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Oxidative stress in proliferative lesions of parathyroid gland

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Deska M., Romuk E., Segiet O., Polczyk J., Buła G., Gawrychowski J.
Polish Journal of Surgery
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2019
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vol. 91(1)
29-34
EN
Background: Primary hyperparathyroidism (PHPT) is one of the most common endocrine disorders and defined as excessive secretion of parathormone. PHPT is a risk factor of several cardiovascular diseases, which could be caused by alterations in oxidant-antioxidant balance. Materials and methods: Blood serum collected from 52 consecutive patients with PHPT treated surgically constituted our study material, whereas 36 healthy volunteers were our control group. Oxidative stress was evaluated in both patients and control subjects by assessment of malondialdehyde (MDA) and lipid hydroperoxides (LHP). Antioxidants were evaluated by the measurement of superoxide dismutase (SOD), ceruloplasmin (CER), catalase (CAT), sulfhydryl (SH) groups, glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione transferase activity (GST) and glutathione reductase (GR). Moreover, total antioxidant capacity (TAC) and total oxidative status (TOS) were measured and oxidative stress index (OSI) was calculated. Results: OSI was increased in patients with PHPT when compared to normal controls, whereas TAC was lower in PHPT. The levels of CER, MnSOD, GR, SH groups and MDA were significantly decreased in PHPT. The levels of serum LHP, catalase and SOD were significantly higher in patients with PHPT than in healthy patients. The erythrocyte CAT activity and GST were significantly increased in patients after parathyroidectomy. The erythrocyte GR and GPx were up-regulated postoperatively, whereas SOD activity decreased. Conclusions: In PHPT there are several alterations in the balance between the production of reactive oxygen species and antioxidant defense system.
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Primary hyperparathyroidism on the example of a 33-year-old female patient with parathyroid adenoma

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Łach J., Dyaczyński M., Buczkowski K.
Polish Journal of Surgery
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2020
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vol. 92(3)
55-61
EN
Parathyroid hyperactivity is the state of over-production and PTH secretion [1]. The most common cause of primary hyperparathyroidism is parathyriod adenoma - about 80% of cases, the remaining are parathyroid hyperplasia around 15%cases [2] [3], and in 1-5% of cases, cancer [2] [3] [4] [5]. The disease is diagnosed inabout 40 people in 100,000 [5] [6] [3] [7]. The most common cause of adenoma is the mutation in gene MEN 1. Less than 5% of cases are chronichyperparathyroidism, which is a component of the MEN 1 MEN 2a endocrine adenocarcinoma syndrome [1]. Excess PTH in the body leads to increased mobilization of calcium from the bones, and henceincreased osteolysis, what also increases the absorption of calcium from thedigestive system, as well as an increased amount of phosphate excretion in the urine. Clinical picture of the disease is multiform and often runs in a latent form. Most often the diseaseoccurs in the form of osteoporosis, chronic recurrent kidney stones, and is also commonpyelonephritis on the basis of urolithiasis. The disease may be accompanied by: dysphagia, abdominal pain, metallic taste in the mouth, persistent constipation. In addition, from the systemnervous: dizziness and headaches, disturbances of consciousness. Arrhythmia the form of additional contractions and paroxysmal tachycardia. Osteolysis, osteoporosis and pathological fractures [1]. The purpose of this article is to bring closer to the reader case of 33 years old woman with primary hyperparathyroidism on the adenoma.
3
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JunGene Expression is Decreased in Parathyroid Adenoma

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Żebracka-Gala J., Waler J., Gawrychowski J., Hasse-Lazar K., Kowalska M., Niemiec A., Szpak-Ulczok S., Jurecka-Lubieniecka B., Buła G., Truchanowski W., Gubała E., Jarząb B.
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issue 10
457-464
EN
The aim of the study was to analyze the gene expression of JUN and CCND1 in a group of parathyroid tissues obtained from patients with primary hyperparathyroidism in comparison to hyperplastic parathyroid and normal/atrophic parathyroid tissues by real-time quantitative PCR. Our goal was to validate the conclusion of Forsberg et al (2005) who reported overexpression of JUN in parathyroid adenomas by a joint microarray and QPCR study.Material and methods. The analysis of JUN, CCND1 was carried out by QPCR in 14 parathyroid adenomas, 8 hyperplasia cases and 50 normal/atrophic parathyroid samples taken intraoperatively. Expression of the examined genes was normalized to the reference index (geometric mean of reference genes expression: EIF3S10, UBE2D2, ATP6V1E).Results. We observed a decrease of JUN expression in parathyroid adenomas in comparison to both normal/atrophic and hyperplastic parathyroids. The fold change value was 0.71 in comparison of adenomas to normal/atrophic samples (p = 0.044) and 0.75 to hyperplastic glands (p = 0.003). For CCND1 we observed one case of parathyroid adenoma with a very clearly increased expression, while 3 adenomas (21.4% of all adenomas) exhibited the increase over the highest value seen in normal parathyroids (fold change = 3.52).Conclusions. In parathyroid adenomas we were not able to confirm any overexpression of JUN gene, as suggested by the previous study. On the contrary, we observed a distinct inhibition of JUN RNA expression in comparison to non-neoplastic parathyroids. For CCND1 gene overexpression in parathyroid adenomas, we report the frequency of 21.4%.
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The profile of ErbB/Her family genes copy number assessed by real-time PCR in parathyroid adenoma and hyperplasia associated with sporadic primary hyperparathyroidism

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Bednarz N., Błaut K., Sworczak K., Osęka T., Bielawski K. P.
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issue 1
83-88
EN
Hyperparathyroidism (pHPT) is a relatively frequent endocrinopathy, however, the molecular mechanisms of its etiology remain poorly understood. This disorder is mainly associated with benign tumours (adenoma) and hyperplasia of the parathyroid, hence, the focus is directed also to genes that are likely to be involved in carcinogenesis. Among such genes are ErbB/Her family genes already used in diagnosis of other tumours (e.g., breast carcinoma) and reported also to play a role in development of endocrine lesions. So far, ErbB-1/Her-1/EGFR expression has been detected in pHPT-associated adenomas and hyperplasia as opposed to no expression in normal parathyroid tissue. Moreover, losses or gains of the fragments of chromosomes where ErbB/Her genes are located have been reported. In this study, the gene dosage of ErbB/Her family genes were determined for the first time in parathyroid adenomas, hyperplasia and morphologically unchanged tissue in order to establish their putative role in the development of the disease. Genomic DNA was isolated from 33 patients with sporadic hyperparathyroidism and the gene copy numbers were assessed using real-time PCR. The ErbB/Her genes' profile was unaltered in most of the examined samples. Two low-level amplifications of ErbB-1/Her-1/EGFR gene, two deletions of ErbB-2/Her-2, and six deletions of ErbB-4/Her-4 were found. The ErbB-3/Her-3 gene remained unaffected. No correlation with clinical parameters was found for any gene. Both the low number of alterations and a lack of their associations with clinical parameters exclude the prognostic value of the ErbB/Her genes family in parathyroid tumourigenesis. Nevertheless, the ErbB-4/Her-4 deletions seem to be interesting for further investigations, especially in the context of PTH secretion.
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