| 2021 | Severe hypocalcaemia in a COVID-19 female patient. | Endocrinol Diabetes Metab Case Rep | Comorbidities are a risk factor for patients with COVID-19 and the mechanisms of disease remain unclear. The aim of this paper is to present a case report of an COVID-19 patient with severe hypocalcaemia. This is a report of an 81-year-old female, suffered from myalgia and fatigue for more than 3-4 weeks. Fever and cough appear 2 days before she presented to the emergency room. On physical examination, she was febrile with a temperature of 38.8°C, accompanied by cough, sore throat, headache, fatigue, and muscle ache. Her past medical history was remarkable with no chronic disease. She had lymphopenia. Laboratory test revealed moderate liver dysfunction, hypoalbuminemia, and severe hypocalcaemia (serum corrected calcium level: 5.7 mg/dL). Parathyroid hormone (PTH) was 107.9 pg/mL (range: 15-65) and 25(OH)2D levels was 4.5 ng/mL (range: 25-80). Chest CT scan detected peripheral ground-glass opacity. Throat swab for coronavirus by RT-PCR assay tested positive for the virus. She was treated with lopinavir/ritonavir, third generation cephalosporin, anticoagulant, daily high-dose calcium acetate, vitamin D3, fresh frozen plasma and oxygen therapy. She was discharged after two negative throat swab tests for coronavirus by conventional RT-PCR.Comorbidities are a risk factor for patients with COVID-19. Laboratory findings are unspecific in COVID-19 patients; laboratory abnormalities include lymphopenia, elevated of LDH, CPK and the inflammatory markers, such as C reactive protein, ferritinemia and the erythrocyte sedimentation rate. In addition to inflammatory markers, in COVID-19 patients it is crucial to check the level of vitamin D and calcium. There may be a correlation between vitamin D deficiency and the severity of COVID-19 disease. |
| 2020 | Seizures and Basal Ganglia Calcification Caused by Hypoparathyroidism. | Cureus | Seizures, not a typical feature of hypoparathyroidism, may present along with myalgia and tetany in patients of hypoparathyroidism. Thorough history and examination, derangement of biochemical parameters such as hypocalcemia, hyperphosphatemia, and inappropriately low levels of parathyroid hormone, along with basal ganglia calcification as seen on imaging, lead to the diagnosis of hypoparathyroidism in a 10-year-old child who presented to us. Treatment with calcium and active vitamin D significantly improved his condition. In this report, we discuss the presentation and treatment of hypoparathyroidism. Early detection and follow-up at clinically appropriate intervals is important to avoid complications. |
| 2017 | Unilateral Submandibular Gland Atrophy and Sialolithiasis Diagnosed on 99mTc-MIBI SPECT/CT in a Patient With Primary Hyperparathyroidism. | Clin Nucl Med | A variety of sequelae of elevated calcium levels are encountered in patients with underlying primary hyperparathyroidism, including stone formation such as calculi in the urinary tract and sialoliths in the salivary glands and ducts. We present a case of a 54-year-old woman with fatigue, myalgia, and poor concentration who was found to have hypercalcemia (corrected calcium, 11.2 mg/dL) and elevated parathyroid hormone level (112 pg/mL), laboratory values consistent with primary hyperparathyroidism. She underwent evaluation with a Tc-MIBI parathyroid SPECT scan that included x-ray CT acquisitions for anatomical localization and attenuation correction. |
| 2016 | Huge Parathyroid Adenoma with Dysphagia Presentation; A Case Report from Southern Iran. | Iran J Med Sci | Parathyroid adenoma is a benign tumor of the parathyroid glands. The cause of most parathyroid adenomas is unknown. Parathyroid adenoma increases the secretion of parathyroid hormone and results in primary hyperparathyroidism. High amounts of parathyroid hormone in the blood cause the imbalance of calcium, which leads to various complications such as kidney stones, depression, lethargy, nausea, vomiting, abdominal pain, myalgia, bone and joint pain, hoarseness, etc. Oropharyngeal dysphagia is defined as having problem in swallowing due to abnormalities in the structure and function of oropharynx and other related organs. The exact prevalence of dysphagia caused by parathyroid adenoma is unknown, but since this complication can lead to increased mortality and morbidity, its diagnosis is important. It is difficult to distinguish parathyroid malignancies from parathyroid adenoma even after surgery. Therefore, the final diagnosis is possible through surgery and histopathological evaluation. Here, a case of parathyroid adenoma with first presentation of generalized weakness and dysphagia has been reported. |
| Oncogenic Osteomalacia From a Primary Phosphaturic Mesenchymal Tumor of the Toe: A Case Report. | J Foot Ankle Surg | Oncogenic osteomalacia is an acquired, rare paraneoplastic syndrome characterized by renal phosphate wasting and subsequent hypophosphatemic osteomalacia. The condition is usually associated with a phosphaturic mesenchymal tumor, which produces fibroblast growth factor 23, the primary circulating factor responsible for reduced tubular phosphate reabsorption. Clinically, adult patients typically present with bone pain, myalgia, recurrent and/or multiple stress fractures, and fatigue, with serum levels typified by low 1,25-(OH)2 vitamin D3, increased alkaline phosphatase, and normal calcium, parathyroid hormone, calcitonin, 25-OH-vitamin D3, and 25,25-(OH)2 vitamin D3 levels. The tumor in question is typically benign and can be of little clinical significance apart from its role in causing hypophosphatemic osteomalacia. Detection of the tumor, therefore, can often be delayed and requires an astute index of suspicion. |
| 2013 | Efficacy and safety of lanthanum carbonate on chronic kidney disease-mineral and bone disorder in dialysis patients: a systematic review. | BMC Nephrol | Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a common complication in CKD patients, particularly in those with end-stage renal disease that requires dialysis. Lanthanum carbonate (LC) is a potent, non-aluminum, non-calcium phosphate binder. This systematic review evaluates the efficacy and safety of LC in CKD-MBD treatment for maintenance-dialysis patients.A systematic review and meta-analysis on randomized controlled trials (RCTs) and quasi-RCTs was performed to assess the efficacy and safety of LC in maintenance hemodialysis or peritoneal dialysis patients. Analysis was performed using the statistical software Review Manager 5.1.Sixteen RCTs involving 3789 patients were identified and retained for this review. No statistical difference was found in all-cause mortality. The limited number of trials was insufficient to show the superiority of LC over other treatments in lowering vascular calcification or cardiovascular events and in improving bone morphology, bone metabolism, or bone turn-over parameters. LC decreased the serum phosphorus level and calcium × phosphate product (Ca × P) as compared to placebo. LC, calcium carbonate (CC), and sevelamer hydrochloride (SH) were comparable in terms of controlling the serum phosphorus, Ca × P product, and intact parathyroid hormone (iPTH) levels. However, LC resulted in a lower serum calcium level and a higher bone-specific alkaline phosphatase level compared with CC. LC had higher total cholesterol and low-density lipoprotein (LDL) cholesterol levels compared with SH. LC-treated patients appeared to have a higher rate of vomiting and lower risk of hypercalcemia, diarrhea, intradialytic hypotension, cramps or myalgia, and abdominal pain. Meta-analysis showed no significant difference in the incidence of other side effects. Accumulation of LC in blood and bone was below toxic levels.LC has high efficacy in lowering serum phosphorus and iPTH levels without increasing the serum calcium. Current evidence does not show a higher rate of adverse effects for LC compared with other treatments, except for a higher incidence of vomiting. Moreover, LC accumulation in blood and bone was below toxic levels. Well-designed studies should be conducted to evaluate the long-term effects of LC. |
| 2012 | Hypocalcemic myopathy secondary to hypoparathyroidism. | WMJ | Myopathy is a rare manifestation of idiopathic hypoparathyroidism. We report a 48-year-old man with a 6-year history of muscle pain and elevated creatine kinase levels. Laboratory analysis revealed low serum calcium, inappropriately low-normal parathyroid hormone, elevated phosphorus, and normal 25-hydroxy vitamin D levels. The patient was diagnosed with idiopathic hypoparathyroidism and treated with calcium and calcitriol. He demonstrated an excellent clinical response and creatine kinase values returned to normal. This case illustrates the subtle nature of hypoparathyroid myopathy and highlights the importance of measuring serum calcium in patients with unexplained myalgia and/or muscle weakness. |
| 2010 | Cinacalcet effect on severe hyperparathyroidism. | Saudi J Kidney Dis Transpl | To determine the efficacy and safety of cinacalcet, a calcimimetic drug that suppress parathyroid hormone (PTH) production, we studied its effect on 20 patients (13 males) on maintenance hemodialysis (HD), 80% of them have persistent high PTH levels (i.e. more than 80 pmol/L), the remaining patients had PTH levels more than 60 pmol/L. Five of 20 (25%) patients dropped out from the study (2 because of severe GIT upset, one showed severe myalgia and arthralgia, one patient due to non compliance and one died at home due to cardiac arrest). The remaining 15 patients (10 males) had a mean age of 40 ± 12.86 years and dialysis duration of 29.13 ± 18.27 months. The follow-up period on cinacalcet was 4 months with a single daily oral dose started with 30 mg/day and increased gradually according to the PTH levels. Nine (60%) patients were on concomitant active vitamin D during the study period with a mean dose of 7.33 ± 3.39 μg/week. There was a significant decrease in the serum PTH levels at the end the study compared to that at the start (46.4 ± 4.7 pmol/L versus 93.3 ± 25.6 pmol/L, respectively, P< 0.000), and the target PTH level (< 31.6 pmol/L) was achieved in 54% of patients. No significant changes in serum Ca and phosphorous levels were observed. We conclude that cinacalcet is an effective therapy to suppress the serum PTH levels and allows favorable management of the serum calcium and phosphorus levels in HD patients. The drug was well tolerated; however, GIT discomfort is a significant side effect that may necessitate drug withdrawal in some patients. |
| 2009 | [The efficacy and safety of intravenous bisphosphonates in the treatment of primary hyperparathyroidism complicated by hypercalcemia crisis]. | Zhonghua Nei Ke Za Zhi | To study the efficacy and adverse events of intravenous bisphosphonates in the treatment of patients of primary hyperparathyroidism (PHPT) complicated by hypercalcemia crisis.From October 2003 to December 2007, 14 patients admitted into our hospital were diagnosed as PHPT complicated by hypercalcemia crisis, which was defined as a serum calcium concentration greater than 3.50 mmol/L. Of them, 6 cases had parathyroid adenoma, 1 had hyperplasia and 7 had parathyroid carcinoma. One of the intravenous bisphosphonates including pamidronate, ibandronate and zoledronic acid was given for 29 times in all the 14 cases. Serum calcium, parathyroid hormone, hematology, and other biochemical markers were monitored. Adverse events were recorded.After intravenous bisphosphonates, the serum total calcium (Ca) levels decreased from (3.85 +/- 0.50) mmol/L to (2.86 +/- 0.39) mmol/L in (1.4 +/- 0.6) days, and were kept below 3.50 mmol/L for (10.14 +/- 8.54) days. There was no significant difference of the magnitude of decrease in serum Ca levels among the patients using pamidronate, ibandronate or zoledronic acid. The change of serum Ca level was associated with the serum Ca level before treatment. The response to intravenous bisphosphonates evaluated by the decrease of serum total calcium levels was more significant in patients with parathyroid adenoma or hyperplasia than those with parathyroid carcinoma. The most common adverse event was pyrexia, which occurred 15 times (51.7%) and 75% of the pyrexia events occurred after the first infusion. Other manifestations included fatigue, flu-like symptom, myalgia, arthralgia and diarrhea with an incidence of 3.4% each (one event in the 29 times of treatment). There were 2 events (6.7%) with mild increase of serum creatinine concentration.Bisphosphonates can decrease serum total calcium levels in hypercalcemia crisis caused by PHPT effectively with mild adverse events. |
| 2005 | A long-term, open-label extension study on the safety of treatment with lanthanum carbonate, a new phosphate binder, in patients receiving hemodialysis. | Curr Med Res Opin | Lanthanum carbonate, a new phosphate binder, is effective in reducing serum phosphorus levels in patients with end-stage renal disease. A 1-year extension study to two randomized controlled studies was conducted to evaluate the long-term safety of lanthanum carbonate in patients who received hemodialysis.Patients from two previous lanthanum carbonate studies were eligible to continue treatment in a 1-year open-label extension. A total of 77 patients (N = 77; 11 from Study 1, 66 from Study 2) were enrolled in this extension. The mean age of patients was 60.9 years (SD +/- 12.5 years); 65% were male and 35% were female. All patients received lanthanum carbonate at the optimal dose for phosphorus control, determined in their previous study. Safety and tolerability were assessed by monitoring adverse events, laboratory parameters, and vital signs. The number of patients who maintained serum phosphorus levels at < or = 5.9 mg/dL (1.9 mmol/L) was recorded, along with serum calcium, calcium x phosphorus product, and parathyroid hormone levels.Lanthanum carbonate was well tolerated and was associated with few treatment-related adverse events. The most commonly reported adverse events were nausea (26.0%), peripheral edema (23.4%), and myalgia (20.8%). No treatment-related serious adverse events occurred. By Week 4, the mean serum phosphorus level had decreased by approximately 1 mg/dL to 5.7 +/- 2.0 mg/dL (1.84 +/- 0.7 mmol/L). At the end of the study, the mean pre-dialysis serum phosphorus level was 5.7 +/- 1.4 mg/dL (1.84 +/- 0.5 mmol/L); 53% of patients had controlled phosphorus levels. Calcium x phosphorus product decreased during Week 1 and remained within a clinically acceptable range thereafter. There were no clinically significant changes in serum calcium, or parathyroid hormone levels.Lanthanum carbonate is well tolerated and is effective for the long-term maintenance of serum phosphorus control in patients with end-stage renal disease. |
| 1990 | Antacid-induced phosphate depletion syndrome presenting as nephrolithiasis. | Aust N Z J Med | A 29-year-old insulin-dependent diabetic woman developed phosphate depletion, nephrolithiasis and bilateral ureteric obstruction due to antacid abuse. Unlike previous descriptions of chronic phosphate depletion, myalgia, weakness and bone pain were absent. Biochemical features included hypophosphataemia, hypercalciuria, hypophosphaturia, elevated plasma, 1,25-dihydroxyvitamin D and low plasma intact parathyroid hormone. These abnormalities were corrected when antacid ingestion was reduced and phosphate intake supplemented. We propose that phosphate depletion secondary to antacid abuse caused 1 alpha-hydroxylase activation and elevation of the plasma 1,25-dihydroxyvitamin D level, leading to marked hypercalciuria. Once diagnosed, antacid abuse is a readily reversible cause of hypercalciuria and renal stones. Moreover, antacid-induced phosphate depletion may present with nephrolithiasis in the absence of musculoskeletal symptoms. This report is intended to draw attention to this important cause of renal stone disease. |