Evaluation of Parathyroid Function in Patients with Hypergastrinaemia and Pernicious Anaemia

Selking, Örjan; Borch, Kurt; Johansson, Henry; Ljunghall, Sverker; Wide, L.

doi:10.3109/03009738209178426

Cited by 8 publications

(7 citation statements)

References 13 publications

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“…This is further supported by a recent observation that mean baseline and stimulated calcitonin levels are significantly higher in patients with high basal gastrin levels than controls [21]. Alternatively, elevated gastrin levels in patients with pernicious anemia could be related to parathyroid hyperfunction, as noted by Selking et al [22], as early as 1982. Although a direct effect of gastrin on the parathyroid glands is unlikely, as gastrin receptors are typically absent from both normal and neoplastic parathyroid tissue [23,24], hypergastrinemia induced by the administration of omeprazole or infusion of gastrin results in increased parathyroid gland weight and PTH gene expression in animal studies [25].…”

Section: Discussionsupporting

confidence: 69%

Primary Hyperparathyroidism in Patients with Gastric Carcinoid Tumors Type 1: An Unusual Coexistence

Thomas

Alexandraki²,

Nikolaou³

et al. 2010

Neuroendocrinology

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Objective: Although a number of familiar syndromes are associated with primary hyperparathyroidism (PHP), there is no information regarding the prevalence of PHP in other sporadic neuroendocrine diseases. The aim of this study is to investigate the prevalence of PHP in our group of patients with gastric carcinoid (GC) type 1 tumors. Methods: Twenty-six patients with biopsy-proven GC type 1 tumors were retrospectively studied. The diagnosis of PHP was suspected following elevated or high-normal serum calcium levels and elevated or inappropriate normal parathyroid hormone levels. Further tests for the localization of the hyperfunctioning parathyroid glands included neck ultrasound, ^99mTc-SESTAMIBI scanning, and cervical or upper mediastinal MR imaging studies. Four control groups were also studied: two age- and sex-matched groups of individuals with (n = 49) and without (n = 34) thyroid autoimmunity and normal endoscopy of the stomach, a third group with nongastric neuroendocrine tumors (n = 68), and a fourth group with atrophic gastritis and hypergastrinemia, without gastric endocrine tumors (n = 30). Results: PHP was diagnosed in 4 (15.38%) patients with GC type 1 tumors compared to none of the 4 control groups. Three of the 4 patients with PHP were operated and proved to have a parathyroid adenoma. No statistically significant differences were observed between patients with or without PHP in mean gastrin and chromogranin A levels, number of lesions, ki-67 labeling index expression, and maximum GC type 1 tumor diameter. Conclusion: PHP seems to be relatively common, approximately 15% in the present cohort, in patients with GC type 1 tumors. PHP should be actively looked for in such patients and treated accordingly.

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Section: Discussionsupporting

confidence: 69%

Primary Hyperparathyroidism in Patients with Gastric Carcinoid Tumors Type 1: An Unusual Coexistence

Thomas

Alexandraki²,

Nikolaou³

et al. 2010

Neuroendocrinology

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“…Indeed, there was an increased prevalence of PHPT in patients with CAAG (8.4 vs 1-3% in the general population (15,16)) and an increased prevalence of CAAG in patients with PHPT (7.4 vs 2% in the general population (3)). Previously, sporadic cases of CAAG and PHPT coexistence had been reported (8,9,10), and an increased prevalence of CAAG in patients with PHPT has been described in three studies (11,12,13), and only one study reported an increased prevalence of PHPT in patients with CAAG (14). In detail, in a retrospective study of 441 patients operated for PHPT, Selking et al (11) found a 1.8% prevalence of pernicious anaemia, which usually occurs in CAAG, compared with a prevalence of 0.3% in the general population.…”

Section: Discussionmentioning

confidence: 99%

“…There is no evidence that hypergastrinemia could influence PTH secretion in humans (11,17,23), whereas hypercalcaemia and/or elevated PTH levels may stimulate gastrin secretion (32,33,34,35). In our study, gastrin and CgA concentrations did not significantly differ in CAAG patients according to the presence or absence of PHPT.…”

Section: Discussionmentioning

confidence: 99%

“…Since the 1970s, sporadic cases of the coexistence of pernicious anaemia and PHPT have been reported (8,9,10), and three studies (11,12,13) have documented the presence of an increased prevalence of CAAG/pernicious anaemia in patients with PHPT (1.8-13.5 vs 0.3-2% in the general population (1,3)). In 2005, Peracchi et al (14) reported an increased prevalence of PHPT in patients with CAAG (5.7% compared with a prevalence of 1-3% in the general population (15,16)).…”

Section: Introductionmentioning

confidence: 99%

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Chronic autoimmune atrophic gastritis associated with primary hyperparathyroidism: a transversal prospective study

Massironi

Cavalcoli

Rossi

et al. 2013

European Journal of Endocrinology

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Design: The coexistence of chronic autoimmune atrophic gastritis (CAAG) and primary hyperparathyroidism (PHPT) has been described previously, even if its extent and underlying mechanisms remain poorly understood. We therefore prospectively evaluated this association in two series of patients, one with CAAG and the other with sporadic PHPT. Methods: From January 2005 to March 2012, 107 histologically confirmed CAAG patients and 149 PHPT patients were consecutively enrolled. Routine laboratory assays included serum calcium, parathyroid hormone (PTH), plasma gastrin and chromogranin A (CgA). In CAAG patients with high PTH levels, ionized calcium and 25(OH)-vitamin D were evaluated. All CAAG and hypergastrinemic PHPT patients received an upper gastrointestinal endoscopy. Exclusion criteria were familial PHPT, MEN1 syndrome, treatment with proton pump inhibitor drugs, Helicobacter pylori infection and renal failure. Results: Of the 107 CAAG patients, nine (8.4%) had PHPT and 13 (12.1%) had secondary hyperparathyroidism stemming from vitamin D deficiency. Among the 149 PHPT patients, 11 (7.4%) had CAAG. Gastrin and CgA levels were similar in the CAAG patients with vs those without hyperparathyroidism (either primary or secondary), and calcium and PTH levels were similar in the PHPT patients with vs those without CAAG. Conclusions: This study confirms a non-casual association between PHPT and CAAG. The prevalence of PHPT in CAAG patients is threefold that of the general population (8.4 vs 1-3%), and the prevalence of CAAG in PHPT patients is fourfold that of the general population (7.4 vs 2%). The mechanisms underlying this association remain unknown, but a potential role for autoimmunity is suggested.

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“…As early as 1982, Selking et al noted an increased prevalence of PA in 441 patients operated for primary HPTH (26), although the same authors could not find a (27). The fact that six out of the seven documented cases with GC and HPTH unrelated to MEN1 (Table 2) were seen in patients with hypergastrinaemia secondary to CAG evokes the question of whether gastrin could be playing a role in the pathogenesis of HPTH in these cases.…”

Section: Discussionmentioning

confidence: 90%

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

Christopoulos

Balatsos²,

Rotas³

et al. 2009

European Journal of Endocrinology

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Objective: To present evidence supporting the hypothesis that the coexistence of gastric carcinoids (GCs) and hyperparathyroidism may represent a distinct clinical entity, not related to multiple endocrine neoplasia type 1 (MEN1). Methods: We studied a cohort of five young siblings (age range 26-42 years), one of whom had been found to have GC and hyperparathyroidism. All siblings underwent serial gastroscopies for the assessment of gastric neuroendocrine cell proliferations over a mean follow-up period of 31.2 months. Imaging, biochemical and hormonal as well as molecular genetic investigations were performed in the direction of MEN1 syndrome. The literature was searched for cases with coexistence of GCs and hyperparathyroidism not associated with MEN1. Results: Four of the siblings, all male, were found to have GCs in a background of Helicobacter pyloriassociated chronic atrophic gastritis and pernicious anaemia, with no serological evidence of gastric autoimmunity. In two of them, asymptomatic hyperparathyroidism was also present. Screening for MEN1 gene mutations or large deletions was negative, and hormone and imaging investigations did not support a diagnosis of familial MEN1 syndrome. A literature search revealed sporadic reports of cases with GC and hyperparathyroidism not attributable to MEN1. Conclusions: The association of GCs and hyperparathyroidism appears to constitute a distinct syndrome that can be encountered in genetically predisposed individuals, and should not be regarded as 'atypical' or 'incomplete' expression of MEN1. Its prevalence and aetiology should be the subject of future studies. Screening for hyperparathyroidism seems to be justified in patients with GC of any type.

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Evaluation of Parathyroid Function in Patients with Hypergastrinaemia and Pernicious Anaemia

Cited by 8 publications

References 13 publications

Primary Hyperparathyroidism in Patients with Gastric Carcinoid Tumors Type 1: An Unusual Coexistence

Primary Hyperparathyroidism in Patients with Gastric Carcinoid Tumors Type 1: An Unusual Coexistence

Chronic autoimmune atrophic gastritis associated with primary hyperparathyroidism: a transversal prospective study

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

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