ABSTRACT
In this prospective study, the role of the intact parathormone (iPHT) levels for the verification of pathologic parathyroid tissue removal during parathyroidectomy, was analyzed in 441 patients diagnosed with primary hyperparathyroidism. The level of intact parathormone was obtained before the initial incision (baseline level) and 10 minutes after the pathologic parathyroid gland removal (control value). In 80 % of cases, the decrease of intact parathormone was more than 50 % of the baseline level. The comparison of preoperative and postoperative intact parathormone levels can also be used as marker of parathyroid hyperplasia or persistent hyperparathyroidism. This method is necessary mainly for performance of focused, miniinvasive approaches as well as in reoperations. This method is of significant benefit in cases of negative preoperative examination methods. The determination of intact parathormone level increases the success of parathyroidectomy (Ref. 26).
Subject(s)
Hyperparathyroidism, Primary/surgery , Parathyroid Hormone/blood , Adult , Aged , Female , Humans , Hyperparathyroidism, Primary/blood , Male , Middle Aged , Monitoring, Intraoperative , Parathyroidectomy , Postoperative Period , Prospective Studies , Thyroid Diseases/blood , Thyroid Diseases/surgery , Thyroidectomy/methods , Treatment OutcomeABSTRACT
Incubation of human platelet-rich plasma (PRP) or washed platelets with merthiolate (MT; sodium ethylmercurithiosalicylate; an inhibitor of lysophosphatide: arachidonoyl transferase) leads to irreversible platelet aggregation which is parallelled by an increase in thromboxane A2 synthesis. MT-induced aggregation is preceded by a pronounced lag-period (0.5-10 min). Duration of the latter is inversely related to the concentration of MT ([MT]). Platelet responses to MT are similar to those triggered by arachidonate (AA) in that the relationships of the aggregation rates both to [MT] and [AA] are threshold and exhibit characteristic super-high values of the apparent Hill coefficients (h > 30). A typical MT-induced response can be subdivided in two sequential phases: i) cyclooxygenase-independent slow aggregation, and ii) indomethacin-abrogated rapid aggregation. MT-induced responses are blocked by PGE1 or ajoene (which inhibits binding of fibrinogen to its cell surface receptor, GPIIb/IIIa). The obtained data are interpreted both quantitatively and qualitatively in terms of a model assuming the existence of: i) a relationship between the rate of MT-inhibitable AA incorporation into phospholipids and the concentration of intracellular free AA, [AA]i; ii) a certain threshold value of [AA]i essential for triggering the second phase of the aggregation.
Subject(s)
Platelet Aggregation/drug effects , Platelet Membrane Glycoproteins/metabolism , Thimerosal/pharmacology , Alprostadil/pharmacology , Arachidonic Acid/metabolism , Disulfides/pharmacology , Humans , Indomethacin/pharmacology , Kinetics , Models, Biological , Plant Extracts/pharmacology , Sulfoxides , Thromboxane A2/biosynthesisABSTRACT
Concentration-response relationships of human platelet aggregation rates were analyzed for a variety of agonists and inhibitors. Their approximation by the Hill equation showed that the values of the Hill coefficient (h) were agonist-dependent and increased as follows: hADP = hL-EPINEPHRINE = hPAF = hPGH2 = hU46619 less than hPMA less than hA23187 less than hMERTHIOLATE = hARACHIDONATE. The results were interpreted in terms of a model assuming varying degrees of cooperativity for each step of signal transduction involved in platelet aggregation. Super-high values of h (greater than 30) obtained with arachidonate and merthiolate, as well as in the case of inhibition of an arachidonate-induced response by indomethacin and PTA2, suggested that at least one region of signal transduction pathway leading to aggregation exhibited supercooperative properties.
