DermKnowledgeBASE: hyperparathyroidism


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The text is the summary of recent articles on hyperparathyroidism at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.

Many patients are asymptomatic or have unspecific complaints [1]. The most sensitive localization procedures for parathyroid adenomas are sonography and Tc-99(m)-MIBI scintigraphy [2]. The biochemical profile of PHPT is characterized by hypercalcemia and high or inappropriately normal PTH concentrations [3]. Among them, 60 patients underwent regular hemodialysis, 60 patients did not undergo Renal replacement therapy and 60 patients were diagnosed as second hyperparathyroidism (SHPT) [4]. Serum samples were collected and tested, and the demographical, clinical and biochemical data were all recorded [5].

There also is a growing body of evidence indicating that the TBS has particular advantages over BMD for specific causes of increased fracture risk, like Chronic Corticosteroid excess, type-2 diabetes, and chronic Kidney disease, and patients being treated with anti-aromatase and primary hyperparathyroidism, conditions wherein BMD readings are often misleading [6]. However, owing to the diverse presentation of hypercalcemia, the diagnosis often goes unnoticed culminating as a continuum of recurrence of symptoms [7]. Therefore, an anterior planar Technetium-99m-sestamibi (MIBI) scintigraphy scan using a single-tracer was done and it identified ectopic anterior mediastinal parathyroid adenoma [8]. Extensive analyses of parathyroid tissues were performed in subgroup [9]. Gene expressions of known parathyroid-related genes were quantified by qRT-PCR [10].

Protein expression profiles determined by liquid chromatography - tandem mass spectrometry (LC-MS/MS) were compared between each type of parathyroid adenomas [11]. LMO3 and S100B showed higher expression in oxyphilic adenoma and may be involve in parathyroid tumorgenesis through the p53 pathway [12]. In all, 115 out of 224 of the patients imaged underwent parathyroid Surgery [13]. The primary hyperparathyroidism (PHP) and cancers are both responsible for about 80 per cent to 90 per cent of causes of hypercalcemia1 [14]. The other causes of the hypercalcemia are Vitamin D overdose, secondary hypercalcemia due to medications intake and familial hypocalciuric hypercalcemia which will be discussed in this article [15].

Par contre, l’étiologie néoplasique est la plus fréquente en milieu hospitalier [16]. We reviewed the literature with the aim of defining if the echographic criteria predictive of unresponsiveness of SHPT to calcitriol therapy are valid also in the cinacalcet era and if drug therapy may reverse nodular hyperplasia of parathyroid Gland (PTG) [17]. She has had no infections since starting dialysis and no other comorbidity, except well-controlled Hypertension and hyperparathyroidism requiring treatment with cinacalcet [18]. Histopathological examination result of the mass was reported as parathyroid Carcinoma [19]. The patient with these findings was operated and pathological examination of excised left lower parathyroid tissue was reported as Carcinoma [20].

The patient subsequently developed liver Metastasis and hypercalcemia with high 1,25 OH Vitamin D and suppressed parathyroid hormone (PTH) levels [21]. Cinacalcet is an allosteric activator of the calcium receptor agonist, and it is used for severe hypercalcemia in patients with primary (benign and malignant) hyperparathyroidism [22]. In our case, not only severe hyperparathyroidism and mediocalcinosis, but also medication (warfarin, calcium and active Vitamin D) was involved [23]. hyperparathyroidism mostly presents with osteolytic lesions, especially in secondary hyperparathyroidism with renal failure [24]. Several factors have been attributed to cause Renal anaemia, amongst which hyperparathyroidism is one of the less recognised reasons [25].

The level of PTH in early stages of Chronic Kidney disease has not been much studied [26]. Calcium phosphate stones are frequently associated with other diseases such as Renal tubular acidosis type 1, urinary tract infections, and hyperparathyroidism [27]. However, the function of MafB in Adult parathyroid tissue is unclear [28]. Subjects and Methods The Nationwide Readmissions Database was queried for parathyroidectomy procedures performed in patients with Chronic Kidney disease between January 2013 and November 2013 [29]. At variance with patients with the Benign counterpart, the phenotype of these patients is characterized by a severe primary hyperparathyroidism (PHPT) [30].

The clinical features are mostly due to the effects of the excessive secretion of PTH by the functioning Tumor and hypercalcemia rather than to the Tumor burden [31]. The prognosis is poor and unmanageable hypercalcemia accounts for death in the majority of cases [32]. Alteration of microRNA profile and methylation pattern have been identified in PCs [33]. To the best of our knowledge, the D707E Mutation has not been identified to date [34]. Only 4 patients with pheochromocytoma with a median age of 37 years were identified [35].

In contrast to the intimal atherosclerotic lesions that characterize cardiovascular disease in the general population, Vascular endothelial dysfunction, medial arterial calcification, and Cardiac dysfunction contribute to cardiovascular pathological conditions in CKD [36]. hypoparathyroidism can cause hypocalcemia and hyperphosphatemia, whereas deficient Vitamin D actions can cause osteomalacia in adults and rickets in Children [37]. hyperparathyroidism, alternatively, can cause hypercalcemia and hypophosphatemia [38]. There were no univariate differences postoperatively for IL-6, HOMA-IR, leptin, or adiponectin [39]. A 70-year-old Woman was found to manifest hypoglycemia with non-suppressed insulinemia and hypercalcemia with elevated PTH level [40].

She was diagnosed as MEN1 based on the manifestation of primary hyperparathyroidism, pituitary adenoma and insulinoma, with genetic variation of MEN1 gene [41]. Primary hyperparathyroidism is generally discovered when asymptomatic but the disease always has the potential to become symptomatic, resulting in Bone loss and kidney stones [42]. In countries where biochemical screening tests are not common, symptomatic primary hyperparathyroidism tends to predominate [43]. Another variant of primary hyperparathyroidism has been described in which the serum calcium concentration is within normal range but parathyroid hormone is elevated in the absence of any obvious cause [44]. Primary hyperparathyroidism can be cured by removal of the parathyroid Gland or glands but identification of patients who are best advised to have Surgery requires consideration of the guidelines that are regularly updated [45].

Diseases in captive individuals, including secondary nutritional hyperparathyroidism, may commonly be associated with Vitamin D deficiencies, and clinical intervention relies on reference data [46]. In a pre-specified analysis of the "Eplerenone in primary hyperparathyroidism" placebo-controlled, randomized trial (ISRCTN 33941607), effects of eight weeks MR-blockade with eplerenone on Bone turnover markers in 97 patients with primary hyperparathyroidism were tested [47]. The causes of hypercalcemia in Children can be classified as parathyroid hormone (PTH)-dependent or PTH-independent, and may be congenital or Acquired [48]. PTH-dependent hypercalcemia is usually caused by parathyroid Tumors, which may give rise to primary hyperparathyroidism (PHPT) or tertiary hyperparathyroidism, which usually arises in association with Chronic renal failure and in the treatment of hypophosphatemic rickets [49]. Acquired causes of PTH-dependent hypercalcemia in neonates include maternal hypocalcemia and extra-corporeal membrane oxygenation [50].

PHPT usually occurs as an isolated non-syndromic and non-hereditary endocrinopathy, but may also occur as a hereditary hypercalcemic disorder such as familial hypocalciuric hypercalcemia, neonatal severe primary hyperparathyroidism, and familial isolated primary hyperparathyroidism, and less commonly, as part of inherited complex syndromic disorders such as Multiple endocrine neoplasia (MEN) [51]. The management of symptomatic hypercalcemia includes interventions such as fluids, anti-resorptive medications and parathyroid Surgery [52].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 ,

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I have varied research interests ranging from eHealth, Health Information Exchange, Clinical Trials and Research, Contact Dermatitis, Bioinformatics, and Cosmetic Dermatology. I have work experience in Canada as an eHealth analyst, and in Dubai and India as a Specialist Dermatologist.


Bell Raj Eapen
Hamilton, ON