Premise
So far we have given the general definition of thrombocytopenia, focusing on the related pathological consequences and on the main causes: in this article we will describe in detail the platelet count gravidic and that induced by pharmacological substances. Finally, we will briefly analyze effective therapies to combat this problem once and for all.
Drug-induced thrombocytopenia
In the previous disquisition we saw how excessive intake of some drugs may be responsible for thrombocytopenia.
It is not uncommon for the drug-induced thrombocytopenia to escape diagnosis, for at least two reasons:
- the triggering causes involved in the reduction of platelets in the blood are very numerous and varied
- the drugs responsible for thrombocytopenia are very many, probably hundreds
In light of these considerations, it is clear that the therapy of choice to treat the disease is not properly the most correct one; often, drug-induced thrombocytopenia is confused with the autoimmune form. Similarly, especially in hospitalized patients, symptoms derived from iatrogenic thrombocytopenia are interpreted as a consequence of sepsis or of the aortic / coronary bypass.
The drugs most involved in thrombocytopenia include: heparins (mainly), quinine, platelet inhibitors in general (eg Eptifibatide), vancomycin, antimicrobials in general, antirheumatic drugs, diuretics (eg chlorothiazide), analgesics (paracetamol, naproxen, diclofenac), chemotherapeutic and, more generally, all synthetic substances able to favor the formation of anti-platelet antibodies.
It is estimated that approximately 10 people per million people are affected each year by thrombocytopenia.
Symptoms
Most patients diagnosed with thrombocytes generally do not experience severe symptoms: more often than not, they present petechial hemorrhages and mild ecchymoses. Rare, though possible, cases of wet purple, which require platelet transfusions and / or corticosteroid administration.
However, with the exception of extreme cases, drug-induced thrombocytopenia can be combated by simply suspending the intake of that drug: this is clearly possible only when the responsible drug is identified with absolute certainty.
Platelet infusion
Even in pregnant women, there have been cases of mild thrombocytopenia: it is estimated that in 10% of future mothers there is a physiological reduction of platelets during pregnancy. However, it should be noted that, under normal conditions, the platelet count almost always remains within the physiological range.
The reduction in the blood level of thrombocytes can be triggered by multiple factors, including gestational thrombocytopenia: from the clinical point of view, we are talking about a benign form, which does not involve either harm to the fetus or to the mother.
Sometimes, the woman suffers from thrombocytopenia even before pregnancy; at other times, the lack of platelets in the blood is diagnosed only during gestation, although already present before pregnancy. Like any other pathology, there are also other, much more serious causes responsible for gestational thrombocytopenia: thrombotic microangiopathies and HELLP syndrome, diseases sometimes so serious that they are fatal; those just described remain clearly extreme cases, therefore the probability that the thrombocytopenia gives unfortunate results remains low.
In the case of severe gravid thrombopenia, therapeutic measures must be immediate and at the same time aggressive, in order to cause as little damage as possible to both the mother and the fetus.
Only in the case of severe thrombocytopenia (platelets <30, 000 per mm3) are pregnant women subjected to cortisone during gestation and to immunoglobulins shortly before delivery.
Diagnosis and therapies
In general, when a patient is diagnosed with a form of thrombocytopenia in the absence of pathologies, it is good to distinguish the actual disease from a possible "false alarm": in this case we speak of pseudopiastrinopenia, a possible event derived from a laboratory error linked to the use of EDTA as an anticoagulant substance. In order to overcome this drawback, it is good to repeat the exam using different diagnostic techniques.
A hypothetically suffering platelet patient is usually subjected to palpation of the spleen; again, an ultrasound or CT scan can be performed to ensure the diagnosis.
Sometimes, laboratory tests are necessary, such as thyroid function, antibodies-platelets, phospholipid antibodies, etc.
The platelet elimination / drop locus can also be accurately identified by radioisotopic methods. Again, in the case of presumed thrombocytopenia, a complete blood count can be performed, useful to highlight any defects in the bone.
In some cases, marrow biopsy is recommended, useful for verifying a possible increase or decrease in the number of megakaryocytes.
As far as therapies are concerned, we have seen that in the case of drug-induced thrombopenia, the suspension of the responsible drug is a must; platelet transfusion is reserved for severe cases (<10, 000 platelets / mm3). The administration of corticosteroids, immunoglobulins and immunosuppressants is useful in the chronic forms of thrombocytopenia.