Parathormone decline levels are better markers of symptomatic hypocalcemia following total thyroidectomy than parathormone alone.

Background: We aimed to assess the predictive value of the absolute and relative intact parathormone (iPTH) decline levels as reliable markers of postoperative hypocalcemia. Materials & methods: iPTH levels were measured 4 h after surgery and the following morning after surgery (postoperative day 1). iPTH, absolute iPTH decline (ΔPTH) and relative iPTH decline (ΔPTH%) were calculated and correlated with symptomatic hypocalcemia. Results: Of the 95 patients, 20% of patients (n = 19) developed symptomatic hypocalcemia. The ΔPTH (U = 206; p < 0.001) and ΔPTH% (U = 127; p < 0.001) were significantly higher in patients with symptomatic hypocalcemia. A ΔPTH% of 20% (sensitivity of 84%; specificity of 91%); and an absolute iPTH decline of 3.75 pg/ml (sensitivity of 74%; specificity of 87%) were highly predictive of symptomatic hypocalcemia. Conclusion: Postoperative ΔPTH and ΔPTH% have the potential to be predictors of symptomatic hypocalcemia following thyroidectomy and could facilitate a safe early discharge.

Screening for Vitamin D Deficiency in Black Americans: Comparison of Total, Free, Bioavailable 25 Hydroxy Vitamin D Levels with Parathyroid Hormone Levels and Bone Mineral Density.

OBJECTIVES: There is debate surrounding the adequacy of total and free 25 hydroxy vitamin D [25(OH)D] levels in black Americans who have inherently high bone mineral density [BMD] and low serum concentration of vitamin D binding proteins [VDBP]. DESIGN: Retrospective analysis of serum samples and BMD analyses from the African American Health Study [AAHS] cohort. SETTING: The AAHS is a population-based longitudinal study initiated to examine issues of disability and frailty among urban-dwelling black Americans in the city of Saint Louis, Missouri. PARTICIPANTS: 122 men and 206 women, age 60.2 ± 4.3 years. INTERVENTION: Retrospective analysis. MEASUREMENTS: Total 25(OH)D, VDBP, PTH, and BMD of the lumbar spine and hip by dual energy x-ray photometry (DXA). Free and bioavailable vitamin D levels were calculated using serum concentrations and affinity constants for the VDBP (Gc1F and Gc1S) phenotypes. RESULTS: Serum total 25(OH)D levels were 14.6 ± 8.9 ng/mL (36 ± 22 nmol/L). Vitamin D insufficiency was estimated by compensatory elevations of PTH above the normal range (> 65 pg/mL). PTH levels were within the normal reference range in > 95% of the samples at total 25(OH)D levels ≥ 20 ng/mL (≥50 nmol/L). There was no difference in the correlation of the reciprocal relationship of vitamin D vs parathyroid hormone between the VDBP phenotypes. Receiver operating characteristic curve analyses indicated that serum total 25(OH)D discriminated sufficiency from insufficiency at least as well as the calculated levels of the free and bioavailable vitamin D. Very low levels of total 25(OH)D (≤ 8 ng/mL, ≤20 nmol/L) were associated with decreased BMD (p=0.02), but higher levels of 25(OH)D did not show statistical differences in BMD. CONCLUSION: Total 25(OH)D levels of ≤ 8ng/mL (≤20 nmol/L) are associated with clinically significant changes in BMD, whereas total 25(OH)D levels ≥ 20 ng/mL (≥50 nmol/L) suppressed PTH and were not associated with deficiencies in BMD. Lower levels of 25(OH)D may be acceptable for bone health in black than in white Americans.

Lack of endogenous parathyroid hormone delays fracture healing by inhibiting vascular endothelial growth factor­mediated angiogenesis.

Intermittent low­dose injections of parathyroid hormone (PTH) have been reported to exert bone anabolic effects and to promote fracture healing. As an important proangiogenic cytokine, vascular endothelial growth factor (VEGF) is secreted by bone marrow mesenchymal stem cells (BMSCs) and osteoblasts, and serves a crucial regulatory role in the process of vascular development and regeneration. To investigate whether lack of endogenous PTH causes reduced angiogenic capacity and thereby delays the process of fracture healing by downregulating the VEGF signaling pathway, a PTH knockout (PTHKO) mouse fracture model was generated. Fracture healing was observed using X­ray and micro­computerized tomography. Bone anabolic and angiogenic markers were analyzed by immunohistochemistry and western blot analysis. The expression levels of VEGF and associated signaling pathways in murine BMSC­derived osteoblasts were measured by quantitative polymerase chain reaction and western blot analysis. The expression levels of protein kinase A (PKA), phosphorylated­serine/threonine protein kinase (pAKT), hypoxia­inducible factor­1α (HIF1α) and VEGF were significantly decreased in BMSC­derived osteoblasts from PTHKO mice. In addition, positive platelet endothelial cell adhesion molecule staining was reduced in PTHKO mice, as determined by immunohistochemistry. The expression levels of HIF1α, VEGF, runt­related transcription factor 2, osteocalcin and alkaline phosphatase were also decreased in PTHKO mice, and fracture healing was delayed. In conclusion, lack of endogenous PTH may reduce VEGF expression in BMSC­derived osteoblasts by downregulating the activity of the PKA/pAKT/HIF1α/VEGF pathway, thus affecting endochondral bone formation by causing a reduction in angiogenesis and osteogenesis, ultimately leading to delayed fracture healing.

Causes and pathophysiology of hypoparathyroidism.

Hypoparathyroidism, a disorder characterized by hypocalcemia ensuing from inadequate parathyroid hormone secretion, is a rather rare disorder caused by multiple etiologies. When not caused by inadvertent damage or removal of the parathyroids during neck surgery, it is usually genetically determined. Epidemiological figures of this disease are still scarce and mainly limited to countries where non-anonymous databases are available and to surgical case series. Both the surgical and non-surgical forms pose diagnostic challenges. For surgical hypoparathyroidism, transient forms have to be ruled out even in the long term, in order to avoid unnecessary chronic replacement therapy with calcium and calcitriol. Regarding non-surgical hypoparathyroidism, once referred to as idiopathic, a systematic clinically and genetically-driven approach to define the precise diagnosis have to be pursued. In the case of syndromic hypoparathyroidism, patients have to be screened for associated abnormalities. Autoimmune, non-genetic hypoparathyroidism is still a diagnosis of exclusion, since no specific autoantibodies are specific for this condition.

Hypoparathyroidism - disease update and emerging treatments.

Parathyroid hormone (PTH) is the primary regulator of blood calcium levels and bone metabolism. Insufficient levels of PTH lead to hypoparathyroidism, characterized by low serum calcium and elevated serum phosphate levels. It is most commonly caused by the inadvertent damage to the parathyroid glands during thyroid surgery. Patients with hypoparathyroidism are currently being treated with oral calcium and active vitamin D, and to avoid worsening hypercalciuria, target serum calcium levels are within the lower end of normal. With current treatment, patients may suffer from large swings in serum calcium and are at a substantial risk of chronic renal failure, nephrocalcinosis, and kidney stones. The recent FDA approval of recombinant human (rh) PTH(1-84) for the treatment of hypoparathyroidism adds PTH replacement therapy to the endocrinologist's armamentarium to treat this chronic disease.

Predicting hypocalcemia after thyroidectomy in children.

BACKGROUND AND AIMS: Hypocalcemia after thyroidectomy is caused by parathyroid trauma. There are no studies regarding the usefulness of intact parathyroid hormone (PTH) as a monitor of postoperative hypoparathyroidism tool in pediatrics. We evaluated the diagnostic accuracy of intra- and postoperative PTH to predict the risk of developing post thyroidectomy hypocalcemia in children. METHODS: A prospective longitudinal cohort study was conducted in 32 pediatric patients (3.2-17.6 years old) undergoing total thyroidectomy. Intact PTH measured by the assays (Immulite Immunoassay System [ICMA] or electrochemioluminescence assay [ECLIA]) at 5 (PTH-5) and 60 (PTH-60) minutes after thyroid removal were considered as predicting variables. The postoperative outcome was hypocalcemia (endpoint variable). Patients were clinically and biochemically monitored regularly for 48 hours after surgery. RESULTS: Of the patients, 47% developed hypocalcemia (15% symptomatic). An ICMA PTH-5 of ≤14 pg/mL or an ECLIA PTH-5 of ≤16 pg/mL predicted hypocalcemia with a sensitivity of 80%, specificity of 100%, positive predictive value (PPV) of 100%, and diagnostic efficiency (DE) of 91%. Using the same cutoff values, PTH-60 presented a sensitivity of 93%, specificity of 82%, PPV of 81%, and DE of 87%. Adjusting for variation in the assays and combining intra- and postoperative PTH determinations, we developed an algorithm that improved sensitivity, specificity, and DE. CONCLUSION: PTH is useful for predicting hypocalcemia after total thyroidectomy in children. The use of our proposed strategy should be considered to (a) initiate preventive treatment in patients identified at high risk for hypocalcemia, (b) shorten the duration of hospitalization, and (c) reduce the clinical and biochemical controls in those who remained normocalcemic.

Dental findings in the diagnosis of idiopathic hypoparathyroidism.

Idiopathic hypoparathyroidism (IHP) is a rare endocrinopathy, characterized by the disturbances in calcium and phosphorous metabolism, owing to deficiency in parathyroid hormone, which leads to tetanic manifestations. Onset of the clinical features occurs early in life, and the severity depends on the extent of chemical imbalance. This article describes a case of 22-year-old patient undiagnosed for 12 years with this endocrinopathy (IHP). Over retained deciduous teeth, delayed eruption, impacted tooth and short roots probably resulting from untreated hypocalcemia during the developmental phase of dentition enabled us to unearth this endocrinopathy through a series of investigations. Thus the article emphasizes the importance of dental findings of this endocrinopathy.

Primary hyperparathyroidism and metabolic risk factors, impact of parathyroidectomy and vitamin D supplementation, and results of a randomized double-blind study.

BACKGROUND: Vitamin D insufficiency may increase the risk for cardio metabolic disturbances in patients with primary hyperparathyroidism (PHPT). OBJECTIVE: To analyze the vitamin D status and indices of the metabolic syndrome in PHPT patients and the effect of vitamin D supplementation after parathyroid adenomectomy (PTX). DESIGN AND METHODS: Double-blinded, randomized clinical trial (ClinicalTrials.gov identifier: NCT00982722) performed at Karolinska University Hospital, Sweden, April 2008 to November 2011. One hundred and fifty consecutive patients with PHPT (119 women) were randomized after PTX, 75 to oral treatment with calcium carbonate 1000 mg daily and 75 to calcium carbonate 1000 mg and cholecalciferol 1600 IU daily over 12 months. Changes in metabolic profile and ambulatory blood pressure (BP) were analyzed. Main outcome measures were changes in metabolic factors, BP, and body composition. RESULTS: The 25-hydroxyvitamin D (25-OH-D)-level was <50 nmol/l in 76% of the patients before PTX. After PTX, glucose, insulin, and IGF1 decreased, while the 25-OH-D and the IGF-binding protein 1 increased and remained unchanged at follow-up after study medication. One year of vitamin D supplementation resulted in lower parathyroid hormone (PTH) (40 (34-52) vs 49 (38-66) ng/l) and higher 25-OH-D (76 (65-93) vs 49 (40-62) nmol/l; P<0.05). Other laboratory parameters were stable compared with after PTX. Systolic BP decreased and total bone mineral content increased in both groups. CONCLUSION: Except for the lowering of the PTH level, no additive effect of vitamin D supplementation was seen. However, PTX proved effective in reducing insulin resistance.

FAM111A mutations result in hypoparathyroidism and impaired skeletal development.

Kenny-Caffey syndrome (KCS) and the similar but more severe osteocraniostenosis (OCS) are genetic conditions characterized by impaired skeletal development with small and dense bones, short stature, and primary hypoparathyroidism with hypocalcemia. We studied five individuals with KCS and five with OCS and found that all of them had heterozygous mutations in FAM111A. One mutation was identified in four unrelated individuals with KCS, and another one was identified in two unrelated individuals with OCS; all occurred de novo. Thus, OCS and KCS are allelic disorders of different severity. FAM111A codes for a 611 amino acid protein with homology to trypsin-like peptidases. Although FAM111A has been found to bind to the large T-antigen of SV40 and restrict viral replication, its native function is unknown. Molecular modeling of FAM111A shows that residues affected by KCS and OCS mutations do not map close to the active site but are clustered on a segment of the protein and are at, or close to, its outer surface, suggesting that the pathogenesis involves the interaction with as yet unidentified partner proteins rather than impaired catalysis. FAM111A appears to be crucial to a pathway that governs parathyroid hormone production, calcium homeostasis, and skeletal development and growth.

Endogenous parathyroid hormone-related protein compensates for the absence of parathyroid hormone in promoting bone accrual in vivo in a model of bone marrow ablation.

To assess the effect of hypoparathyroidism on osteogenesis and bone turnover in vivo, bone marrow ablation (BMXs) were performed in tibias of 8-week-old wild-type and parathyroid hormone-null (PTH(-/-)) mice and newly formed bone tissue was analyzed from 5 days to 3 weeks after BMX. At 1 week after BMX, trabecular bone volume, osteoblast numbers, alkaline phosphatase-positive areas, type I collagen-positive areas, PTH receptor-positive areas, calcium sensing receptor-positive areas, and expression of bone formation-related genes were all decreased significantly in the diaphyseal regions of bones of PTH(-/-) mice compared to wild-type mice. In contrast, by 2 weeks after BMX, all parameters related to osteoblastic bone accrual were increased significantly in PTH(-/-) mice. At 5 days after BMX, active tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts had appeared in wild-type mice but were undetectable in PTH(-/-) mice, Both the ratio of mRNA levels of receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG) and TRAP-positive osteoclast surface were still reduced in PTH(-/-) mice at 1 week but were increased by 2 weeks after BMX. The expression levels of parathyroid hormone-related protein (PTHrP) at both mRNA and protein levels were upregulated significantly at 1 week and more dramatically at 2 weeks after BMX in PTH(-/-) mice. To determine whether the increased newly formed bones in PTH(-/-) mice at 2 weeks after BMX resulted from the compensatory action of PTHrP, PTH(-/-) PTHrP(+/-) mice were generated and newly formed bone tissue was compared in these mice with PTH(-/-) and wild-type mice at 2 weeks after BMX. All parameters related to osteoblastic bone formation and osteoclastic bone resorption were reduced significantly in PTH(-/-) PTHrP(+/-) mice compared to PTH(-/-) mice. These results demonstrate that PTH deficiency itself impairs osteogenesis, osteoclastogenesis, and osteoclastic bone resorption, whereas subsequent upregulation of PTHrP in osteogenic cells compensates by increasing bone accrual.

Extracellular calcium-sensing receptor/PTH knockout mice colons have increased Wnt/ß-catenin signaling, reduced non-canonical Wnt signaling, and increased susceptibility to azoxymethane-induced aberrant crypt foci.

Epidemiological evidence suggests increased dietary calcium and dairy products reduce the onset of colon cancer. To understand a role of the colonic extracellular calcium-sensing receptor (CaSR) in calcium-mediated chemoprevention of colon cancer, we induced formation of aberrant crypt foci (ACF) caused by azoxymethane (AOM) injection in 'rescued' CaSR-/PTH- (C-/P-) double knockout colons compared with colons from control CaSR+/PTH+ (C+/P+) mice. C-/P- colonic epithelia had increased Wnt/ß-catenin signaling as evidenced by 3-8-fold increases in Wnt3a, CyclinD1, and MMP-7 proteins compared with C+/P+ colonic epithelia. The C-/P- colonic epithelia had reduced Wnt5a and Ror2, and a three-fold increase in TNFR1 compared with C+/P+ epithelia. The C-/P- colons and small intestine had extensive neutrophil infiltration with myeloperoxidase (MPO) levels 18-fold higher then C+/P+ small intestine and colon. Saline-injected C-/P- colons had the same number of ACF/cm(2) as C+/P+ colons, which were injected with AOM. However, there were eight times more ACF/cm(2) in the C-/P- injected with AOM compared with C+/P+ colons, which received AOM. Together our results suggest both inflammation and Wnt/ß-catenin signaling are increased in the epithelia of 'rescued' CaSR/PTH double knockout colons, and the capacity for non-canonical Wnt signaling through Wnt5a/Ror2 engagement is reduced. The loss of the colonic CaSR increased the number of ACF/cm(2) in response to AOM injection, suggesting colonic CaSR may mediate the chemoprotective effect of increased dietary calcium against colorectal cancer observed in humans.

Intraoperative serum parathyroid hormone level is an indicator of hypocalcaemia in total thyroidectomy patients.

Postoperative hypocalcaemia is the most frequent and common complication after total thyroidectomy. It is necessary to diagnose or to predict hypocalcaemia immediately after total thyroidectomy for minimizing complications. A prospective observational study was carried out in the Department of Clinical Pathology in collaboration with Department of Microbiology & Immunology, Department of Surgery, Department of Otolaryngology, Bangabandhu Sheikh Mujib Medical University (BSMMU) and Department of Otolaryngology, Dhaka Medical College & Hospital (DMC&H), Dhaka, during the period of September 2010 to August 2011 to evaluate intraoperative (20 minutes after total thyroidectomy) parathyroid hormone (PTH) measurement as a predictor of post thyroidectomy hypocalcaemia. Total 65 patients were enrolled in this study those came for total thyroidectomy. Postoperative hypocalcaemia developed in 25 cases. Intraoperative PTH was assessed and significant correlation was found between intraoperative PTH level and development of hypocalcaemia. The sensitivity, specificity, accuracy, positive predictive value, negative predictive value of intraoperative serum PTH for prediction of post total thyroidectomy hypocalcaemia were 84.0%, 85.0%, 84.6%, 77.8%, and 89.5% respectively. Because of the high sensitivity, specificity and accuracy of intraoperative serum PTH of this study, the early prediction of hypocalcaemia could be made by single assay of intraoperative serum PTH level at 20 minutes after total thyroidectomy.

22q11.2 deletion presenting with severe hypocalcaemia, seizure and basal ganglia calcification in an adult man.

We report a 40-year-old man who was found to have profound hypocalcaemia and hypoparathyroidism when investigated for multiple, generalized, tonic/clonic seizures and a chest infection. Computed tomography scan of the brain revealed extensive symmetric bilateral calcification within the cerebellum, thalamus and basal ganglia. Molecular cytogenetic testing by fluorescent in situ hybridization using the commercial Vysis LSI DiGeorge/VCFS dual colour probe set showed a deletion of 22q11.2. The extraordinary feature of this case is the adult presentation of hypocalcaemia, hypoparathyroidism and basal ganglia calcification due to 22q11.2 deletion.

Parathyroid hormone deficiency after total thyroidectomy: incidence and time.

BACKGROUND: Parathyroid hormone (PTH) deficiency or hypoparathyroidism after total thyroidectomy is not an uncommon postoperative complication. Patients who have PTH deficiency will develop profound hypocalcemia if not properly treated with oral calcium supplementation and activated vitamin D (1,25-dihydroxycholecalciferol or calcitriol). However, there is little published on the long-term outcomes of these patients. The aim of this study was to determine the incidence of PTH deficiency and the time course to resolution after total thyroidectomy. METHODS: We identified 271 consecutive patients who underwent total thyroidectomy from January 2006 to December 2008. All patients had serum PTH levels tested 4 h after surgery and the morning after surgery. Patients were diagnosed with PTH deficiency if their serum PTH was <10 pg/mL. The outcomes of patients with PTH deficiency (group 1) were then compared with patients who did not have PTH deficiency (group 2). Patients in group 1 were evaluated for parathyroid function by measuring serum PTH levels as well as documenting usage of supplemental calcium and 1,25-dihydroxycholecalciferol. RESULTS: Of the 271 patients, 33 (12%) were found to have PTH deficiency. In comparing PTH deficient patients (group 1) with patients in group 2, there were no differences in age, gender, thyroid pathology, the incidence of thyroiditis, or other factors that would predict hypoparathyroidism. Twenty-four patients (73%) had recovery of their PTH levels to > or =10 pg/mL at their 1 wk follow-up appointment, while 9 (27%) patients still had PTH levels <10 pg/mL. With long term follow-up, 27 (82%) patients had recovered with a PTH level of > or = 10 pg/mL, while 6 (18%) patients had a serum PTH level <10 pg/mL. However, three of the 33 patients in group 1 (9%) required long-term 1,25-dihydroxycholecalciferol, but only two of these patients had undetectable PTH levels. Thus, the overall rate of hypocalemia requiring 1,25-dihydroxycholecalciferol was <1% (two of 271 total patients). CONCLUSIONS: We concluded that approximately 12% (33 of 271) of patients undergoing total thyroidectomy will develop PTH deficiency. Of the PTH deficient patients, 73% will return to normal parathyroid function within 1 wk of surgery. Furthermore, 82% of these PTH deficient patients will return to normal parathyroid function with long-term follow-up. Less than 1% (two of 271) of patients undergoing total thyroidectomy will require 1,25-dihydroxycholecalciferol for long-term hypocalcemia.

Skeletal and hormonal effects of magnesium deficiency.

Magnesium (Mg) is the second most abundant intracellular cation where it plays an important role in enzyme function and trans-membrane ion transport. Mg deficiency has been associated with a number of clinical disorders including osteoporosis. Osteoporosis is common problem accounting for 2 million fractures per year in the United States at a cost of over $17 billion dollars. The average dietary Mg intake in women is 68% of the RDA, indicating that a large proportion of our population has substantial dietary Mg deficits. The objective of this paper is to review the evidence for Mg deficiency-induced osteoporosis and potential reasons why this occurs, including a cumulative review of work in our laboratories and well as a review of other published studies linking Mg deficiency to osteoporosis. Epidemiological studies have linked dietary Mg deficiency to osteoporosis. As diets deficient in Mg are also deficient in other nutrients that may affect bone, studies have been carried out with select dietary Mg depletion in animal models. Severe Mg deficiency in the rat (Mg at <0.0002% of total diet; normal = 0.05%) causes impaired bone growth, osteopenia and skeletal fragility. This degree of Mg deficiency probably does not commonly exist in the human population. We have therefore induced dietary Mg deprivation in the rat at 10%, 25% and 50% of recommended nutrient requirement. We observed bone loss, decrease in osteoblasts, and an increase in osteoclasts by histomorphometry. Such reduced Mg intake levels are present in our population. We also investigated potential mechanisms for bone loss in Mg deficiency. Studies in humans and and our rat model demonstrated low serum parathyroid hormone (PTH) and 1,25(OH)(2)-vitamin D levels, which may contribute to reduced bone formation. It is known that cytokines can increase osteoclastic bone resorption. Mg deficiency in the rat and/or mouse results in increased skeletal substance P, which in turn stimulates production of cytokines. With the use of immunohistocytochemistry, we found that Mg deficiency resulted in an increase in substance P, TNFalpha and IL1beta. Additional studies assessing the relative presence of receptor activator of nuclear factor kB ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), found a decrease in OPG and an increase in RANKL favoring an increase in bone resorption. These data support the notion at dietary Mg intake at levels not uncommon in humans may perturb bone and mineral metabolism and be a risk factor for osteoporosis.

Vitamin D metabolite-mediated hypercalcemia with suppressed parathormone concentration in Pneumocystis jiroveci pneumonia after kidney transplantation.

Pneumocystis jiroveci pneumonia (PJP) is a severe complication in immunocompromised hosts including transplant recipients. Hypercalcemia (HCa) is not a classic symptom of the disease. However, HCa (mean [SD; range], 2.90 [0.20; 2.71-3.17] mmol/L) was detected in 5 patients with PJP at diagnosis. The HCa was associated with decreased concentrations of circulating parathormone (PTH), from 294 (292) ng/L 3 to 6 months previously to 20 (23.5; 7-53) ng/L. Concentrations of 1,25-(OH)2 vitamin D, measured in 3 patients, were in the high normal range (54.66 [7.23; 225-66] microg/L), whereas 25-(OH) vitamin D concentrations were low (13.9 [2.17; 20-60] microg/L). After treatment with trimethoprim-sulfamethoxazole for 21 days, 4 patients recovered and 1 died. Calcium and PTH concentrations rapidly returned to normal (2.36 [0.05] mmol/L and 89 [29.7] ng/L, respectively) at 2 months after the acute phase of the disease. Although fewer than 10 cases of PJP-associated HCa have been reported to date, it is possible that this association is more frequent than previously thought because our cases were detected during 2 years. As in other granulomatous disease-induced HCa, including fungal infections, it is likely that endogenous extrarenal production of 1-alpha-hydroxylase by activated macrophages and by interferon-gamma involved in granuloma formation results in increased conversion from 25-(OH) vitamin D to 1,25-(OH)2 vitamin D and, consequently, in transient HCa and suppression of PTH secretion. Fortuitous detection of HCa in transplant recipients with pulmonary symptoms must raise suspicion of PJP or fungal infection.

A case of magnesium deficiency associated with insufficient parathyroid hormone action and severe osteoporosis.

The relationship between osteoporosis and magnesium (Mg) deficiency is still controversial. Here we report a case of an 82-year-old woman with a giant adenomatous goiter and severe osteoporosis with multiple vertebral fractures, whose clinical course indicated that her osteoporosis was probably due to Mg deficiency. She visited our hospital for treatments of tetany. Laboratory data showed the existence of hypomagnesemia, hypocalcemia, hypokalemia, vitamin D deficiency, and slightly elevated intact PTH. Intravenous administration of Mg not only improved these electrolyte abnormalities but also increased serum levels of intact PTH, bone formation markers, 1,25-dihydroxyvitamin D, as well as bone resorption markers in the urine, and lowered urinary phosphate reabsorption. Hypomagnesemia on admission seemed to arise from long-lasting poor food intake and malnutrition, because it improved after the disappearance of dysphagia with a goiter resection. After the operation, BMD values at the lumbar spine and femoral neck obviously increased during 6 months of Mg supplementation without any specific therapies for osteoporosis. Mg deficiency in this case seemed to cause impaired secretion of PTH from the parathyroid and the refractoriness of bone and kidney to the hormone, which led to the suppression of both bone remodeling and renal vitamin D production. These processes were probably linked to her severe osteoporosis, which was reversed by Mg supplementation.