scholarly journals Functional hypoparathyroidism: causes, pathogenesis, clinical significance in Bone tissue pathology

2018 ◽  
Vol 21 (2) ◽  
pp. 30-35
Author(s):  
Guzel M. Nurullina ◽  
Guzyal I. Akhmadullina ◽  
Irina S. Maslova

Parathyroid hormone (PTH) regulates the maintenance of serum calcium concentration in strict limits through direct effects on bones and kidneys and indirectly due to the effect on the gastrointestinal tract. PTH also regulates phosphorus metabolism. Secondary hyperparathyroidism develops in response to a decreased serum calcium and vitamin D levels, leading to an increased bone resorption. However, the increase in parathyroid hormone above the reference values is not observed in all cases of vitamin D deficiency or hypocalcemia. Supressed or inadequately normal PTH in these conditions is referred to as functional hypoparathyroidism. Various theories have been suggested to explain the functional hypoparathyroidism: magnesium deficiency, intestinal calcistat, lower reference values for plasma PTH compared to current cut off interval, biological variations of vitamin D-binding protein. However, at present none of these theories are generally accepted. The clinical significance of functional hypoparathyroidism may be that vitamin D deficiency, hypocalcemia, and hypomagnesemia are associated with a risk of fracture, regardless PTH level.

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Hafsa Majid ◽  
Aysha Habib Khan ◽  
Tariq Moatter

Single nucleotide polymorphisms (SNPs), R990G and A986S of the calcium sensing receptor (CaSR) gene, are shown to influence response of parathyroid hormone (PTH) in subjects with optimal vitamin D levels. This cross-sectional study was conducted in subjects with vitamin D deficiency (VDD) to observe associations between CaSR polymorphisms, plasma iPTH, and serum calcium levels. Adult females (n=140) with known VDD, intact parathyroid hormone (iPTH), and calcium levels were recruited for genotype analysis. The frequencies of the 986 alleles GG, GT, and TT were 68%, 25%, and 7%, respectively, whereas the frequencies of the 990 alleles AA, AG, and GG were 80%, 8.9%, and 11.1%, respectively. The subjects with GG genotype of R990G polymorphism had higher iPTH levels (148.65 versus 91.47 and 86.1 pg/mL for GG versus AA, AG, resp.,P= 0.008 ) and lower calcium levels (8.4 versus 9.04 and 9.07 mg/dL for GG versus AA, AG, resp.,P= 0.002). No such association of A986S polymorphism with plasma iPTH or serum calcium levels was observed in the present study. Patients with VDD bearing the GG genotype of R990G SNPs are prone to have higher iPTH levels and lower calcium.


2011 ◽  
Vol 4 ◽  
pp. CMED.S7116 ◽  
Author(s):  
Evgenia Korytnaya ◽  
Nagashree Gundu Rao ◽  
Jane V. Mayrin

Objective To present a case of hypercalcemia associated with thyrotoxicosis in a patient with vitamin D deficiency and review biochemical changes during the course of treatment. Methods We report a case, describe the changes in serum calcium, phosphorus, parathyroid hormone in Graves’ disease and concomitant Vitamin D deficiency. We compare our findings to those reported in literature. Results Our patient had hypercalcemia secondary to thyrotoxicosis alone, which was confirmed by low parathyroid hormone level and resolution of hypercalcemia with treatment of thyrotoxicosis. The case was complicated by a concomitant vitamin D deficiency. Serum calcium elevation in patients with thyrotoxicosis occurs secondary to hyperthyroidism alone or due to concurrent hyperparathyroidism. Hypercalcemia from thyrotoxicosis is usually asymptomatic and is related to bone resorption. Vitamin D deficiency can be seen in patients with thyrotoxicosis because of accelerated metabolism, poor intestinal absorption and increased demand during bone restoration phase. Coexistence of hypercalcemia and Vitamin D deficiency in patients with thyrotoxicosis is rare, but possible, and 25-hydroxyvitamin D levels should be checked. The definite treatment for hypercalcemia in thyrotoxicosis is correction of thyroid function. Conclusion Hypercalcemia in thyrotoxicosis should be distinguished from concomitant hyperparathyroidism and confirmed by resolution of hypercalcemia with control of thyrotoxicosis. Patients with hypercalcemia and thyrotoxicosis may also have vitamin D deficiency and 25-OH Vitamin D levels should be checked.


Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Mahrukh Khalid ◽  
Vismay Deshani ◽  
Khalid Jadoon

Abstract Background/Aims  Vitamin D deficiency is associated with more severe presentation of primary hyperparathyroidism (PTHP) with high parathyroid hormone (PTH) levels and reduced bone mineral density (BMD). We analyzed data to determine if vitamin D levels had any impact on PTH, serum calcium and BMD at diagnosis and 3 years, in patients being managed conservatively. Methods  Retrospective analysis of patients presenting with PHPT. Based on vitamin D level at diagnosis, patients were divided into two groups; vitamin D sufficient (≥ 50 nmol/L) and vitamin D insufficient (≤ 50 nmol/L). The two groups were compared for age, serum calcium and PTH levels at diagnosis and after mean follow up of 3 years. BMD at forearm and neck of femur (NOF) was only analyzed in the two groups at diagnosis, due to lack of 3 year’s data. Results  There were a total of 93 patients, 17 males, mean age 70; range 38-90. Mean vitamin D level was 73.39 nmol/L in sufficient group (n = 42) and 34.48 nmol/L in insufficient group (n = 40), (difference between means -38.91, 95% confidence interval -45.49 to -32.33, p < 0.0001). There was no significant difference in age, serum calcium and PTH at the time of diagnosis. After three years, there was no significant difference in vitamin D levels between the two groups (mean vitamin D 72.17 nmol/L in sufficient group and 61.48 nmol/L in insufficient group). Despite rise in vitamin D level in insufficient group, no significant change was observed in this group in PTH and serum calcium levels. BMD was lower at both sites in vitamin D sufficient group and difference was statistically significant at NOF. Data were analyzed using unpaired t test and presented as mean ± SEM. Conclusion  50% of patients presenting with PHPT were vitamin D insufficient at diagnosis. Vitamin D was adequately replaced so that at 3 years there was no significant difference in vitamin D status in the two groups. Serum calcium and PTH were no different in the two groups at diagnosis and at three years, despite rise in vitamin D levels in the insufficient group. Interestingly, BMD was lower at forearm and neck of femur in those with sufficient vitamin D levels and the difference was statistically significant at neck of femur. Our data show that vitamin D insufficiency does not have any significant impact on PTH and calcium levels and that vitamin D replacement is safe in PHPT and does not impact serum calcium and PTH levels in the short term. Lower BMD in those with adequate vitamin D levels is difficult to explain and needs further research. Disclosure  M. Khalid: None. V. Deshani: None. K. Jadoon: None.


2005 ◽  
Vol 25 (4) ◽  
pp. 362-366 ◽  
Author(s):  
Nirav Shah ◽  
Judith Bernardini ◽  
Beth Piraino

Background Peritoneal dialysis (PD) patients are at risk for 25(OH) vitamin D deficiency due to effluent loss in addition to traditional risk factors. Objectives To measure 25(OH) vitamin D deficiency in prevalent PD patients, to evaluate a replacement dose, and to determine the effects of correction. Methods 25(OH) vitamin D levels were drawn on prevalent PD patients. Patients deficient in 25(OH) vitamin D were given ergocalciferol, 50 000 IU orally once per week for 4 weeks. Patients scored muscle weakness, bone pain, and fatigue on a scale of 0 (none) to 5 (severe). Serum calcium, phosphate, parathyroid hormone (PTH), and 25(OH) vitamin D, and 1,25(OH)2 vitamin D levels were obtained before and after treatment. Results 25(OH) vitamin D levels were measured in 29 PD patients. Deficiency (<15 ng/mL) was found in 28/29 (97%); 25/29 (86%) had undetectable levels (<7 ng/mL). One course of ergocalciferol corrected the deficiency in all but 1 patient, who required a second course. Scores for muscle weakness and bone pain fell from pre- to posttreatment ( p < 0.001). 1,25(OH)2 vitamin D levels rose post ergocalciferol (from 20 to 26 pg/mL, n = 20, p = 0.09). Serum calcium, phosphate, and PTH levels did not change with ergocalciferol. Conclusions Most PD patients had marked 25(OH) vitamin D deficiency, which was readily and safely corrected with one course of 50000 IU ergocalciferol, having no effect on serum calcium, phosphorus, or PTH, but complaints of muscle weakness and bone pain decreased. A prospective, placebo-controlled double-blinded study is needed to determine whether replacement of 25(OH) vitamin D is beneficial in PD patients.


2016 ◽  
Vol 41 (7) ◽  
pp. 735-740 ◽  
Author(s):  
Enrico Heffler ◽  
Matteo Bonini ◽  
Luisa Brussino ◽  
Paolo Solidoro ◽  
Giuseppe Guida ◽  
...  

Exercise-induced dyspnea is common among adolescents and young adults and often originates from exercise-induced bronchoconstriction (EIB). Sometimes, dyspnea corresponds to exercise-induced laryngospasm (EILO), which is a paradoxical decrease in supraglottic/glottic area. Vitamin D deficiency, which occurs frequently at northern latitudes, might favor laryngospasm by impairing calcium transport and slowing striate muscle relaxation. The aim of this study was to evaluate whether vitamin D status has an influence on bronchial and laryngeal responses to exercise in young, healthy athletes. EIB and EILO were investigated during winter in 37 healthy competitive rowers (24 males; age range 13–25 years), using the eucapnic voluntary hyperventilation test (EVH). EIB was diagnosed when forced expiratory volume in the first second decreased by 10%, EILO when maximum mid-inspiratory flow (MIF50) decreased by 20%. Most athletes (86.5%) had vitamin D deficiency (below 30 ng/mL), 29 mild-moderate (78.4%) and 3 severe (8.1%). EVH showed EIB in 10 subjects (27%), EILO in 16 (43.2%), and combined EIB and EILO in 6 (16.2%). Athletes with EILO had lower vitamin D (19.1 ng/mL vs. 27.0 ng/mL, p < 0.001) and higher parathyroid hormone (30.5 pg/mL vs. 19.2 pg/mL, p = 0.006) levels. The degree of laryngoconstriction (post-EVH MIF50 as a percentage of pre-EVH MIF50) was related directly with vitamin D levels (r = 0.51; p = 0.001) and inversely with parathyroid hormone levels (r = –0.53; p = 0.001). We conclude that vitamin D deficiency is common during winter in young athletes living above the 40th parallel north and favors laryngospasm during exercise, probably by disturbing calcium homeostasis. This effect may negatively influence athletic performance.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A281-A282
Author(s):  
Alexandra Povaliaeva ◽  
Liudmila Ya Rozhinskaya ◽  
Ekaterina A Pigarova ◽  
Larisa K Dzeranova ◽  
Nino N Katamadze ◽  
...  

Abstract Objective: to assess the state of vitamin D metabolism in patients hospitalized with COVID-19 infection. Materials and methods: We examined 49 patients, which were hospitalized for inpatient treatment of COVID-19 infection from May to June 2020. Study group included 24 men (49%) and 25 women (51%), median age 58 years [48; 70], BMI 26.4 kg/m2 [24.3; 30.5]. All patients were diagnosed with pneumonia due to SARS-CoV-2 with median percent of lung involvement equal to 29% [14; 37], 22 patients (45%) required oxygen support upon admission. Median SpO2 was equal to 95% (92; 97), median NEWS score was equal to 3 [2; 6]. Participants were tested for vitamin D metabolites (25(OH)D3, 1,25(OH)2D3, 3-epi-25(OH)D3, 24,25(OH)2D3 and D3) by UPLC-MS/MS, free 25(OH)D and vitamin D-binding protein by ELISA, as well as PTH by electrochemiluminescence immunoassay and routine biochemical parameters of blood serum (calcium, phosphorus, albumin) at the time of admission. Results: patients had in general very low 25()D3 levels - median 10.9 ng/mL [6.9; 15.6], corresponding to a pronounced vitamin D deficiency in half of the patients. Levels of 24,25(OH)2D3 were also low – 0.5 ng/mL [0.2; 0.9], and resulting vitamin D metabolite ratios (25(OH)D3/24,25(OH)2D3) were high-normal or elevated in most patients – 24.1 [19.0; 39.2], indicating decreased activity of 24-hydroxylase. Levels of 1,25(OH)2D3, on the contrary, were high-normal or elevated - 57 pg/mL [46; 79], which, in accordance with 25(OH)D3/1,25(OH)2D3 ratio (219 [134; 266]) suggests an increase in 1α-hydroxylase activity. Median level of 3-epi-25(OH)D3 was 0.7 ng/mL [0.4; 1.0] and D3 metabolite was detectable only in 6 patients. Median DBP level was 432 mg/L [382; 498], median free 25(OH)D was 5.6 pg/mL [3.3; 6.7], median calculated free 25(OH)D was 2.0 pg/mL [1.4; 3.3]. Most patients had albumin-adjusted serum calcium level in the lower half of reference range (median 2.24 mmol/L [2.14; 2.34]). Seven patients had secondary hyperparathyroidism and one patient had primary hyperparathyroidism, the rest of the patients had PTH levels within the normal range.25(OH)D3 levels showed significant negative correlation with percent of lung involvement (r = -0.36, p&lt;0.05) and positive correlation with SpO2 (r = 0.4, p&lt;0.05). 1,25(OH)2D3 levels correlated positively with 25(OH)D3 levels (r = 0.38, p&lt;0.05) and did not correlate significantly with PTH levels (p&gt;0.05). Conclusion: Our data suggests that hospitalized patients with COVID-19 infection have significant impairment of vitamin D metabolism, in particular, an increase in 1α-hydroxylase activity, which cannot be fully explained by pre-existing conditions such as vitamin D deficiency and secondary hyperparathyroidism. The observed profound vitamin D deficiency and association of vitamin D levels with markers of disease severity indicate the importance of vitamin D supplementation in these patients.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A180-A180
Author(s):  
Iqra Iqbal ◽  
Artem Minalyan ◽  
Muhammad Atique Alam Khan ◽  
Glenn A McGrath

Abstract Introduction: About 30% cases of sarcoidosis have extrapulmonary manifestations but only 7% of patients present without any lung involvement. Among those 7%, most of the patients have manifestations on the skin but isolated bone marrow sarcoidosis has not been commonly reported. This case represents an unusual manifestation of isolated bone marrow sarcoidosis presenting with very high calcium levels. Case Presentation: A 58-year-old female presented to us with fatigue, poor appetite, and nausea. She did not report any weight changes. Her cancer screening was up to date. On examination, she appeared dehydrated. No neck swelling was appreciated. Cardiac, respiratory, abdominal, and neurological examinations were normal. Complete blood count showed hemoglobin of 10.6 mg/dL, white blood cell count of 3.8 k/dL, and platelet count of 87 x109/L. Metabolic panel revealed hypercalcemia with corrected calcium levels as high as 12.6 mg/dL. Ionized calcium was 8.1 mg/dL (normal 4.8 - 5.6). Her parathyroid hormone (PTH) level was elevated up to 64.6 mg/dL and then further increased to 134.3 mg/dL. A 24-hour urinary calcium level was normal. 1, 25-dihydroxy (1,25-OH) and 25-OH vitamin D levels were 97 mg/dL (normal 18–72) and 31.2 mg/dL, respectively. Serum protein electrophoresis and light chain analysis were normal. Hyperparathyroidism was suggested as a cause of hypercalcemia. Ultrasound of the neck and sestamibi scan showed a right lower pole parathyroid adenoma. Paraneoplastic hypercalcemia was also one of the differentials. Parathyroid hormone related peptide (PTHrP) was 9 pg/mL (normal 14 - 27). Colonoscopy was normal. Computerized tomography showed normal lungs, liver and spleen. No masses and lymphadenopathy was seen. A bone marrow biopsy was done for pancytopenia. Patient underwent parathyroid adenoma removal followed by a drop in serum calcium level (8.2 mg/dL). Patient was discharged on calcium carbonate and vitamin D tablets. Upon outpatient follow-up, calcium level started to rise again up to 9.8 mg/dL. Despite discontinuation of supplemental calcium and vitamin D, calcium continued to uptrend (11.5 mg/dL 4 weeks later). Angiotensin converting enzyme (ACE) level came back as high as 129 (normal level &lt; 40 mcg/L). Meanwhile, the bone marrow biopsy results showed that 40% of bone marrow was occupied by non-caseating granulomas suggesting sarcoidosis. Patient was started on steroids for isolated bone marrow sarcoidosis, and eventually her serum calcium level normalized. Conclusion: An isolated bone marrow sarcoidosis is an extremely rare manifestation of extrapulmonary sarcoidosis. It can present with pancytopenia and should be sought in patients with persistent hypercalcemia. In addition, our case was challenging due to the presence of a concurrent hyperparathyroidism which was initially thought to be the only explanation of our patient’s hypercalcemia.


2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Kamis Gaballah ◽  
Sami Kenz ◽  
Raeefa Anis ◽  
Omar Kujan

Osteolytic lesions of the jaw are not uncommon. Such lesions usually arise from local pathologies, but some have systemic backgrounds. We describe a 12-year-old girl who presented with an asymptomatic left mandibular swelling. The bony swelling was corresponding to a radiolucent lesion in the left premolar/molar region. This lesion could have represented an inflammatory and developmental odontogenic jaw cyst, giant cell lesion, and odontogenic tumor. However, the workup investigations revealed secondary hyperparathyroidism due to vitamin D deficiency. A vitamin D replacement was initiated with a single I.M. injection of 300,000 I.U followed by 10,000 I.U orally, weekly. Six weeks later, her Vitamin D and parathyroid hormone were normalized, and she showed significant clinical and radiological improvement of the jaw lesion. At 18 months, follow-up the panoramic image revealed complete resolution of the radiolucency and stable normal parathyroid hormone and vitamin D levels. In conclusion, Jaw bone lesions can develop secondary to hyperparathyroidism due to vitamin D deficiency, and this should be ruled out before any surgical intervention. Treatment of such lesions lies in the correction of parathyroid excess with a careful and systematic approach. This may prevent unnecessary surgical intervention in such patients.


2019 ◽  
Vol 160 (4) ◽  
pp. 612-615 ◽  
Author(s):  
Bradley R. Lawson ◽  
Andrew M. Hinson ◽  
Jacob C. Lucas ◽  
Donald L. Bodenner ◽  
Brendan C. Stack

Objective To quantify how frequently intraoperative parathyroid hormone levels increase during thyroid surgery and to explore a possible relationship between secondary hyperparathyroidism due to vitamin D deficiency and elevation in intraoperative parathyroid hormone. Study Design Case series with chart review. Setting Tertiary academic center. Subjects and Methods A total of 428 consecutive patients undergoing completion and total thyroidectomy by the senior author over a 7-year period were included for analysis. All patients had baseline and postexcision intraoperative parathyroid hormone levels as well as vitamin D levels from the same laboratory. Institute of Medicine criteria were employed for vitamin D stratification (>30, normal; 20-29.9, insufficient; <20, deficient) . Other data analyzed include sex, age, neck dissection status, and parathyroid autotransplantation. Results A total of 118 patients (27.6%) had an intraoperative parathyroid hormone elevation above baseline. Patients with vitamin D deficiency were significantly more likely to experience hormone elevation ( P = .04). When parathyroid hormone rose, it did so by a mean 32.1 pg/mL. Patients with vitamin D deficiency demonstrated significantly larger hormone increases ( P = .03). Conclusion Elevation in intraoperative parathyroid hormone levels above baseline after completion and total thyroidectomy occurs in over one-fourth of cases and is significantly associated with vitamin D deficiency. This study is the first to report this observation. We hypothesize that vitamin D deficiency in these patients may create a subclinical secondary hyperparathyroidism that leads to intraoperative parathyroid hormone elevation when the glands are manipulated. Additional studies will be needed to explore this physiologic mechanism and its clinical significance.


1989 ◽  
Vol 256 (4) ◽  
pp. E483-E487 ◽  
Author(s):  
G. G. Kwiecinksi ◽  
G. I. Petrie ◽  
H. F. DeLuca

Vitamin D deficiency reduces mating success and fertility in female rats, but it is not known if the reduction in reproductive performance is a direct action of vitamin D or the hypocalcemia associated with vitamin D deficiency. The effect of vitamin D deficiency with normocalcemia on fertility and reproductive capacity in female rats was investigated. Female weanling rats were maintained on vitamin D-deficient or vitamin D-replete diets until maturity and mated to age-matched, normal, vitamin D-replete males. Three groups of vitamin D-deficient females were maintained on diets varying in calcium and Pi concentrations to test the effect of vitamin D deficiency with different serum calcium and Pi concentrations on reproductive performance. Vitamin D-deficient females were capable of reproduction, but successful matings by all groups of vitamin D-deficient females were markedly reduced regardless of serum calcium concentration, when compared with matings with vitamin D-replete females. Fertility was also drastically reduced in litters from all groups of vitamin D-deficient females regardless of serum calcium concentration, when compared with litters from vitamin D-replete females. Vitamin D-deficient female rats that received vitamin D or 1,25-dihydroxyvitamin D3 were capable of successfully mating and giving rise to normal, healthy litters. These results indicate that vitamin D and not hypocalcemia is directly responsible for reduced reproductive capacity and fertility in vitamin D-deficient female rats.


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