scholarly journals Hypoparathyroidism and pseudohypoparathyroidism

2006 ◽  
Vol 50 (4) ◽  
pp. 664-673 ◽  
Author(s):  
Sergio S. Maeda ◽  
Erika M. Fortes ◽  
Ulisses M. Oliveira ◽  
Victoria C.Z. Borba ◽  
Marise Lazaretti-Castro

The principal function of the parathyroid hormone (PTH) is maintenance of calcium plasmatic levels, withdrawing the calcium from bone tissue, reabsorbing it from the glomerular filtrate, and indirectly increasing its intestinal absorption by stimulating active vitamin D (calcitriol) production. Additionally, the PTH prompts an increase in urinary excretion of phosphorus and bicarbonate, seeking a larger quantity of free calcium available in circulation. Two mechanisms may alter its function, limiting its control on calcium: insufficient PTH production by the parathyroids (hypoparathyroidism), or a resistance against its action in target tissues (pseudohypoparathyroidism). In both cases, there are significantly reduced levels of plasmatic calcium associated with hyperphosphatemia. Clinical cases are characterized by nervous hyperexcitability, with paresthesia, cramps, tetany, hyperreflexia, convulsions, and tetanic crisis. Abnormalities such as cataracts and basal ganglia calcification are also typical of these diseases. Treatment consists of oral calcium supplementation associated with increased doses of vitamin D derivatives.

1993 ◽  
Vol 184 (1) ◽  
pp. 47-61
Author(s):  
D. F. Stiffler

Calcium is present in amphibian blood at a concentration similar to that in other vertebrates, about 1–2 mmol l-1. The fraction of free calcium in amphibians is lower than that in other tetrapod vertebrates because about 50% of the plasma Ca2+ is bound to plasma proteins and perhaps other molecules. Plasma [Ca2+] varies seasonally, increasing in spring and summer and decreasing in winter. Changes in plasma [Ca2+] also occur during larval development, as the concentration of this ion increases in larval forms as they approach metamorphosis. Calcium is exchanged at a variety of sites in animals. There is evidence for Ca2+ uptake across the skin and gills of larval anurans. It is also transported into the blood from the small intestine (especially the duodenum) and reabsorbed in renal tubules from the glomerular filtrate. The possibility of Ca2+ absorption from urine stored in the urinary bladder has not been confirmed, however. Calcium is stored in bone and in specialized endolymphatic sacs. This Ca2+ can be mobilized when the need arises. There are a number of endocrine and other humoral factors that appear to be involved in amphibian calcium metabolism. These include parathyroid hormone, calcitonin, vitamin D and prolactin.


2020 ◽  
Vol 24 (2) ◽  
pp. 206
Author(s):  
Jayaprakash Sahoo ◽  
Rajan Palui ◽  
RashmiRanjan Das ◽  
Ayan Roy ◽  
Sadishkumar Kamalanathan ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A184-A185
Author(s):  
Ahmad Zare ◽  
Sara Choudhry

Abstract Physiological intracranial calcification occurs in about 0.3–1.5% of cases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. A 21-year-old female who was initially evaluated by neurology team for headache and diplopia, underwent MRI of brain which revealed Calcifications involving the bilateral basal ganglia, thalami, dentate nuclei as well as juxtacortical frontal lobes. She reported Fatigue and muscle pain, usually in her arms especially after playing sports which had been going on for many years. She had no history of fractures, seizures, psychiatric disorders, developmental delay or obvious cognitive impairments. She denied any family history of calcium disorders or autoimmune diseases. As she had been generally healthy in her whole life, she never had any lab testing done. On examination, Height 5’1”, Chvostek’s sign was positive. Fundoscopy was normal. she had no dysmorphic features or shortened 4th metacarpal. Investigations revealed serum calcium less than 5.0 mg (N 8.3 - 10.1 mg/dl), PTH 205.1 pg/ml (N 18.4 - 80.1 pg/ml), phosphate 7.1 mg (N 2.5 - 5 mg), Vitamin-D 36.2 ng/ml (N 30.0 - 100.0 pg/ml),magnesium 2.0 m (N 1.6 - 2.6 mg/dl) with normal albumin, alkaline phosphatase and renal function test. She was diagnosed with pseudohypoparathyroidism and started on calcium and active vitamin D supplement and was referred for genetic testing study. She reported significant improvement in myalgia after a few weeks of starting calcium and active vitamin D supplementations and repeat lab testing showed improved hypocalcemia and hyperphosphatemia. This case illustrates unusual presentation of PTH resistance with basal ganglia calcification as initial presentation prompting further workup. She likely has pseudohypoparathyroidism type 1b. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, determination of serum calcium, phosphorus, and parathyroid hormone is mandatory in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism.


2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Hao ◽  
Yun Qin ◽  
Wanjun Zhao ◽  
Lingyun Zhang ◽  
Han Luo

Background: In postthyroidectomy patients, hypocalcemia is the most common complication to prolong hospital stay and decrease patients’ satisfaction. Based on current evidence, it is recommended to supply vitamin D to patients with high risk of developing hypocalcemia. However, how to stratify the risk of patients remains challenging.Aim: We conducted a prospective study to evaluate the effect of vitamin D supplement (calcitriol) on high-risk hypocalcemia patients based on relative decline of parathyroid hormone (RDP).Method: RDP was calculated by the difference between preoperative and postoperative first-day PTH divided by preoperative PTH and presented as percentage. Patients who underwent total thyroidectomy in addition to bilateral central compartment dissection were enrolled prospectively and were divided into two cohorts: Cohort I: patients with RDP ≤70% and Cohort II: patients with RDP >70%. Patients in Cohort I were then randomly assigned to Group A or B, and patients in Cohort II were randomly assigned to Group C or D. All groups received oral calcium, and patients in Groups B and D also received calcitriol. All patients were followed for one year. In the study, standard procedure dictates that only oral calcium is given to patients whose RDP ≤70% and that oral calcium and calcitriol are given to patients whose RDP >70%. Therefore, Cohort I Group A and Cohort II Group D are controls in this study.Results: The incidence of clinical hypocalcemia in Groups A and D (the controls) was 11.0% (10/91), and 17.6% (16/91) required additional intravenous calcium. Of note, no patients developed permanent hypocalcemia. Furthermore, calcitriol supplement did not have significant impact on clinical outcomes between Group A and B in Cohort I. By contrast, calcitriol supplement distinctly improved clinical outcome by comparing Groups C and D (Cohort II), as marked by clinical hypocalcemia, need of requiring intravenous calcium, and long-termed decreased levels of PTH.Conclusion: Supplying calcitriol based on RDP cutoff of 70% may be a wise practice in thyroidectomy patients, and RDP 70% may be a useful predictor to stratify high-risk patients.


Author(s):  
Francesco Trepiccione ◽  
Giovambattista Capasso

Ca2+ homeostasis is achieved through a fine balance among three main organs: the intestine, the kidney, and bone. Blood levels of Ca2+ are accurately tuned through the Ca2+ sensing receptors and regulated by several hormones, including parathyroid hormone (PTH), active vitamin D, and calcitonin. The most recent findings in Ca2+ handling are described. The role of the Ca2+ sensing receptor, as well as Klotho, a new player participating in Ca2+ homeostasis, are described. Finally, the effects of diuretics, calcineurin inhibitors, and the link between hypertension and Ca2+ metabolism are reviewed.


2009 ◽  
Vol 50 (4) ◽  
pp. 420-424 ◽  
Author(s):  
André Russowsky Brunoni ◽  
Ana C.G. Nakata ◽  
Teng Chei Tung ◽  
Geraldo F. Busatto

2017 ◽  
Vol 6 (8) ◽  
pp. 589-594 ◽  
Author(s):  
A Chinoy ◽  
M Skae ◽  
A Babiker ◽  
D Kendall ◽  
M Z Mughal ◽  
...  

Background Hypoparathyroidism is characterised by hypocalcaemia, and standard management is with an active vitamin D analogue and adequate oral calcium intake (dietary and/or supplements). Little is described in the literature about the impact of intercurrent illnesses on calcium homeostasis in children with hypoparathyroidism. Methods We describe three children with hypoparathyroidism in whom intercurrent illnesses led to hypocalcaemia and escalation of treatment with alfacalcidol (1-hydroxycholecalciferol) and calcium supplements. Results Three infants managed with standard treatment for hypoparathyroidism (two with homozygous mutations in GCMB2 gene and one with Sanjad-Sakati syndrome) developed symptomatic hypocalcaemia (two infants developed seizures) following respiratory or gastrointestinal illnesses. Substantial increases in alfacalcidol doses (up to three times their pre-illness doses) and calcium supplementation were required to achieve acceptable serum calcium concentrations. However, following resolution of illness, these children developed an increase in serum calcium and hypercalciuria, necessitating rapid reduction to pre-illness dosages of alfacalcidol and oral calcium supplementation. Conclusion Intercurrent illness may precipitate symptomatic hypocalcaemia in children with hypoparathyroidism, necessitating increase in dosages of alfacalcidol and calcium supplements. Close monitoring is required on resolution of the intercurrent illness, with timely reduction of dosages of active analogues of vitamin D and calcium supplements to prevent hypercalcaemia, hypercalciuria and nephrocalcinosis.


Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 531-536 ◽  
Author(s):  
Miquel Sánchez ◽  
Alejandro de la Sierra ◽  
Antonio Coca ◽  
Esteban Poch ◽  
Vicent Giner ◽  
...  

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