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A standard definition of an optimal 25OHD level has been the concentration above which PTH cannot be suppressed further, or the concentration below which PTH levels begin to rise. Part of this uncertainty may reside with standardization and operator variability in 25OHD assays 32 because a variety of methods to measure 25OHD are available and different extraction procedures are used. Calcium absorption is one index. It is much more difficult to use bone mineral density 33 and reductions in fractures 35 , 36 to establish a threshold.

This illustrates the importance of establishing an international consensus on a reference range for 25OHD, if we are to improve the reference range of PTH by excluding subjects with vitamin D insufficiency. Further studies are required to establish reference intervals for second- and third-generation PTH assays using large population cohorts that are comprised of vitamin D-replete subjects and also to stratify according to age, sex, race, GFR, and possibly body mass index.

Exceptions to this rule have been described so far in about 10 patients who overexpressed N-PTH 12 , 13 , 43 , some in the setting of a severe form of PHPT or parathyroid cancer 12 , In all cases, this has been paradoxically detected by the finding of higher third-generation than second-generation PTH assay results 12 , 13 , Only four studies have so far compared the sensitivity of second-generation vs.

They are summarized in Table 2 , which has been modified from a recent publication These studies summarize hypercalcemic patients with the disease, proven surgically It was the upper normal range defined by the kit supplier in two studies 41 , 44 , or an upper range defined in 70 normocalcemic postmenopausal women in another 45 , or a vitamin D-sufficient range defined in 74 normal subjects in the last study The second-generation, Nichols Allegro Intact PTH assay identified of subjects with elevated PTH values adding the results of two studies 41 , 44 , a sensitivity of For third-generation assays, the Scantibodies Whole PTH assay identified of elevated PTH values when results of the four studies were combined 41 , 44—46 , resulting in a sensitivity of If the four studies are combined 41 , 44—46 for second- and third-generation PTH assays, taking the mean of the two second-generation and the two third-generation PTH assays in the Boudou et al.

All Nichols commercial PTH assays were removed from the market in These results indicate that the sensitivity of second- and third-generation PTH assays in detecting elevated PTH values is similar. It remains to be demonstrated whether these results will differ when reference ranges are established using large population cohorts that are restricted to vitamin D-replete subjects, and stratified according to age, sex, race, and possibly body mass index.

There is no overall difference between second- and third-generation assays for the diagnostic evaluation of PHPT; however, both of these newer generation assays represent an improvement over the first-generation PTH assay. The value of genetic testing in familial hyperparathyroidism and other genetic forms of PHPT is considered in this section.

Gene sequencing is available from both academic and commercial laboratories. For the present discussion, genetic tests are directed at identifying the carrier state for a genetic hyperparathyroid disorder. They are not recommended for use in direct evaluation of DNA in a parathyroid tumor because such testing is not useful for syndrome diagnosis or for tumor staging.

A possible exception could be tumor HRPT2 mutation testing for diagnosis of parathyroid carcinoma, but this requires further study. Traditionally, genetic tests were based on highly penetrant traits. Examples in MEN1 would include serum calcium or, as more recently recognized, skin angiofibromas. Assessment of such traits still has an important place, particularly when DNA testing is not a good option. Genetic tests, and particularly gene sequence tests have several different and related roles.

First, a syndrome may be confirmed in a proband. Confirming a syndrome provides information regarding possible pathological processes that may develop, such as increased incidence of parathyroid carcinoma in hyperparathyroidism-jaw tumor syndrome. The pretest level of suspicion of a syndrome may be variable. For example, families with atypical FHH may rarely be identified by DNA analysis, leading to avoidance of inappropriate parathyroid surgery.

Second, testing in the proband can determine whether a shortcut or exon-specific test can be offered to relatives in that family.

Because all carriers in one syndromal family share an identical mutation, only a small zone of sequence about that mutation needs to be amplified for testing. Third, and in parallel with the above, testing in asymptomatic relatives can establish or refute a member as a silent carrier. In the latter situation, a negative test will spare the subject forever from the need for ongoing biochemical and other screening. When a mutation cannot be identified in an affected family member, the same gene can sometimes be screened by linkage or haplotype testing with nearby polymorphisms.

Assessment of the so-called asymptomatic relative might theoretically include the possibility of prenatal or preimplantation testing, which has rarely been done in a hyperparathyroid syndrome. Fourth, trait testing in a known carrier should be done periodically to screen for emergence of potentially morbid syndromal tumors in parathyroid and other tissues.

Fifth, a positive test may lead to a major intervention. An example of this is the presence of an activating mutation in the RET gene in asymptomatic relatives, with consideration given to early thyroidectomy to prevent or cure medullary thyroid carcinoma. At the present time, preventive parathyroidectomy is not recommended for any of the familial hyperparathyroid syndromes, with the possible exception of hyperparathyroidism-jaw tumor syndrome for the prevention of the possible parathyroid carcinoma.

FHH has traditionally been diagnosed in families by the presence of hypercalcemia and relative hypocalciuria. Hypercalcemia is present in virtually all carriers including neonates 48 , It is recommended that all family members be evaluated once the diagnosis is established.

Hypercalcemia is seen in children under the age of 10 in FHH, a finding that is almost never present in other forms of familial hyperparathyroidism. The calcium to creatinine clearance ratio is of particular value and is usually below 0.

There is a modest overlap in these values. It is important to ensure that other causes of hypercalcemia and relative hypocalciuria are excluded, including concurrent treatment with thiazide diuretics or lithium. The approach to a first case, or an isolated case, or a proband is different from the assessment of kindred. Features suggestive of FHH are hypercalcemia and relative hypocalciuria, hypercalcemia with normal PTH in the normal reference range, and persistent hypercalcemia after an attempted parathyroidectomy.

Definitive diagnosis requires genetic studies of the CASR gene. Rare families with the same syndrome are caused by mutation of one of two unidentified genes mapped by linkage to chromosome 19p and 19q. Presumably, there are CASR mutations for example the promoter region is not tested routinely invisible to current methods. Expense, limited need, and the high false-negative rate limit the use of CASR testing. Testing serum and urine calcium in three relatives has a lower false-negative rate in family diagnosis than doing a DNA sequence in a proband.

However, a genetic test for a CASR mutation in a case of unclear hypercalcemia can avoid unnecessary surgery. CASR gene testing is of greater value in the following circumstances: Its purpose is essentially to confirm the diagnosis and ensure that inappropriate parathyroid surgery is avoided.

Family members being evaluated for FHH should have serum calcium tested, preferably before the age of In MEN1 there is a predisposition to tumors of the parathyroid, pancreatic, and pituitary glands Familial MEN1 requires MEN1 to be present in the presence of one or more first-degree relatives with at least one of the three tumors. This definition does not imply that all MEN1 cases are from the same gene.

We will focus upon the hyperparathyroidism of MEN1. Gastrinoma is less frequent but potentially carries a greater morbidity due to the presence of excessive gastric acid production and the possibility of metastatic disease.

This trait in MEN1 is expressed somewhat similarly to that in sporadic parathyroid adenoma. Important differences are an average onset age 20 yr that is 30 yr younger than in adenoma, a 1: Onset has been noted as early as age 8, but kidney stones and advancing hypercalcemia have not been noted before age The earlier onset is associated with osteopenia at an earlier age than in adenoma.

Before gene identification in , trait testing was the sole method for diagnosis excluding rarely used linkage or haplotype testing about chromosome 11q The traits that have been most useful for diagnosis are ionized calcium, PTH, and prolactin. Skin tumors such as facial angiofibroma and truncal collagenoma are common and very specific for MEN1, however their usefulness in screening has not been established.

Since , MEN1 sequence testing has been offered in academic and commercial labs. Its roles are as listed above. The main role is to give long-term information to patients, relatives, and care providers. Periodic screening for nonparathyroid tumors in known carriers is not covered further here. MEN2A is another autosomal dominant disorder. DNA analysis for mutations in the RET oncogene is of value in considering prophylactic thyroidectomy to prevent the development of medullary thyroid carcinoma.

Silent parathyroid tumors in MEN2A may also be discovered during such a procedure. This is an autosomal dominant disorder. Parathyroid tumors are the most common manifestation, often with the asynchronous development of multiple adenomas 49 , Other features include ossifying fibromas of the mandible and maxilla, and renal lesions such as cysts and hamartomas.

Heritable HRPT2 mutations are also found in a subset of patients with sporadic presentation of parathyroid carcinoma 58 and in a minor proportion of kindreds with FIH HRPT2 DNA testing in relatives can result in the identification and surveillance of individuals at risk for malignant parathyroid disease, raising new questions about treatments and enabling preventative or curative treatment, and this should be seriously considered in these contexts.

FIH is a broad category used for the familial syndromes that do not fit into any of the categories above excluding neonatal severe PHPT that we do not cover due to its rarity. It has no specific features, and some cases must represent occult presentation of an above-mentioned syndrome 49 , Most cases have unknown causes, probably unrelated to the four main genes above Family features that might make a syndromal mutation more likely include multigland parathyroid disease, parathyroid cancer, and onset of hypercalcemia before age I love video , and I'm a foodie duh.

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