An ti-Mülle rian hor mo ne (AMH) is a glycop ro tein be lon gi ng to the tran sfor mi ng growth fac to rs (TGF-β). AMH plays a fun da men tal ro le in the regres sion of Mülle rian duc ts in ma le em bryo. In its ab sen ce, Mülle rian duc ts de ve lop in to fe ma le in ner rep ro duc ti ve or ga ns. In boys, it is sig ni fi can tly pro du ced in Ser to li cel ls of tes tes un til pu ber ty and then slowly dec rea ses to re si dual va lues for the re st of the me n's li fe. AMH ser ves as a bioc he mical mar ker of the pre sen ce of tes tes in cryptor chi dic ma les. In fe ma les, AMH is sec re ted by gra nu lo sa cel ls of sma ll fol lic les in the ova ry. Se rum va lues are al mo st un de tec tab le du ri ng in fan cy and then ra pid ly in crea se wi th the on set of pu ber ty, refl ec ti ng the ini tial rec ruit me nt of pri mor dial fol lic les. AMH is pro du ced in growi ng fol lic les un til they rea ch a sta ge when do mi na nt fol lic le is de tac hed from a co ho rt of an tral fol lic les. The mea su re me nt of se rum AMH le ve ls du ri ng wo ma n's rep ro duc ti ve li fe rep re sen ts an ideal tool for the as ses sme nt of the ova rian fol li cu lar re ser ve. The ad van ta ge of AMH in re la tion to the ova rian ste roid hor mo nes is that se rum le ve ls do not fl uc tua te sig ni fi can tly du ri ng the men strual cycle. In ad di tion, cir cu la ting AMH stron gly cor re la tes wi th an tral fol lic le cou nt (AFC), vi sua li zed by ul tra sou nd in the fol li cu lar pha se of the cycle. As the num ber and qua li ty of the oo cytes di mi ni sh throug hout the wo ma n's rep ro duc ti ve li fe, se rum con cen tra tio ns of AMH gra dual ly dec rea se and fa ll be low de tec tab le le ve ls in me no pau se. This cou ld be of par ti cu lar in te re st in sub fer ti le and in fer ti le wo men un der goi ng as sis ted rep ro duc ti ve tec hniques (ART) in ac hie vi ng preg nan cy. Key wor ds: an ti-Mülle rian hor mo ne; ova rian re ser ve; sper ma to ge ne sis; in fer ti li ty; sex-diff e ren tia tion Review In tro duc tionAn ti-Mülle rian hor mo ne (AMH) is a 140-kDa di meric glycop ro tein hor mo ne and be lon gs to the transfor mi ng growth fac to r-β (TGF-β) fa mi ly. AMH is synthe si zed as a lar ge pre cur sor wi th a sho rt sig nal sequen ce fol lowed by the pre-pro hor mo ne that for ms ho mo di me rs. Prior to sec re tion, the ma tu re hor mo ne un der goes glyco syla tion and di me ri zation to pro du ce a 144-kDa di mer com po sed of iden ti cal di sul phi de-lin ked 72-kDa mo no mer subu ni ts. Ea ch mo no mer con tai ns an N-ter mi nal domain (al so cal led the "pro re gio n") and a C-ter minal do main (al so cal led the "ma tu re re gio n"); it is be lie ved that N-ter mi nal do main ac cen tua tes the ac ti vi ty of the C-ter mi nal do main in whi ch re si des the bioac ti vi ty of the mo le cu le (1). Du ri ng cytoplas mic tran sit, be tween 5 and 20% of AMH is cleaved at a spe ci fi c si te be tween the N-ter mi nal and the C-ter mi nal do main of the 72-kDa mo no mer, to fo rm tw...
Hypersecretion of prolactin by lactotroph cells of the anterior pituitary may lead to hyperprolactinemia in physiological, pathological and idiopathic conditions. Most patients with idiopathic hyperprolactinemia may have radiologically undetected microprolactinomas, but some may present other causes of hyperprolactinemia described as macroprolactinemia. This condition corresponds to the predominance of higher molecular mass prolactin forms (big-big prolactin, MW > 150 kDa), that have been postulated to represent prolactin monomer complexed with anti-prolactin immunoglobulins or autoantibodies. The prevalence of macroprolactinemia in hyperprolactinemic populations between 15-46% has been reported. In the pathophysiology of macroprolactinemia it seems that pituitary prolactin has antigenicity, leading to the production of anti-prolactin autoantibodies, and these antibodies reduce prolactin bioactivity and delay prolactin clearance. Antibody-bound prolactin is big enough to be confi ned to vascular spaces, and therefore macroprolactinemia develops due to the delayed clearance of prolactin rather than increased production. Although the clinical symptoms are less frequent in macroprolactinemic patients, they could not be diff erentiated from true hyperprolactinemic patients, on the basis of clinical features alone. Although gel fi ltration chromatography (GFC) is known to be the gold standard for detecting macroprolactin, the polyethylene glycol precipitation (PEG) method has off ered a simple, cheap, and highly suitable alternative. In conclusion, macroprolactinemia can be considered a benign condition with low incidence of clinical symptoms and therefore hormonal and imaging investigations as well as medical or surgical treatment and prolonged follow-up are not necessary.
Introduction: Macroprolactinaemia is a well-known analytical problem in diagnostics of hyperprolactinaemia usually detected with polyethylene glycol (PEG) precipitation method. Since there is no harmonization in macroprolactin detection and reporting results, this study proposes and evaluates the usefulness of in-house developed algorithm. The aims were to determine the most suitable way of reporting results after PEG treatment and the possibilities of rationalizing the precipitation procedure. Materials and methods: This is a retrospective study based on extracted data for 1136 patients. Prolactin concentrations were measured before and after PEG precipitation on Roche cobas e601. Macroprolactinaemia was defined by percentage recovery and post-PEG prolactin concentrations. Results: Prevalence of macroprolactinaemia using recovery criteria of ≤ 40%, ≤ 60%, and post-PEG prolactin concentrations was 3.3%, 8.8% and 7.8%, respectively. Raising the cut-off value from the upper limit of the manufacturer’s reference interval to 32.9 μg/L does not drastically change detected macroprolactinaemia with recovery criteria. Post-PEG prolactin concentrations showed more than half of the patients with macroprolactinaemia would be overlooked. Regardless of the criteria, a cut-off of 47.0 μg/L would miss most of the macroprolactinaemic patients. Repeated recovery measurements of follow-up patients showed there is a significant difference with mean absolute bias of 9%. Conclusions: Post-PEG prolactin concentration with corresponding reference interval is the most suitable way of reporting results. All samples with prolactin concentration above the upper limit of the manufacturer’s reference interval should be submitted to PEG precipitation. Follow-up period could be prolonged since the difference between the recoveries of repeated measurements is not clinically significant.
Introduction Evaluation of thyroid function is often requested and therefore defining paediatric reference intervals (RIs) is of vital importance. Currently, there is a distinct lack of paediatric RIs for thyroid function tests in Croatia. Thus, we established RIs for thyroid stimulating hormone (TSH), total triiodothyronine (TT3), total thyroxine (TT4), free triiodothyronine (FT3) and free thyroxine (FT4) in the Croatian paediatric population. Materials and methods Reference intervals were calculated from 397 apparently healthy children, aged from 2 days to < 19 years. Serum samples were analysed for thyroid function tests on the Abbott Architect i2000. Age- and sex-specific 95% RIs with 90% confidence intervals were established according to Clinical and Laboratory Standards Institute guidelines. To express the magnitude of sex and age variation, standard deviation ratio (SDR) was calculated using two-level nested ANOVA. The criterion for considering partitioning reference values was set to SDR > 0.3. Results All thyroid function tests required age partitioning, confirmed by SDR above 0.3. There was no need for sex partitioning, confirmed by SDR below 0.3. Still, FT3 was partitioned due to visually noticeable sex related difference for the oldest group (12 years to < 19 years). Conclusion This is the first study to establish RIs for thyroid function tests in the Croatian paediatric population. We propose RIs for widely used Abbott platform, thus giving laboratories method- and population-specific paediatric RIs for thyroid function tests that should improve clinical test interpretation.
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