parathyroidectomy (PTX) on mild PHPT on renal function and markers for bone turnover, cardiovascular disease (CVD), and vascular inflammation.
METHODS: Prospective randomized controlled trial. ClinicalTrials.gov: NCT00522028.
METHODS: Eight Scandinavian referral centers.
METHODS: From 1998 to 2005, 191 patients with mild PHPT were included in Sweden, Norway, and Denmark. Of these 150 were included in the present analyses.
METHODS: Seventy patients were randomized to PTX and 80 to observation without intervention (OBS).
METHODS: e-GFR was calculated based on creatinine and cystatin C. Markers of CVD and systemic inflammation: osteoprotegerin, vascular cell adhesion molecule 1, soluble CD40 ligand, interleukin-1 receptor antagonist, von Willebrand factor. Bone turnover markers: C-terminal telopeptide of type 1 collagen (CTX-1) and serum Procollagen type 1 N-terminal propeptide.
RESULTS: No differences in the development of renal function or vascular and systemic inflammation were detected. CTX-1 was lower in PTX after 10 years.
CONCLUSIONS: Secondary analyses of a randomized controlled trial.
CONCLUSIONS: PTX does not appear to affect renal function or markers of CVD and vascular inflammation in mild PHPT in a ten-year perspective.

BACKGROUND: The ability to differentiate sporadic primary hyperparathyroidism (sPHPT) caused by a single parathyroid adenoma (PTA) from multiglandular disease (MGD) pre-operatively, as well as definitely diagnose sPHPT in difficult patients, would enhance surgical decision making.
OBJECTIVE: Identify miRNA (miR) signatures for MGD, single- and double-PTA, as well as cell-free miRNA (cfmiR) in plasma samples from patients with single-PTAs to use as biomarkers.
METHODS: 47 patients with sPHPT (single-PTA n=32, double-PTA n=12, MGD n=9). Pre-operative plasma samples from 16 single-PTA and 29 normal healthy donors (NHD).
METHODS: All specimens were processed and analyzed for 2,083 miRs using HTG EdgeSeq miR whole transcriptome assay and normalized using DESeq2 to identify differentially expressed (DE) miRs. MiR classifiers were identified using Random Forest.
METHODS: ROC curves and AUC.
RESULTS: MiR signatures distinguished normal parathyroid from MGD and PTA as well as MGD from PTA in tissue samples. Common miRs were found in the single-PTA and double-PTAs. Data integration identified a 27-miR signature in single-PTA tissue samples compared to the rest of the tissue samples. In plasma samples analysis, significant cfmiRs were DE in single-PTA patients compared to NHD. Of those, only 9 miRNAs/cfmiRs were found DE in both tissue and plasma samples from patients diagnosed with a single-PTA (AUC=76%).
CONCLUSIONS: Twenty-seven miRs were consistently found DE in single-PTA tissue and plasma samples. Data integration showed a 9-cfmiR signature with potential clinical utility to pre-operatively diagnose sPHPT caused by a single-PTA, which could decrease more invasive parathyroid explorations.

Primary hyperparathyroidism (PHPT) is a common endocrine disease characterized by hypercalcemia due to inappropriately high parathyroid hormone secretion. While in the typical, symptomatic form of the disease diagnosis is set easily and standard management is surgical removal of the hyperfunctioning parathyroid (HP), this may not be the case in more subtle forms of PHPT, such as the asymptomatic and the normocalcemic PHPT. Localization of the HP could also be challenging, especially in small-sized adenomas, ectopic lesions or multiglandular disease. An experienced surgical team is essential to achieve curative parathyroidectomy. In this article, we used illustrative clinical vignettes to dissect the approach to the patient with PHPT, from the diagnosis establishment to the suggested investigation to identify classical and non-classical PHPT features and the methodology to locate the abnormal tissue. Accordingly, we elaborated on appropriate management, both surgical and conservative.