Correction: Late Recovery of Parathyroid Function after Total Thyroidectomy: A Case-Control Study

Author(s):  
Juan José Díez ◽  
Emma Anda ◽  
Julia Sastre ◽  
Begoña Pérez Corral ◽  
Cristina Álvarez-Escolá ◽  
...  
Author(s):  
Juan José Díez ◽  
Emma Anda ◽  
Julia Sastre ◽  
Begoña Pérez Corral ◽  
Cristina Álvarez-Escolá ◽  
...  

AbstractThe clinical characteristics of patients with postoperative hypoparathyroidism who recover parathyroid function more than 12 months after surgery have not been studied. We aimed to evaluate whether the intensity of replacement therapy with calcium and calcitriol is related to the late recovery of parathyroid function. We compared the demographic, surgical, pathological, and analytical features of two groups of patients: cases, i. e., late recovery patients (those who recover parathyroid function>1 year after thyroidectomy, n=40), and controls, i. e., patients with permanent hypoparathyroidism (n=260). Replacement therapy with calcium and calcitriol was evaluated at discharge of surgery, 3–6 months, 12 months, and last visit. No significant differences were found in clinical, surgical, pathological, or analytical characteristics between cases and controls. The proportion of cases who required treatment with calcium plus calcitriol at 12 months was significantly lower than that found in controls (p<0.001). Furthermore, daily calcium and calcitriol doses in controls were significantly higher than those in cases at 3–6 months (p=0.014 and p=0.004, respectively) and at 12 months (p<0.001 and p=0.043, respectively). In several models of logistic regression analysis therapy with calcium and calcitriol at 12 months was negatively related to late recovery of parathyroid function. Although delayed recuperation of parathyroid function after total thyroidectomy is uncommon (13%), follow-up beyond 12 months is necessary in patients with postoperative hypoparathyroidism, especially in those whose needs of treatment with Ca and calcitriol are reducing over time.


2017 ◽  
Vol 11 (3) ◽  
pp. 124-135
Author(s):  
Marilla Dickfos ◽  
Robert Franz

Цель. Амиодарон является жизненно важным лекарством, но способным провоцировать развитие амиодарон-индуцированного тиреотоксикоза (АмИТ) – угрожающего жизни побочного эффекта, который может вызвать серьезную сердечную дисфункцию и привести к развитию сердечной недостаточности. Небольшая часть пациентов не отвечает на терапию, а степень сердечной дисфункции у них продолжает расти. Больным из этой группы обычно выполняют тотальную тиреоидэктомию. Без хирургического удаления щитовидной железы смертность этих пациентов достигает 30–50%. Хотя хирургические вмешательства считаются более безопасными у эутиреоидных пациентов, продление медикаментозной терапии может привести к ухудшению сердечной функции и повышению хирургических рисков. Исследование направлено на изучение безопасности хирургического лечения АмИТ у пациентов, для которых медикаментозная терапия оказалась неэффективной. Методы. Мы проводили сравнение пациентов, подвергшихся хирургическому лечению АмИТ, и пациентов, перенесших тотальную тиреоидэктомию по другим показаниям. Нами были проанализированы демографические данные пациентов, сведения об их ASA-статусах, весе щитовидной железы, осложнениях (возникших в результате хирургического лечения и наркоза) и частоте тиреотоксического криза. Результаты. Это исследование позволило продемонстрировать, что тотальная тиреоидэктомия является относительно безопасной процедурой для лечения АмИТ, который не поддается медикаментозной терапии. Выявлена сходная частота развития осложнений у пациентов двух групп. Выводы. Тотальная тиреоидэктомия является безопасной процедурой и может выполняться у пациентов с АмИТ. Актуальность. Наши данные дают хирургам возможность объяснить пациенту реальные риски при данной операции. Они также обеспечивают лечащему врачу уверенность в безопасности процедуры у больных с амиодарон-индуцированным тиреотоксикозом.


2019 ◽  
Author(s):  
Forough Saki ◽  
azita salehifar ◽  
Seyed Reza Kassaee ◽  
Gholamhossein Ranjbar omrani

Abstract Background:FGF23 controls serum l,25(OH)2D3 levels and phosphate homeostasis. This study evaluates the effects of Ferritin on intact PTH, FGF23 and l,25(OH)2D3 in patients with major thalassemia. It evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH function in human. Methods:In this case-control study,25 patients with major-beta thalassemia with hypoparathyroidism and their age- and gender-matched patients with major-beta thalassemia having normal parathyroid function were enrolled. Biochemical studies assessed serum calcium, albumin phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH)D, 1,25(OH)2D3, Ferritin and Fractional excretion of phosphorous. Results:FGF23 was higher in the patients with hypoparathyroidism compared to controls(p=0.002). Fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite of high FGF23(p=0.001). There was a correlation between serum1,25(OH)2D3 and FGF23 with ferritin in the controls(P=<0.001and P=<0.001,respectively). Conclusions: The present study suggested that rise in FGF23 in patients with thalassemia, may be due to either stimulating effect of PTH and 1,25(OH)2D3 on FGF23 production, or might be direct stimulating effect of ferritin. It seems that in hypoparathyroid patients with insufficient PTH action, the FGF23 is not able to exert its full function in reducing serum phosphorus level by its phosphaturic action.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yanhong Guo ◽  
Qin Wang ◽  
Chunyan Lu ◽  
Pianpian Fan ◽  
Jing Li ◽  
...  

Abstract Background Patients with primary hyperparathyroidism (PHPT) may be asymptomatic, and some may present with normocalcemic PHPT (NPHPT). Patients with vitamin D deficiency may also be asymptomatic, with normal calcium and elevated PTH concentrations. These latter patients are usually diagnosed with vitamin D deficiency-induced secondary hyperparathyroidism (VD-SHPT). Therefore, it is very difficult to distinguish PHPT and NPHPT from VD-SHPT based on calcium or PTH concentrations in clinical settings. In this case-control study, we aimed to verify the diagnostic power of a new parathyroid function index (PFindex = Ca*PTH/P). Methods This study enrolled 128 patients with surgically and pathologically confirmed PHPT, including 36 with NPHPT, at a hospital in West China between January 2009 and September 2017. Thirty-seven patients with VD-SHPT and 45 healthy controls were selected from the population of a cross-sectional epidemiological study as the SHPT and healthy groups, respectively. We used the PFindex to describe the characteristics of PHPT, NPHPT, and VD-SHPT.. Differences between the four groups were compared, and a receiver operating characteristic (ROC) curve analysis was used to evaluate the diagnostic power of PFindex. Results The PHPT group had the highest PFindex (454 ± 430), compared to the other three groups (NPHPT: 101 ± 111; SHPT: 21.7 ± 6.38; healthy: 12.2 ± 2.98, all p < 0.001). A PFindex cut-off value of 34 yielded sensitivity and specificity rates of 96.9 and 97.6% and of 94.4 and 94.6% for the diagnoses of PHPT and NPHPT, respectively. The use of a PFindex > 34 to differentiate NPHPT from VD-SHPT yielded the highest positive likelihood ratio and lowest negative likelihood ratio. Conclusion The PFindex provided excellent diagnostic power for the differentiation of NPHPT from VD-SHPT. This simple tool may be useful for guiding timely decision-making processes regarding the initiation of vitamin D treatment or surgery for PHPT.


1999 ◽  
Vol 51 (4) ◽  
pp. 503-508 ◽  
Author(s):  
Marcocci ◽  
Bruno-Bossio ◽  
Manetti ◽  
Tanda ◽  
Miccoli° ◽  
...  

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Forough Saki ◽  
Azita Salehifar ◽  
Seyed Reza Kassaee ◽  
Gholamhossein Ranjbar Omrani

Abstract Background FGF23 controls serum l,25(OH)2D3 levels and phosphate homeostasis. This study evaluates the effects of ferritin on intact PTH, FGF23, and l,25(OH)2D3 in patients with major thalassemia. It also evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH functioning in human. Methods In this case-control study, 25 major-beta thalassemia patients with hypoparathyroidism were age- and gender-matched with major-beta thalassemia patients having normal parathyroid function. Biochemical studies assessed the serum calcium, albumin, phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH) D, 1,25(OH)2D3, ferritin, and the fractional excretion of phosphorous. Results FGF23 was higher in the patients with hypoparathyroidism than the controls (P = 0.002). The fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite the high level of FGF23 (P = 0.001). There was a correlation between serum 1,25(OH)2D3 and FGF23 with ferritin in the controls (P = < 0.001and P = < 0.001, respectively). Conclusions The present study showed a strong positive correlation between serum ferritin and levels of FGF23 and 1,25(OH)2D3. We hypothesized that ferritin could have a stimulatory effect on the production of 1,25(OH)2D3. Moreover, a rise in FGF23 in patients with thalassemia, might be either associated with the stimulating effect of PTH and 1,25(OH)2D3, or directly related to the stimulating effect of ferritin.


2021 ◽  
Vol 21 (4) ◽  
pp. 123
Author(s):  
Shahram Paydar ◽  
Roham Borazjani ◽  
Hamid Reza Abbasi ◽  
Shahram Bolandparvaz ◽  
Mohammad Hossein Dabbaghmanesh

2021 ◽  
Vol 21 (3) ◽  
pp. 61
Author(s):  
Marcello Picchio ◽  
Annalisa Romina Di Filippo ◽  
Martina Spaziani ◽  
Simone Orelli ◽  
Riccardo Bellagamba ◽  
...  

2019 ◽  
Author(s):  
Forough Saki ◽  
Azita Salehifar ◽  
Seyed Reza Kassaee ◽  
gholamhossein Ranjbar omrani

Abstract Background FGF23 controls serum l,25(OH) 2 D 3 levels and phosphate homeostasis. This study evaluates the effects of Ferritin on intact PTH, FGF23 and l,25(OH) 2 D 3 in patients with major thalassemia. It also evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH function in human.Methods In this case-control study, 25 patients with major-beta thalassemia with hypoparathyroidism and their age- and gender-matched patients with major-beta thalassemia having normal parathyroid function were enrolled. Biochemical studies assessed the serum calcium, albumin phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH)D, 1,25(OH)2D3, Ferritin and Fractional excretion of phosphorous.Results FGF23 was higher in the patients with hypoparathyroidism compared to the controls (p=0.002). Fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite the high level of FGF23(p=0.001). There was a correlation between serum1, 25(OH)2D3, and FGF23 with ferritin in the controls ( P =<0.001and P =<0.001, respectively).Conclusions The present study showed a strong positive correlation between serum ferritin and FGF23 and 1,25(OH)2D3. We hypothesized that ferritin could have stimulatory effect on production of 1,25(OH)2D3. Also, rise in FGF23 in patients with thalassemia, might be associated with either stimulating effect of PTH and 1,25(OH)2D3, or might be related to direct stimulating effect of ferritin.


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