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IPTs
may also have pharmacological causes.
A
typical example is a therapy with anticonvulsant agents, due to the
induction of hepatic enzymes which bring about an increase in the meta-bolism
and clearance of exogenous vitamin D (Phenobarbital).
In
actual fact sodium valproate and carbamazepine, which do not have a
marked hepatic enzymatic induction effect, have a smaller effect on
calcium and vitamin D serum levels. Another therapy which may lead to
IPTs is that with cortisone agents owing to a deficiency in intestinal
conveyance of calcium and a conse-quent decrease in intestinal absorption
of cation.
Besides
the case of pharmacological treatments, IPTs may also occur as a result
of resistance to 1,25(OH)2D3.
This
is an inability to respond to physiological amounts of vitamin D, as
in the rare cases of vitamin D resistant rickets, as well as in the
event of resistance to 1,25(OH)2D3, which is often found in elderly
people owing to the decline in the function of the various tissues and
organs.
This
condition affecting elderly people combines with the reduced efficiency
of renal hydroxylation of vitamin D, with significant consequences on
the calcium-phosphoric metabolism.
Finally, IPTs is a frequent complication of hypercalciuric conditions,
such as the idiopathic hypercalciuria syndrome, characterised by an
increased renal calcium excretion. Patients affected by hypercalciuria
related to renal excretion suffer from a constant calcium loss even
when fasting.
This situation is associated with a proneness to hypocalcemia, with
a consequent increase in PTH secretion - which is regarded as secondary
compared to the renal losses - and in 1,25(OH)2D3 levels.
This
disorder is corrected through the administration of thiazidic agents.
10. Hyperparathyroidism treat-ment IPTp and IPTt are still treated surgically,
whereas for secondary forms the use of vitamin D is certainly advisable.
Depending on the cause, the addition of calcium to the patient's diet
may be recommended.
Furthermore,
the type of vitamin D (native o calcitriol) will be decided based on
the pathogenesis of the secondary hyperparathyroid patho-logy (for instance,
calcitriol will have to be used in the IPTs caused by IRC). Today, the
treatment of IPTp is still based on the possibility of entrusting surgery
to a "parathyroid expert".
The
objective of surgical treatment of IPTp is the resolution of parathyroid
hyperfunction and the restoration of a stably normal function of the
parathyroid glands. It is therefore clear that the strategy differs
depending on the anatomic and patho-logic substrate of IPTp: adenoma
or hyperplasia. If IPTp is supported by adenoma (Picture 8), the exeresis
of the adenoma can solve the problem leaving behind a situation of functional
balance assured by the other glands.
The
task is more difficult when IPTp is caused by a multiple glandular patho-logy,
which may also involve all the glands.
The
removal of all the pathologic tissue would demand total para-thyroidectomy
with consequent secon-dary hypo-parathyroidism. In practice, in order
to assure parathyroid activity, surgeons resort to a 7/8 para-thyroidec-tomy
surgery or to parathyroidectomy with auto-transplantation, with a risk
of relapse and of hypoparathyroidism due to the insufficient function
of the residual tissue or of the transplanted tissue.
This outline of the problem implies the possibility of a diagnosis,
prior or during the operation, between adenoma and hyperplasia, which
can be very difficult to carry out unless an expert is involved.
The
recent progress made in parathyroid surgery has led to the acknowledgement
of the great importance of PTH measure-ment during surgery in order
to evaluate at that stage the need for the exeresis of the whole pathologic
tissue. As regards parathyroidectomy surgery through videoscopy, the
results achie-ved do not demonstrate a superiority of this method compared
to the traditional one, the former certainly being not advisable in
the event of hyperplasia.
Researchers
are currently investigating molecules which are able to stimulate CaR,
which could act as calcium-antagonists (without causing hyper-calcemia!)
and stop the secretion of the hyperfunctioning parathyroid tissue. The
results obtained from the research work carried out so far are encouraging.
This
could represent the future pharma-co-logical approach to IPTp therapy.
11.
Hypoparathyroid syndromes Hypoparathyroid syndromes belong to the large
medical segment represented by hypocalcemias, which fall into two classes:
hypocalcemias due to para-thyroid causes (table II) and hypo-calcemias
not due to parathyroid causes (table III).
Although on the one hand an excessive function of the parathyroid tissue
brings about the clinical condition known as hyperparathyroidism, on
the other hand for this endocrine tissue a reduced function leads to
hormonal deficiency conditions known as hypo-parathyroidism (IpoPT).
Secon-dary hypoparathyroidism (IpoPTs) is certainly the most frequent
form, with neck surgery (mainly of the thyroid gland and of the parathyroids)
with consequent ablation or devascularisation of the parathyroid glands.
Primary hypo-parathyroidism (IpoPTp), on the other side, certainly has
great clinical interest, as it is represented by an heterogeneous galaxy
of genetically caused conditions, whose acknowledgement is important
especially during the first years of life. Advanced physiology, biochemistry,
molecular biology and genetics know-ledge of the mechanisms in charge
of hormonal regulation of calcium, and in special way of PTH and vitamin
D, have aided the characterisation of the pathogenesis of primary hypopara-thyroid
syndromes.
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