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Hypercalcaemia – Presentation and Management

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Hypercalcaemia – Presentation and Management CME ENDOCRINOLOGY Clinical Medicine 2017 Vol 17, No 3: 270–3 Hypercalcaemia – presentation and management Author: J e r e m y J O T u r n e r H y p e r c a l c a e m i a i s a c o m m o n d i s o r d e r n o r m a l l y c a u s e d renal colic and abdominal pain related to constipation or peptic by primary hyperparathyroidism (PHPT) or malignancy. ulceration. Symptomatic patients may also experience polyuria A proportion of cases present as an emergency, which and polydipsia secondary to nephrogenic diabetes insipidus carries a significant mortality. Emergency management of and intellectual obtundation. As the severity of hypercalcaemia hypercalcaemia is based on intravenous rehydration with progresses, nausea, vomiting, QT shortening potentially ABSTRACT normal saline but when this is inadequate, bisphosphonate leading to ventricular fibrillation arrest, confusion and coma therapy is used; more recently the novel anti-resorbtive may occur. Physical signs of hypercalcaemia are relatively few agent denosumab has been shown to have a useful role in but include band keratopathy, although this is very rare, and treatment. It is estimated that up to 10% of all cases of PHPT signs related to the aetiology of the hypercalcaemia. Classical presenting under the age of 45 years have an underlying radiographic features of PHPT, although rarely seen, include genetic predisposition; nine potentially causative genes are now resorption of the distal ends of the clavicles, sub periosteal recognised and may be screened in routine clinical practice. erosions on the radial borders of the middle or terminal Although parathyroidectomy is the only curative treatment for phalanges, brown tumours and ‘pepperpot skull’. PHPT, this is indicated in a minority of cases. Many cases can be adequately managed conservatively and guidance from the 4th Differential diagnosis international workshop on the management of asymptomatic PHPT has recently been updated in a consensus statement. The two commonest causes of hypercalcaemia are PHPT and malignancy. Other causes include tertiary hyperparathyroidism, granulomatous disorders (principally Introduction sarcoidosis), thyrotoxicosis, drugs (principally thiazides but Hypercalcaemia is a common disorder, accounting for poorly monitored therapy with alfacalcidol and calcitriol are approximately 0.6% of all acute medical admissions.1 I t s important causes of hypercalcaemia, and lithium therapy prevalence in the general population is up to 1/1,000. It is may also be associated with hypercalcaemia due to Li-induced most commonly due to primary hyperparathyroidism or PHPT), excessive ingestion of calcium carbonate (‘milk alkali malignancy although there are numerous other causes.2 syndrome’), vitamin D toxicity, vitamin A intoxication, The classical symptomatic presentation of hypercalcaemia is seen relatively rarely in the developed world, the commonest Key points presentation being asymptomatic detection on biochemical testing. Management of hypercalcaemia depends on the Nine potentially causative genes are now implicated in primary presentation and underlying cause; while severe hypercalcaemia hyperparathyroidism (PHPT) (>3.5 mmol/L) requires emergency management, 3 a significant proportion of asymptomatic mild hypercalcaemia is due to Guidance on management of asymptomatic PHPT was recently primary hyperparathyroidism (PHPT) and is amenable to updated in the 4 th international consensus guidelines conservative management. Cinacalcet is licensed for PHPT and its role is recognised in the Presentation 4 th international consensus guidelines The commonest presentation is detection of a raised serum calcium concentration on a biochemical screen. If symptoms Denosumab is recognised to have a role in the emergency are present, classically they are ‘moans, bones, stones and management of hypercalcaemia groans’ referring to depressed mood, musculoskeletal pain, Pre-operative parathyroid imaging is increasingly being performed by SPECT CT Author: Consultant endocrinologist and clinical director, Department of Diabetes & Endocrinology, Norfolk and Norwich KEYWORDS: Hypercalcaemia, hyperparathyroidism, malignancy, University Hospital; honorary professor, Norwich Medical School; co parathyroidectomy, SPECT ■ director, NIHR CRN:Eastern Research Network, Norwich, UK . 270 © Royal College of Physicians 2017. All rights reserved. CCMJv17n3-Turner.inddMJv17n3-Turner.indd 227070 115/05/175/05/17 1:121:12 PPMM CME Endocrinology Table 1. Genes potentially implicated in primary > True ectopic production of PTH is very rare. Of course, a diagnosis of carcinoma does not rule out the simultaneous hyperparathyroidism presence of PHPT, which is common. Disorder Gene MEN1 MEN1 Investigations MEN2 RET It is assumed throughout that calcium levels are adjusted for the MEN4 CDKN1B albumin concentration according to the widely used formula: HPT-JT CDC73 Adjusted calcium = Total calcium – 0.02 (40–Albumin) FIHPT MEN1, CDC73, CASR, CDKN1A, CDKN2B, CDKN2C where calcium is measured in mmol/L and albumin in g/L. NSPHPT CASR There is, however, some debate as to whether this formula is universally appropriate or whether individual labs should nsPHPT PTH derive local adjustment formulae.7 MEN1/2/4 = multiple endocrine neoplasia type 1/2/4; HPT-JT = Broadly speaking, if PTH is detectable in the presence = hyperparathyroidism jaw tumour syndrome; FIHPT familial isolated of hypercalcaemia then the cause of the hypercalcaemia is hyperparathyroidism; NSPHPT = neonatal severe primary hyperparathyroidism; nsPHPT = non syndromic primary hyperparathyroidism. usually primary (sometimes tertiary) hyperparathyroidism. Conversely, if the PTH level is suppressed, then the cause is likely malignancy, although consideration of other PTH- immobilisation, familial hypocalciuric hypercalcaemia (FHH) independent pathologies should be undertaken. However, two and untreated Addison's disease. caveats to this approach should be considered. Firstly, while Tertiary hyperparathyroidism occurs in the context of most laboratories will quote a reference range for PTH in the long-standing secondary hyperparathyroidism where some region of 1.6–6.9 pmol/L, the lower limit of this reference range degree of autonomy of parathyroid function arises and thus is very close to the lower limit of detection of the assay and the calcium level rises inappropriately. FHH is a rare inherited therefore results at the lower end of the range require careful disorder of calcium metabolism in which the set point for interpretation, specifically asking if the result is appropriate serum calcium concentration is elevated, usually due to an for the clinical presentation. When in doubt, repeating the 4 inactivating mutation of the calcium sensing receptor gene, assay, discussing with the local laboratory and proceeding with leading to lifelong and usually asymptomatic elevation of other investigations to rule out other possible pathology are all serum calcium with normal or slightly elevated PTH levels and reasonable approaches. Secondly, FHH and PHPT may have reduced urinary calcium excretion. indistinguishable serum biochemistry and conventionally, the only way to separate these two conditions is by urinary Primary hyperparathyroidism biochemistry – specifically, the calcium to creatinine clearance ratio (FHH<0.01 versus PHPT>0.01). This is calculated from Approximately 85% of all PHPT arises because of a solitary simultaneous measurements of urine and plasma calcium and parathyroid adenoma, 1% are due to parathyroid carcinoma creatinine concentrations using the following formula: and the remainder are due to multiple adenomata or multi-gland hyperplasia. 5 Although the majority of PHPT CaCl/CrCl = (urine calcium × plasma creatinine)/(plasma is sporadic, a proportion arises on the background of a calcium × urine creatinine) familial predisposition and abnormalities in a number of potential genes are now recognised (Table 1 ). 6 Thus, during The plasma creatinine concentration needs to be converted to clinical assessment of PHPT, a family history should always the same units as the other parameters (mmol/L). be sought and the physician should remain vigilant for other The 25 OH vitamin D level should be measured when endocrinopathies as may be seen in, for example, multiple investigating hypercalcaemia. This allows the detection endocrine neoplasia (MEN)1. Occurrence of PHPT at a young of vitamin D toxicity and, more importantly, vitamin D age (approximately <45 years) and/or presence of multi-gland deficiency, which is common in PHPT and should be corrected disease should also prompt consideration of this possibility. as part of the management. Other investigations should be performed depending on the M a l i g n a n c y results of the initial investigations, as follows: 1 Parathyroid localisation should be carried out if surgical Up to 20% of all cases of carcinoma will be affected by management is appropriate, but it should be noted that the hypercalcaemia at some point during their clinical course. 2 purpose of such imaging is not to confi rm the diagnosis of Several mechanisms account for hypercalcaemia due to PHPT but rather to localise the target gland pre-operatively. malignancy: Conventional practice has been to perform ultrasound and > Humoral hypercalcaemia of malignancy arises because of Sesta-MIBI nuclear imaging, although the literature gives secretion of PTHrP. wide ranges for sensitivity for these, with typical values > O s t e o l y t i c m e t a s t a s e s . often in the region of 50–70%,8
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