Result Of Hyperparathyroidism Research Articles

Acute Pancreatitis Caused by Hypercalcemia as an Initial Manifestation of Primary Hyperparathyroidism (PHPT): A Rare Case Report

Acute pancreatitis (AP) is a frequent gastrointestinal emergency with gallstones and chronic alcohol consumption being the most common causes. Other etiologies can also be identified such as hypercalcemia, which remains a rare yet deadly cause of acute pancreatitis. In this case, hypercalcemia is usually the result of hyperparathyroidism. The latter’s causative diseases must be investigated carefully. Herein, we report the case of AP related to hypercalcemia from a parathyroid adenoma. By reporting this case and reviewing the literature, we aim to raise the practitioners’ attention to this association as it is crucial for timely diagnosis and appropriate management of these cases.

Hypercalcemia related pancreatitis

Common etiological factors of acute pancreatitis are alcohol, gallstone disease, drugs, trauma, viral infection and hyperlipidemia. Hypercalcemia as a cause of pancreatitis is very rarely reported. Hypercalcemia is usually the result of hyperparathyroidism (HPT) and the most common cause of HPT is parathyroid adenoma. We present a case of recurrent pancreatitis, which helped in diagnosing an otherwise clinically silent parathyroid adenoma.

Biologic Effects of Parathyroid Hormone Metabolites: Implications for Renal Bone Disease

Renal bone disease or renal osteodystrophy is the term used to describe the spectrum of histologic abnormalities encountered in patients with chronic kidney disease (CKD). The patterns of bone histology encountered in the setting of CKD range from states of high bone turnover, such as osteitis fibrosa, the result of hyperparathyroidism, to states of abnormally low bone turnover, such as adynamic bone.1 The major factors involved in the pathogenesis of secondary hyperparathyroidism include phosphate retention as glomerular filtration rate decreases and low levels of calcitriol as renal mass is reduced. Both of these factors may lower serum calcium and therefore stimulate parathyroid hormone (PTH) secretion. In addition to these indirect effects, low levels of calcitriol and high serum phosphorus have been shown to have direct effects on the parathyroid gland to increase PTH secretion. The pathogenetic factors involved in the development of adynamic bone disease are less well understood, but it appears that oversuppression of PTH and the use of vitamin D compounds may play a role. Thus, in the management of renal osteodystrophy, it is important to be able to monitor and treat hyperparathyroidism effectively while at the same time avoiding oversuppression of PTH. In this regard, accurate measurements of circulating PTH levels are an essential guide in the management of renal bone disease. It is well accepted that PTH is present in the circulation in the form of both the intact 84-amino acid peptide and a variety of truncated fragments.2–4 Although the role of the intact PTH molecule as a major regulator of mineral ion homeostasis is well established, the actions of PTH fragments have remained poorly understood. In this review, we discuss the generation of PTH metabolites and the evidence supporting their biologic activity and their potential role in renal bone disease.

Immunoreactive parathyroid hormone levels in platyrrhini and catarrhini: A comparative analysis with three different assays.

Serum concentrations of the hormonal form of vitamin D3-1,25-dihydroxy-vitamin D3 [1,25-(OH)2-D3]-are elevated in many genera of platyrrhines when compared to catarrhines; this elevation is presumed to result from a decrease in the ability of the target cell receptor effectively to recognize 1,25-(OH)2-D3. The activity of the renal 25-hydroxyvitumin D3-1α-hydroxylase, the mammalian enzyme which synthesizes the majority of the circulating 1,25-(OH)2-D3, is accelerated by parathyroid hormone (PTH). In order to determine whether the elevated serum concentrations of 1,25-(OH)2-D3 in platyrrhines were the result of relative hyperparathyroidism, we measured serum levels of immunoreactive parathyroid hormone (iPTH) in normocalcemic platyrrhines, catarrhines, and human subjects with assays that recognize different domains of the human PTH molecule. Antisera directed against the biologically active, aminoterminus of PTH yielded comparable mean values for iPTH among three test groups. The mean concentration of iPTH as assessed by a "proximal" midregion assay was significantly reduced in platyrrhine serum when compared to either human or catarrhine serum. A "distal" midregion assay yielded a reduced mean value for iPTH in both platyrrhine and catarrhine serum when compared to human serum. These data suggest that 1) high circulating levels of 1,25-(OH)2-D3 in New World primates are not the result of hyperparathyroidism; and 2) structural homology between human and primate PTH diminishes progressively as one moves toward the carboxyterminus of the molecule and is lost more rapidly in the platyrrhine than in the catarrhine hormone.