Studies on the elevated amniotic fluid SP1 in Meckel's syndrome: modified glycosylation of SP1.

Pregnancy-specific beta 1-glycoprotein (Schwangerschaftsprotein, SP1) is elevated in the amniotic fluid in Meckel's syndrome. In an attempt to clarify this phenomenon, we studied fetal tissues by immunohistochemistry for the distribution of SP1 in normal fetuses and fetuses with Meckel's syndrome. The amount of SP1 was increased in two out of ten Meckel placentae, as semiquantitatively shown by the immunoperoxidase method, but was normal in the rest of the cases. There was no difference in the SP1 distribution or content in the other fetal tissues studied. Fetal cerebrospinal fluid contained only very low levels of SP1 and thus cannot provide a source for elevated amniotic fluid SP1. In addition, binding of amniotic fluid SP1 to concanavalin A (Con-A) was studied in pregnancies with normal fetuses and Meckel's syndrome using affinity chromatography. The proportion not bound to Con-A in normal amniotic fluids decreased with advancing gestation and was lowest when the total SP1 concentrations were highest. An especially low percentage of SP1 not bound to Con A was found in Meckel's syndrome, suggesting an altered carbohydrate structure of SP1 in these amniotic fluids.

Pregnancy-specific beta 1 glycoprotein (SP1) in the cerebrospinal fluid.

Pregnancy-specific beta 1 glycoprotein (SP1) was assayed by Particle Counting Assay in the cerebrospinal fluid (CSF) from 26 non-neurological patients, from 190 patients with various neurological disorders and from 84 patients with malignant hemopathies. With a sensitivity limit of 0.5 microgram/l, SP1 was undetectable in normal CSF. High levels were observed in CSF from one pregnant woman with herpetic encephalitis and from another woman with post-puerperal thrombophlebitis as a result of high serum concentrations and leakage of the blood-brain barrier. SP1 was detected at low levels in the CSF from 1 patient out of 5 with Creutzfeldt-Jakob disease and from a patient with Behçet's disease. Seven patients out of 84 with malignant hemopathies presented cerebral involvement; 3 of them had detectable SP1. However, SP1 was also detected in the CSF of 2 patients in apparently complete remission. The determination of SP1 in CSF appears to be of limited value in the diagnosis of neurological disorders and in the early detection of a cerebral localization of malignant hemopathies.

Schwangerschaftsprotein 1 (SP1) in serum and cerebrospinal fluid of patients with gestational trophoblastic disease.

The beta subunit of human chorionic gonadotrophin (beta-hCG) and Schwangerschaftsprotein 1 (SP1) were measured by radioimmunoassay in the serum and cerebrospinal fluid (CSF) of 46 postmolar and postpartum patients who developed gestational trophoblastic disease. There was a significant correlation between beta-hCG and SP1 serum levels. The mean serum SP1 level in high-risk patients was significantly higher than that in low-risk patients. There was a significant correlation between serum and CSF beta-hCG levels. The ratio of serum to CSF beta-hCG levels was low in the three patients with clinical evidence of intracranial metastasis. SP1 was present in the CSF of only one of these three patients, but it could be detected in the CSF of another four patients without clinical evidence of metastases in the central nervous system. The two low-risk patients with SP1 present in the CSF showed poor response to intramuscular methotrexate.

Pregnancy-specific beta 1-glycoprotein-like material in human cerebrospinal fluid.

Human cerebrospinal fluid (CSF) from 34 unselected neurological patients was studied for pregnancy-specific beta 1-glycoprotein (SP1) activity because of the recent finding of SP1 production by cultured glial cells. An organic central nervous system lesion was diagnosed in 9 patients, but not in the other 25. Low levels of SP1 immunoreactivity were found in CSF by RIA, and the adsorption of anti-SP1 antiserum with concentrated CSF abolished the positive immunohistochemical staining of placental tissue obtained with the unadsorbed antiserum. By means of immunoadsorption using monoclonal anti-SP1 antibodies, it was possible to isolate SP1 immunoreactive material from CSF and to demonstrate that it had the same electrophoretic mobility in sodium dodecyl sulfate-polyacrylamide gel electrophoresis as purified placental SP1. These results show that CSF contains SP1-like material that is closely related, if not identical, to placental SP1. The amount of SP1 in CSF has no direct correlation to an organic central nervous system lesion or to abnormality of the CSF.

Concentrations of SP1 and beta-hCG in serum and cerebrospinal fluid and concentrations of hCG in urine in patients with trophoblastic tumour.

Using immunological techniques urinary hCG, pregnancy-specific beta 1-glycoprotein (SP1) and beta-subunit of hCG (beta-hCG) levels were measured in the serum and cerebrospinal fluid of patients with trophoblastic tumours. After removal of hydatidiform moles, urinary hCG, beta-hCG and SP1 levels were similar, but SP1 levels tended to exceed serum beta-hCG levels. SP1 usually disappeared first. In patients with metastatic choriocarcinoma, SP1 levels appeared to be lower than beta-hCG values in serum and cerebrospinal fluid, but urinary hCG, beta-hCG and SP1 concentrations all decreased during chemotherapy. Measurements of SP1 levels may well be useful in the monitoring of patients being treated for trophoblastic tumours.