PubMed Health⌕ Search

Biomedical subjects

T Stallmach

Publications and source records attributed to T Stallmach.

At least 55 records · Page 3Linked to original sources
PubMed1998

Incidental choriocarcinoma confined to a near-term placenta.

A large solitary choriocarcinoma was found incidentally in a placenta from a 36-week gestation following caesarean section performed because of intrauterine fetal distress. Macroscopically, there appeared to be a large old infarct in the centre of the placenta proper. Microscopically, there was extensive central necrosis with a rim of viable trophoblastic tumour that had the typical morphology of choriocarcinoma. Although the tumour was floating within maternal blood and was also detected in direct contact with fetal vessels, no metastatic disease was reported in the subsequent 1 1/2 years either in the mother or in the child. Placental infarcts are often not examined histologically, and an intraplacental tumour may thus be missed. Central friability and an unusual colour should alert the pathologist and lead to histological clarification. The management of an incidentally discovered intraplacental choriocarcinoma should be an expectant one, consisting of extensive workup for any evidence of metastases and serial beta-HCG measurements in both mother and child.

Adult↗
PubMed1998

Fetuses from preeclamptic mothers show reduced hepatic erythropoiesis.

The fetal liver is the main hematopoietic organ during intrauterine life. Morphometrical studies were performed on liver sections to detect changes occurring with intrauterine growth retardation and preeclampsia. Compared with the controls (n = 10), fetuses from preeclamptic mothers showed a severe reduction of erythroid cells by 60% on average (n = 18). Closer examination revealed that the erythroid cells at early stages of differentiation were more affected (80% reduction) than at later stages (55%). Seven out of 18 fetuses from preeclamptic mothers did not show growth retardation but exhibited severely reduced hepatic erythropoiesis. We suggest that the prime factor for impaired red blood cell production is preeclampsia itself rather than intrauterine growth retardation. Regulation of erythropoiesis in utero might depend on the interaction of many hematopoietic growth factors, and preeclampsia might alter the balance. To test this notion, we quantitated erythropoietin in fetal blood and various cytokines in the amniotic fluid. An elevation of erythropoietin and interleukin (IL)-3 levels was seen in babies born under the conditions of preeclampsia, whereas the concentrations of granulocyte/macrophage-colony-stimulating factor (CSF), granulocyte-CSF, and IL-1 beta were reduced, and the levels of IL-6 and IL-8 remained constant. With preeclampsia, a discrepancy between elevation of erythrocyte numbers in peripheral blood and depression of hematopoiesis at the main production site, the fetal liver, is seen. Concomitantly, there is elevation of some but reduction of other hematopoietic cytokines. We envision that during the course of preeclampsia quantitation of hematopoietic growth factors might allow to predict the deterioration of in utero life conditions.

Amniotic Fluid↗
PubMed1997

Hypoplastic thymus and T-cell reduction in EECUT syndrome.

We report on a patient with EEC/EECUT syndrome and concomitant hypoplasia of the thymus and reduction of T cells in secondary lymphatic organs. The patient was born prematurely at 35 weeks of gestational age and exhibited ectodermal dysplasia, ectrodactyly, cleft palate and urinary tract abnormalities. On the left side, a large ureterocele was present. On the right side, an atretic ureter was found. Both conditions had led to intrauterine hydronephrosis, renal dysplasia, oligohydramnios, pulmonary hypoplasia, and death of the child. Ureteral malformations are thought to be of epithelial origin. Autopsy showed only small rudiments of thymic tissue containing single epithelial cells, but were completely devoid of Hassall corpuscules. Again, this clearly points to an ectodermal defect. Although there was severe reduction of T cells in secondary lymphatic organs, the thymic defect would not have necessarily led to immunological deficiency; perhaps this is the reason that an epithelial defect in the thymus of patients with EEC syndrome has not yet been reported. With regard to an updating of the diagnosis of the EEC/EECUT syndrome, an "EEC/EECUT plus" syndrome is suggested.

Abnormalities, Multiple↗
PubMed1997

Lethal multiple pterygium syndrome: suggestion for a consistent pathological workup and review of reported cases.

We report on 2 brothers with lethal multiple pterygium syndrome (LMPS) born to non-consanguineous parents as late spontaneous abortions. Both fetuses presented with massive nuchal edema, and facial anomalies including cleft palate and broad ribs. Apparently, several subgroups of LMPS exist. Differentiation is difficult, as there is no consistent agreement on a workup protocol for autopsies. We compared the findings in the literature on cases with LMPS, and we suggest a standardized workup as an initial step for more efficient differentiation between various subgroups.

Abnormalities, Multiple↗
PubMed1997

Familial progressive tubulo-interstitial nephropathy and cholestatic liver disease -- a newly recognized entity?

UNLABELLED: We describe two siblings (female and male) with progressive tubulo-interstitial nephropathy and cholestatic liver disease. The main characteristics were progressive renal failure and elevated liver enzymes (AST, ALT and gamma-GT). Dialysis was started at the age of 1.9 and 6.5 years, respectively. Renal histology disclosed sclerosed glomeruli and atrophic tubules; the interstitium was fibrotic and infiltrated by lymphocytes. Endoscopic retrograde cholangiopancreatography revealed segmental irregularities and narrowing of the intrahepatic bile ducts, consistent with early primary sclerosing cholangitis. Liver histology showed enlarged portal triads, mild proliferation and inflammation of bile ducts, and fibrosis. At 5.9 years the girl underwent a successful renal transplantation whereas the boy is still on dialysis. CONCLUSION: The association of progressive tubulointerstitial nephropathy and cholestatic liver disease, consistent with early primary sclerosing cholangitis, constitutes a distinct autosomal recessive entity.

Biopsy↗
PubMed1997

Lethal maternal sepsis caused by Campylobacter jejuni: pathogen preserved in placenta and identified by molecular methods.

Campylobacter jejuni is one of the most common organisms in the etiology of febrile diarrhea. Bacteremia is reported to be rare. In pregnant women, however, C. jejuni (previous name, Vibrio fetus) can cause fetal death. We report the case of a pregnant woman with enterocolitis and sepsis that caused the death of the fetus and, 11 days later, the death of the mother. C. jejuni was detected by culture techniques at the time of the first symptoms but not during the subsequent course of disease. Bacteria were detected by silver staining and electron microscopic examination in the placenta, but for identification, we used molecular methods. From formalin-fixed, paraffin-embedded placental tissues, a part of the bacterial 16S rRNA was amplified by broad-range polymerase chain reaction, which resulted in a 461-nucleotide sequence. Direct sequencing and comparison to reference sequences revealed C. jejuni as the causative agent for the sepsis and deaths. With this approach, the adverse outcome could be related etiologically to the same infectious agent identified at the onset of the disease. From this and other recent reports, we conclude that C. jejuni must be considered an important pathogen in pregnancy.

Adult↗
PubMed1996

Diaphragmatic defects, limb deficiencies, and ossification defects of the skull: a distinctive malformation syndrome.

We report on prenatal and postnatal findings in 4 consecutive fetuses with a pattern of severe congenital anomalies who were born to a healthy nonconsanguineous couple. The spectrum of malformations includes diaphragmatic defects, hypoplastic lungs, omphalocele, limb deficiencies, syndactyly of toes, and ossification defects of the skull. This specific spectrum of anomalies is not fully compatible with that of any established syndrome. No prenatal exposure to any possible teratogen was found. Family history is suggestive for autosomal recessive inheritance, even though germ-line mosaicism in one of the parents cannot completely be excluded.

Abnormalities, Multiple↗
PubMed1996

Autocrine regulation of growth by insulin-like growth factor (IGF)-II mediated by type I IGF-receptor in Wilms tumor cells.

Wilms tumor is a common embryonic tumor in childhood. Two Wilms tumor-suppressor genes, WT1 and WT2, are located on chromosome 11p, WT2 at 11p15.5 close to the IGF-II gene, which is highly expressed in some Wilms tumors. We established Wilms tumor cell lines to investigate the regulation of tumor cell growth by IGF-II. We demonstrated that Wilms tumor cells produce more IGF-II than normal kidney cells. Both types I and II IGF receptors reside on these cells. In serum-free culture medium, tumor cell growth is reversibly inhibited by suramin via interfering with IGF-II binding. Wilms tumor cell growth is also arrested by IGF binding protein-3, capturing the continuously produced IGF-II, and by alpha IR-3, a type I IGF receptor-blocking antibody. Thus, we demonstrated the whole loop of elevated synthesis, secretion, receptor binding, and autocrine growth stimulation of IGF-II through type I IGF receptor in Wilms tumor cell cultures. We concluded that IGF-II plays a crucial role in the regulation of growth of this embryonic tumor. Overproduction of IGF-II by the tumor cell is the limiting step for Wilms tumor growth, supporting its important role as an embryonic growth factor.

Animals↗
PubMed1996

Image cytometric DNA analysis of adrenocortical neoplasms as a prognostic parameter: a clinico-pathologic study of 13 patients.

Formalin-fixed paraffin-embedded material of thirteen adrenocortical neoplasms were examined by conventional microscopy, and by DNA image cytometry in Feulgen-stained tissue sections and cytospin preparations. The subsequent clinical course of each patient was reviewed. Seven of the neoplasms were classified according to the histologic criteria of Weiss as adenomas and six as carcinomas. The DNA content and indices of all 13 adrenocortical neoplasms were measured by image cytometry. For the internal standard, the DNA values of the adjacent normal adrenal cells in 10 cases and of nuclei of fibrocytes of the tumour stroma were determined. DNA values in all seven adenomas, in normal adrenal cells, and in the nuclei of fibrocytes were unequivocally diploid. The six carcinomas expressed aneuploid, tetraploid or hypertetraploid DNA values. DNA values of normal adrenal cells seemed to provide a better internal control than those of connective tissue cells. Of the seven adenoma patients with a follow-up between 8 and 124 months (mean 59 months), six were alive without evidence of tumour; one patient died from other causes. Of the six carcinoma patients with a follow-up ranging from 5 days to 36 months, three patients died from the disease; one patient was alive with metastases, and only two patients were alive without evidence of the disease for 25 and 36 months, respectively. Our results strongly suggest that image cytometric DNA analysis is a valuable method to distinguish between benign and malignant adrenocortical neoplasms.

Adrenal Cortex Neoplasms↗
PubMed1995

The role of perforin-expression by granular metrial gland cells in pregnancy.

The pregnant uterus of humans and rodents contains a population of granulated lymphoid cells, which, in the mouse, are called granular metrial gland (GMG) cells and have been described to express high levels of perforin. Since there is evidence for cytolytic activity of these cells and since perforin is a crucial effector molecule for the lytic action of cytotoxic T cells and natural killer cells, we evaluated the function of perforin in the pregnant uterus by using perforin-deficient mice. Perforin-deficient female mice were found to reproduce as efficiently as normal control females when bred either with syngeneic or allogeneic males. However, perforin-deficient mice differed from normal mice in that the frequency of GMG cells was significantly higher within maternal blood spaces and within several compartments of the feto-maternal interface. Proliferating GMG cells, identified by [3H] thymidine incorporation, were observed during more advanced stages of pregnancy when compared to normal controls. In contrast to normal mice, perforin-deficient mice did not display GMG cells attached to degenerating trophoblasts; instead perforin-deficient GMG cells were often observed in association with small maternal lymphocytes. In addition, the lack of transmission of lymphocytic choriomeningitis virus from infected pregnant perforin-deficient mice to the fetuses argued against a role of perforin expression by GMG cells in prevention of virus transmission from the mother to the fetus. Our data indicate that functional perforin is not necessary for successful pregnancies. The morphological changes in the pregnant uterus of perforin-deficient mice might, however, point to a certain, as-yet undefined function of perforin in the uterus of pregnant normal mice, which is functionally compensated in perforin-deficient mice.

Animals↗
PubMed1995

Prenatal sonographic diagnosis of autosomal recessive polycystic kidney disease (ARPKD) during the early second trimester.

Autosomal recessive polycystic kidney disease (ARPKD) is a rare hereditary disease with a high neonatal mortality. Currently, prenatal diagnosis is possible only during the second half of pregnancy, when bilaterally enlarged, echogenic kidneys are visible by ultrasound. We describe a case in which a diagnosis of ARPKD was sought in the first half of pregnancy. High-resolution ultrasonography revealed echogenic, normal-sized kidneys at 15 + 4 weeks. Microsatellite DNA analysis of a chorionic villus sample, parental blood, and blood of an affected sibling showed that the fetus had the maternal haplotype and a recombination of the paternal haplotype. Thus, no distinction between homo- and heterozygosity for the ARPKD mutation in the fetus was possible. A further ultrasound examination at 19 + 4 weeks confirmed the previous results, indicating that the fetus was likely to be affected. After termination of the pregnancy, the diagnosis was confirmed on microscopic examination.

Adult↗
PubMed1995

[Placental site trophoblastic tumor. Morphology, differential diagnosis and prognosis].

A placental-site trophoblastic tumor is a rare neoplasia that is derived from the cells of the intermediate trophoblast. Morphological, biochemical, and Doppler ultrasound findings are presented regarding differential diagnosis using material from three recent cases. Essentially, placental-site trophoblastic tumors can be diagnosed if infiltration of the myometrium is seen by a monomorphic trophoblastic proliferation that is not interrupted by decidual cells. Necrosis and hemorrhages are not features of placental-site trophoblastic tumors. However, there is a peculiar behavior towards the uterine vasculature as spiral arteries are dilated and transformed the same way as occurs at the site of physiological implantation of pregnancy. It appears that as a result of this phenomenon there is a characteristic finding in ultrasound. Examination of this type of tumor demonstrates cystic spaces that can be defined as blood vessels by their Doppler signal. In two of the three cases a hysterectomy was performed, and criteria for the assumption of malignant placental-site tumors are therefore presented. However, only the mitosis rate seems to possess some predictive value.

Adult↗
PubMed1995

Expression pattern of cytokines in the different compartments of the feto-maternal unit under various conditions.

Concentrations of five cytokines, GM-CSF, G-CSF, IL-1, IL-6 and IL-8, were determined within five compartments under four different conditions: at the time of a Caesarean section performed between 25 and 38 weeks' gestational age in normal pregnancy without uterine contraction (n = 12), in normal pregnancy with labour already established (n = 8), in pregnancy complicated by amniotic infection (n = 11), or under the conditions of preeclampsia with fetal intrauterine dystrophy (n = 13), cytokine concentrations were determined in fetal arterial and venous blood, in amniotic fluid, and in retroplacentally obtained maternal blood and peripheral maternal blood. With dystrophy, the concentrations of GM-CSF, G-CSF and IL-1 were about 20-50% lower (P < 0.01) in the amniotic fluid, and IL-6 and IL-8 were elevated in maternal peripheral blood (P < 0.01) but not within maternal retroplacental blood. Thus, preeclampsia/intrauterine dystrophy is characterized by reduction of some cytokines within the amniotic fluid compartment and concomitant reactive augmentations of other cytokines within the maternal and fetal organism. With amniotic fluid infection, concentrations of G-CSF, IL-6 and IL-8 were elevated in all compartments (P < 0.001) but GM-CSF and IL-1 showed a significant rise only within amniotic fluid and retroplacental maternal blood (P < 0.001), a rise that was apparently not transmitted to peripheral maternal or fetal blood. Care was taken to exclude the presence of uterine contractions in the group of controls, because this condition by itself causes severe elevation of cytokine concentrations, which are pronounced within amniotic fluid.

Amniotic Fluid↗
PubMed1995

[Transvaginal ultrasound of "placental-site trophoblastic tumor"].

The case of a placental-site trophoblastic tumor (PSTT) is described. Transvaginal sonography revealed a vascularized tumor mass with a deep invasion of the myometrium, partly with echogenic, solid parts and partly multiple echo-free cystic lesions. The maximum size of an echo-free cystic lesion was 4.4 cm. Doppler exploration indicated the presence of blood flow in all these cystic lesions. Distinctly abnormal low flow indices were prominent in the whole tumor area. According to the clinical results and the slightly positive levels of human chorionic beta-gonadotropin (100-1,000 IU/l postpartum), this tumor was classified as malignant trophoblastic disease, most likely PSTT. The authors conclude that, in the case of a patient with suspected trophoblastic disease and in view of the sonographic findings, PSTT may be a valid differential diagnosis, particularly if larger cystic lesions of more than 3 cm in diameter are found in the tumor bed together with evident blood flow at a low vascular resistance.

Adult↗
PubMed1995

Cytokine production and visualized effects in the feto-maternal unit. Quantitative and topographic data on cytokines during intrauterine disease.

BACKGROUND: A large array of cytokines show high activity in amniotic fluid. Attempts have been made to quantify the concentrations or to track rising levels for diagnostic purposes when examining disturbances of the feto-maternal unit. However, the kinetics of cytokine production in the amniotic fluid are not well understood, and there is lack of knowledge about concomitant levels in fetal and maternal blood. EXPERIMENTAL DESIGN: The presence of cytokines in fetal and placental cells was demonstrated by immunohistochemistry using mAb. Cytokines were quantified by enzymimmunoassay in amniotic fluid and fetal and maternal blood. This was done with regard to two disease states that quite frequently complicate the course of pregnancy, namely chorioamnionitis and intrauterine growth retardation. The cytokines examined were G-CSF, GM-CSF, TNF-alpha, IL-1, IL-6, and IL-8. RESULTS: In chorioamnionitis, all cytokines, except GM-CSF, were elevated about 100 times in the amniotic fluid. An accompanying increase in maternal and fetal blood was only found for IL-6 and G-CSF; IL-8 was elevated in fetal blood only. Intrauterine growth retardation was characterized by elevated levels of TNF-alpha in the amniotic fluid, whereas G-CSF, GM-CSF, and IL-1 beta were significantly reduced. Immunohistochemistry showed that under normal conditions the cytokines are to be found in a characteristic distribution in certain cell types in the fetus, the placenta, and the placental bed. With rising concentrations, more cells seemed to be recruited for cytokine production, especially macrophages and decidual cells. In chorioamnionitis, fetal extramedullary granulopoiesis was augmented, and in intrauterine growth retardation, erythropoiesis as well as granulopoiesis were depressed. CONCLUSIONS: Not only inflammatory disease but also intrauterine growth retardation is characterized by a changing cytokine pattern. Alterations in fetal hematopoiesis observed at postmortem examination of perinatal deaths can be correlated to changes in cytokine production within the feto-maternal unit.

Amniotic Fluid↗
PubMed1994

[Detection of the intermediate trophoblast as evidence of intrauterine pregnancy].

With spontaneous abortion the conceptus is often expelled and lost right at the beginning, and uterine curettings then contain only endometrial fragments and clotted blood. Even complete embedding of all available material for histologic examination will not reveal any chorionic villi, and ectopic pregnancy can thus not be excluded. In such cases, the intermediate trophoblast can sometimes still be demonstrated within the endometrial tissue. This highly invasive trophoblast is difficult to identify using conventional staining, but cytokeratin antibodies are reliable markers of this cell type. Using immunohistochemistry, these fetal components could be demonstrated in 27 of 95 specimens (28.5%), proving the intrauterine nature of the aborted pregnancy. In some cases the fetal derivation of intermediate trophoblast was demonstrated by using in situ hybridisation to mark repetitive sequences on the Y-chromosome in the interphase nucleus.

Abortion, Spontaneous↗
PubMed1994

Augmentation of fetal granulopoiesis with chorioamnionitis during the second trimester of gestation.

Chorioamnionitis is a major hazard to pregnancy in the second trimester. It affects the fetomaternal unit, causing febrile illness in the mother. The fetus eventually is expelled because uterine contractions can no longer be suppressed after a certain stage of the disease. To determine the effects of chorioamnionitis on the fetus we examined fetal hematopoiesis, which is, for the most part, located extramedullarily during the second trimester of gestation. The study was performed morphometrically on sections of fetal tissues; the results are given as an increase of cells per square millimeter. In chorioamnionitis the fetuses (n = 18) showed increased granulopoiesis in the parenchyma of the liver (x12), in the spleen (x 5), in the portal triads of the liver (x3), and in the bone marrow (x1.35). Erythropoiesis and total hematopoiesis were reduced in all compartments. Inflammatory disease in the mother other than chorioamnionitis did not alter fetal hematopoiesis (n = 13). Under normal conditions fetal liver granulopoiesis is at a very low level within the sinusoids, but an early and substantial increase can be seen most easily in this location during infection; chorioamnionitis can thus be diagnosed from the fetal liver alone. Alterations in fetal hematopoiesis might be caused by cytokines generated at the fetomaternal interface during chorioamnionitis.

Bone Marrow↗