OBJECTIVE: There is no specific recommendation for management in pregnant women: the aim of this review, based on a clinical case study, is to clarify its development, complications, risk factor and treatment.
METHODS: A review of the literature was performed by consulting the Pubmed, Cochrane Library, and Science Direct databases.
RESULTS: Primary hyperparathyroidism is defined as excessive production of parathyroid hormone resulting in hypercalcemia. The prevalence of primary hyperparathyroidism during pregnancy is not known. Indeed, the symptomatology, related to hypercalcemia, is not very specific and easily confused with the clinical manifestations of pregnancy. The physiological changes specific to the pregnant state frequently lead to a slight hypocalcemia which may complicate the diagnosis of primary hyperparathyroidism. Primary hyperparathyroidism results from a parathyroid adenoma in the majority of cases and is detected by ultrasound during pregnancy. Primary hyperparathyroidism in pregnancy causes significant risks to both mother and fetus. The maternal complication rate is 14-67%, however, the most serious complication is hypercalcemic crisis, which requires increased surveillance in the postpartum period. Obstetrical complications are also induced by primary hyperparathyroidism, such as acute polyhydramnios, or intrauterine growth retardation. The fetal complication rate can reach 45-80% of cases with neonatal hypocalcemia as the main complication. If medical treatment is based on hyperhydration, only surgical treatment is curative.
CONCLUSIONS: Surgery should be proposed to symptomatic patients or those with high blood calcium levels, discussed in interdisciplinary committee and should be organized ideally in the second trimester to avoid maternal and fetal complications.

The sigma-1 and sigma-2 receptors were first discovered in the 1960s and were thought to be a form of opioid receptors initially. Over time, more was gradually learned about these receptors, which are actually protein chaperones, and many of their unique or unusual properties can contribute to a range of important new therapeutic applications. These sigma receptors translocate in the body and regulate calcium homeostasis and mitochondrial bioenergetics and they also have neuroprotective effects. The ligands to which these sigma receptors respond are several and dissimilar, including neurosteroids, neuroleptics, and cocaine. There is controversy as to their endogenous ligands. Sigma receptors are also involved in the complex processes of cholesterol homeostasis and protein folding. While previous work on this topic has been limited, research has been conducted in multiple disease states, such as addiction, aging. Alzheimer\'s disease, cancer, psychiatric disorders, pain and neuropathic pain, Parkinson\'s disease, and others. There is currently increasing interest in sigma-1 and sigma-2 receptors as they provide potential therapeutic targets for many disease indications.

Calcium homeostasis is regulated by the dyad of parathyroid hormone and calcitriol, whereas kidney, intestine, and bone are the primary target sites. Elevation of serum calcium levels and hypercalcemia are likely markers of pathological conditions, particularly malignancy and hyperparathyroidism. Similarly, several dysfunctions within the body can direct hypercalcemia. Furthermore, chemicals and drugs can also drive this condition. Owing to the significant role of the kidney in calcium homeostasis, renal abnormalities lead to hypercalcemia and increased calcium levels can have pathological effects on the kidney. This review is designed to highlight some of the commonly known causes of hypercalcemia and their effects on the kidney.

Mitochondria are the main sites for oxidative phosphorylation and synthesis of adenosine triphosphate in cells, and are known as cellular power factories. The phrase \"secondary mitochondrial diseases\" essentially refers to any abnormal mitochondrial function other than primary mitochondrial diseases, i.e., the process caused by the genes encoding the electron transport chain (ETC) proteins directly or impacting the production of the machinery needed for ETC. Mitochondrial diseases can cause adenosine triphosphate (ATP) synthesis disorder, an increase in oxygen free radicals, and intracellular redox imbalance. It can also induce apoptosis and, eventually, multi-system damage, which leads to neurodegenerative disease. The catechin compounds rich in tea have attracted much attention due to their effective antioxidant activity. Catechins, especially acetylated catechins such as epicatechin gallate (ECG) and epigallocatechin gallate (EGCG), are able to protect mitochondria from reactive oxygen species. This review focuses on the role of catechins in regulating cell homeostasis, in which catechins act as a free radical scavenger and metal ion chelator, their protective mechanism on mitochondria, and the protective effect of catechins on mitochondrial deoxyribonucleic acid (DNA). This review highlights catechins and their effects on mitochondrial functional metabolic networks: regulating mitochondrial function and biogenesis, improving insulin resistance, regulating intracellular calcium homeostasis, and regulating epigenetic processes. Finally, the indirect beneficial effects of catechins on mitochondrial diseases are also illustrated by the warburg and the apoptosis effect. Some possible mechanisms are shown graphically. In addition, the bioavailability of catechins and peracetylated-catechins, free radical scavenging activity, mitochondrial activation ability of the high-molecular-weight polyphenol, and the mitochondrial activation factor were also discussed.

With the extensive application of titanium dioxide nanoparticles (TiO2 NPs), their impacts on calcium homeostasis have aroused extensive attention from scholars. However, there are still some controversies in relevant reports. Therefore, a systematic review was performed followed by a meta-analysis to explore whether TiO2 NPs could induce the imbalance in calcium homeostasis in vivo and in vitro through Revman5.4 and Stata15.0 in this research. Fourteen studies were included through detailed database retrieval and literature screening. Results indicated that the calcium levels were significantly increased and the activity of Ca2+-ATPase was significantly decreased by TiO2 NPs in vivo and in vitro. Subgroup analysis of the studies in vivo showed that TiO2 NPs exposure caused a significant increase in calcium levels in rats, exposure to large-sized TiO2 NPs (>10 nm) and long-term (>30 days) exposure could significantly increase calcium levels, and the activity of Ca2+-ATPase showed a concentration-dependent downward trend. Subgroup analysis of the studies in vitro revealed that intracellular calcium levels increased significantly in animal cells, exposure to small-sized TiO2 NPs (≤10 nm) and high concentration (>10 μg/mL) exposure could induce a significant increase in Ca2+ concentration, and the activity of Ca2+-ATPase also showed a concentration-dependent downward trend. This research showed that the physicochemical properties of TiO2 NPs and the experimental scheme could affect calcium homeostasis.

Alzheimer\'s disease is a neurological condition that causes the disruption of neuronal connections in the human brain. It is progressive and targets about 10% of the United States population over the age of 65.3 to date, there is no cure to the disease. Physicians can treat symptoms but lack the ability to stop the progression of the disease. However, promising research has come to the surface in recent years. A collection of these therapeutic targets, which have yielded positive results in mice models, are presented in this article. They include targets such as meningeal lymphatics, mitochondrial homeostasis, genomic instability, calcium homeostasis, and cold-shock proteins such as RNA-binding motif protein 3 and reticulon-3, high-density lipoprotein, and antibodies.

The prevalence of atrial fibrillation (AF) is bound to increase globally in the following years, affecting the quality of life of millions of people, increasing mortality and morbidity, and beleaguering health care systems. Increasingly effective therapeutic options against AF are the constantly evolving electroanatomic substrate mapping systems of the left atrium (LA) and ablation catheter technologies. Yet, a prerequisite for better long-term success rates is the understanding of AF pathogenesis and maintenance. LA electrical and anatomical remodeling remains in the epicenter of current research for novel diagnostic and treatment modalities. On a molecular level, electrical remodeling lies on impaired calcium handling, enhanced inwardly rectifying potassium currents, and gap junction perturbations. In addition, a wide array of profibrotic stimuli activates fibroblast to an increased extracellular matrix turnover via various intermediaries. Concomitant dysregulation of the autonomic nervous system and the humoral function of increased epicardial adipose tissue (EAT) are established mediators in the pathophysiology of AF. Local atrial lymphomononuclear cells infiltrate and increased inflammasome activity accelerate and perpetuate arrhythmia substrate. Finally, impaired intracellular protein metabolism, excessive oxidative stress, and mitochondrial dysfunction deplete atrial cardiomyocyte ATP and promote arrhythmogenesis. These overlapping cellular and molecular alterations hinder us from distinguishing the cause from the effect in AF pathogenesis. Yet, a plethora of therapeutic modalities target these molecular perturbations and hold promise in combating the AF burden. Namely, atrial selective ion channel inhibitors, AF gene therapy, anti-fibrotic agents, AF drug repurposing, immunomodulators, and indirect cardiac neuromodulation are discussed here.

This systematic review assessed genotypes and changes in calcium homeostasis. A literature search was performed in EMBASE, Medline and CENTRAL on 7 August 2020 identifying 1012 references. Studies were included with any human population related to the topic of interest, and genetic variations in genes related to calcium metabolism were considered. Two reviewers independently screened references, extracted relevant data and assessed study quality using the Q-Genie tool. Forty-one studies investigating Single Nucleotide Polymorphisms (SNPs) in relation to calcium status were identified. Almost half of the included studies were of good study quality according to the Q-Genie tool. Seventeen studies were cross-sectional, 14 case-control, seven association and three were Mendelian randomization studies. Included studies were conducted in over 18 countries. Participants were mainly adults, while six studies included children and adolescents. Ethnicity was described in 31 studies and half of these included Caucasian participants. Twenty-six independent studies examined the association between calcium and polymorphism in the calcium-sensing receptor (CASR) gene. Five studies assessed the association between polymorphisms of the Vitamin D receptor (VDR) gene and changes in calcium levels or renal excretion. The remaining ten studies investigated calcium homeostasis and other gene polymorphisms such as the CYP24A1 SNP or CLDN14. This study identified several CASR, VDR and other gene SNPs associated with calcium status. However, to provide evidence to guide dietary recommendations, further research is needed to explore the association between common polymorphisms and calcium requirements.

Mineral derangements are a common consequence of chronic kidney disease (CKD). Despite the well-established role of phosphorus in the pathophysiology of CKD, the implications of calcium disturbances associated with CKD remain equivocal. Calcium plays an essential role in numerous physiological functions in the body and is a fundamental structural component of bone. An understanding of calcium metabolism is required to understand the potential adverse clinical implications and outcomes secondary to the (mal)adaptation of calcium-regulating hormones in CKD. The first part of this two-part review covers the physiology of calcium homeostasis (kidneys, intestines and bones) and details the intimate relationships between calcium-regulating hormones (parathyroid hormone, calcitriol, fibroblast growth factor 23, α-Klotho and calcitonin) and the role of the calcium-sensing receptor.

BACKGROUND: Parathyroid disease is uncommon in pregnancy. During pregnancy, multiple changes occur in the calcium regulating hormones which may make the diagnosis of primary hyperparathyroidism more challenging. Close monitoring of serum calcium during pregnancy is necessary in order to optimize maternal and fetal outcomes. In this review, we will describe the diagnosis and management of primary hyperparathyroidism during pregnancy.
METHODS: We searched MEDLINE, CINAHL, EMBASE and Google scholar bases from 1 January 1990 to 31 December 2020. Case reports, case series, book chapters and clinical guidelines were included in this review.
CONCLUSIONS: Medical management options for primary hyperparathyroidism during pregnancy are severely limited due to inadequate safety data with the various potential therapies available, and surgery is advised during the 2nd trimester of pregnancy in the presence of severe hypercalcemia (calcium adjusted for albumin greater than 3.0 mmol/L (12.0 mg/dL)). Hypercalcemia should be avoided during pregnancy in order to minimize maternal and fetal complications.