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Macroprolactin is an antigen–antibody complex of higher molecular mass than prolactin (>150 kDa), consisting of monomeric prolactin and immunoglobulin G. The term ‘macroprolactinemia’ is used when the concentration of macroprolactin exceeds 60% of the total serum prolactin concentration determined by polyethylene glycol precipitation. The gold standard technique for the diagnosis of macroprolactinemia is gel filtration chromatography. The prevalence of macroprolactinemia in hyperprolactinemic populations varies between 15% and 35%. Although the pathogenesis of these antibodies is not clear, it is possible that changes in the pituitary prolactin molecule represent increased antigenicity to the immune system, leading to the production of anti-prolactin antibodies. Mild hyperprolactinemia usually occurs because macroprolactin is not cleared readily from the circulation due to its higher molecular weight. Moreover, the hypothalamic negative feedback mechanism for autoantibody-bound prolactin is inactive because macroprolactin cannot access the hypothalamus, resulting in hyperprolactinemia. Reduced in-vivo bioactivity of macroprolactin may be the reason for the lack of hyperprolactinemic symptoms. It also seems that anti-prolactin autoantibodies may compete with prolactin molecules for receptor binding, resulting in low bioactivity. Additionally, the large molecular size of macroprolactin confined in the intravascular compartment prevents its passage through the capillary endothelium to the target cells, which may be the reason for the lack of symptoms. Macroprolactinemia is considered to be a benign clinical condition in patients with normal concentrations of bioactive monomeric prolactin, with a lack, or low incidence, of hyperprolactinemic symptoms and negative pituitary imaging. In such cases with resistance to anti-prolactinaemic drugs, no pharmacological treatment, diagnostic investigations or prolonged follow-up are required. However, macroprolactinemia may also occur in patients with conventional symptoms of hyperprolactinemia who cannot be differentiated from patients with true hyperprolactinemia. These symptoms are mainly attributed to excess levels of monomeric prolactin, and this is of concern. The diagnosis of macroprolactinemia is misleading and inappropriate. A multitude of physiological, pharmacological and pathological causes, including stress, prolactinomas, hypothyroidism, renal and hepatic failure, intercostal nerve stimulation and polycystic ovary disease, can contribute to increased levels of monomeric prolactin. It is important for patients with elevated monomeric prolactin levels to undergo routine evaluation to identify the exact pathological state and introduce adequate treatment, regardless of the presence of macroprolactin. In addition, macroprolactinemia occasionally occurs due to macroprolactin associated with pituitary adenomas, with biological activity of macroprolactin comparable with that of monomeric prolactin. In cases when excess macroprolactin occurs with clinical manifestations of hyperprolactinemia, macroprolactinemia should be regarded as a pathological biochemical variant of hyperprolactinemia. An individualized approach to the management of such patients with macroprolactinemia may be necessary, and pituitary imaging, dopamine treatment and prolonged follow-up should be applied. [ABSTRACT FROM AUTHOR]

A case of combined interstitial and intrauterine pregnancies after bilateral salpingectomy and in-vitro fertilization with embryo transfer is reported. The case was incorrectly diagnosed ultrasonographically as intrauterine triplets at 7 weeks gestation. The patient suffered from intra-abdominal bleeding at 14 weeks gestation. At laparotomy, a ruptured left interstitial pregnancy with a non-viable fetus was found in the left abdominal quadrant. The uterine defect was successfully repaired and gestational contents and blood were evacuated from the abdominal cavity. The intrauterine twin pregnancy progressed without incident, and a Caesarean section was performed at 36 weeks gestation, resulting in healthy male and female infants. [ABSTRACT FROM AUTHOR]

A case of combined interstitial and intrauterine pregnancies after bilateral salpingectomy and in-vitro fertilization with embryo transfer is reported. The case was incorrectly diagnosed ultrasonographically as intrauterine triplets at 7 weeks gestation. The patient suffered from intra-abdominal bleeding at 14 weeks gestation. At laparotomy, a ruptured left interstitial pregnancy with a non-viable fetus was found in the left abdominal quadrant. The uterine defect was successfully repaired and gestational contents and blood were evacuated from the abdominal cavity. The intrauterine twin pregnancy progressed without incident, and a Caesarean section was performed at 36 weeks gestation, resulting in health male and female infants. [ABSTRACT FROM PUBLISHER]

A case of simultaneous bilateral tubal pregnancy resulting from in-vitro fertilization and embryo transfer is presented. Repeated transvaginal ultrasound examinations confirmed an intrauterine sac but no fetus. A diagnosis of early missed abortion was incorrectly made and a curettage was performed. The pathological examination showed the presence of decidua and Arias-Stella phenomenon but no chorionic villi. Diagnostic laparoscopy and laparotomy performed 40 days after embryo transfer (eighth week of gestation), revealed bilateral tubal pregnancy. Bilateral salpingectomy was performed. [ABSTRACT FROM AUTHOR]

A case of simultaneous bilateral tubal pregnancy resulting from in-vitro fertilization and embryo transfer is presented. Repeated transvaginal ultrasound examinations confirmed an intrauterine sac but no fetus. A diagnosis of early missed abortion was incorrectly made and a curettage was performed. The pathological examination showed the presence of decidua and Arias-Stella phenomenon but no chorionic villi. Diagnostic laparoscopy and laparotomy performed 40 days after embryo transfer (eighth week of gestation), revealed bilateral tubal pregnancy. Bilateral salpingectomy was performed. [ABSTRACT FROM PUBLISHER]