Bilirubin found in syndrome of hemolysis, elevated liver enzymes, and low platelet count.
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Biomedical subjects
Publications and source records attributed to T Tamada.
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To study the interrelationship between preeclampsia, the syndrome of hemolysis, elevated liver enzymes, and low platelet count, and acute fatty liver of pregnancy, 41 liver specimens from 41 preeclamptic women with and without liver dysfunction were examined for the amount of fat deposited in hepatocytes. All 41 specimens stained with oil red O on frozen sections showed a significant amount of microvesicular fat droplets in varying degrees. In contrast, only 11 of the 41 stained conventionally (with hematoxylin-eosin) showed significant fatty infiltration. The density of hepatocellular fat correlated positively with plasma urate concentration and negatively with the platelet count. These findings suggest that preeclampsia may be one of several microvesicular fatty diseases of the liver and that acute fatty liver of pregnancy may be the most severe form.
Thirty-three patients with PCO were studied, focusing on the serum LH profile appearing during their menstrual cycles. The elevated LH level declined gradually after ovulation to the normal or near-normal range at the end of the luteal phase and the early follicular phase. The once declined LH level gradually elevated again with the increasing days from the beginning of menstrual flow and remained at a high level until the next ovulation. The LH response to LH-RH increased with the elevating basal LH level. These results may suggest that the timing of hormonal analysis is important for correct diagnosis of PCO.
To evaluate the prevalence of hyperprolactinemia in patients with polycystic ovarian syndrome (PCO), 72 patients with oligo- or anovulation were studied. All of the patients had persisting elevated LH (greater than 25 mIU/ml), normal FSH, high LH/FSH ratio (greater than 2.5), and exaggerated LH responses to LHRH. Mean testosterone and androstenedione concentrations were appreciably increased in these patients. Out of 171 samples for prolactin (PRL) determination from these 72 patients, only 5 patients had a PRL value above 30 ng/ml during the first sampling. The next sampling from these same 5 women disclosed that they were transiently hyperprolactinemic because the next samples showed a normal PRL value. To further investigate the PRL secretory capacity 500 micrograms of TRH and 10 mg of metoclopramide (MCP) were administered to these 72 and 44 patients, respectively. The PRL response to MCP was significantly blunted in these patients compared to normal women while the PRL response to TRH in these patients was not indistinguishable from that in normal women. These results indicate that the true prevalence rate of hyperprolactinemia in PCO may be low rather than high and the association of hyperprolactinemia with PCO may be coincidental rather than a pathogenically related phenomenon.
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A case of liver cirrhosis with large portacaval shunt from the superior mesenteric vein is reported. The portal blood flow was diagnosed as reversed on admission, but normalized with treatment. Blood flow was measured noninvasively and repeatedly using an ultrasonic Doppler duplex system. The reversed portal flow led to the superior mesenteric vein, right (and some left) internal inguinal vein, and inferior vena cava. This rare collateral pathway was clearly demonstrated by percutaneous transhepatic portalgraphy. A link between shunt and an appendectomy carried out 22 yr ago is considered, and the possibility of the temporarily reversed portal blood flow on admission being due to deteriorated hepatic hemodynamic conditions is discussed.
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To assess the clinical significance of an elevated liver enzyme (sGOT) on the outcome of preeclamptic pregnancy, the charts of 145 preeclamptic/eclamptic patients who had sGOT determination during 7 days before and 2 days after delivery were reviewed. Of these, 60 patients exhibited a sGOT value above 30U/L (elevated sGOT group). This group was compared with the remaining 85 patients who showed a normal sGOT value related to clinical backgrounds and clinical outcome. The elevated sGOT group had a significantly low platelet count (16.4 +/- 8.4 vs. 21.4 +/- 6.7 X 10(4)/cumm, p less than 0.001) as well as a significantly high perinatal mortality rate (23.8 vs. 6.3%, p less than 0.01). There was a trend to a higher boy-to-girl ratio in the elevated sGOT group than in the normal sGOT group (1.10 vs. 0.83). In a group of 31 patients who were complicated with both elevated sGOT and thrombocytopenia, the perinatal mortality rate increased further to 42.4% and the boy-to-girl ratio was significantly higher than in the group of 66 patients who showed both a normal sGOt and normal platelet count (2.00 vs. 0.85, p less than 0.05). These results may indicate that 1) preeclamptic pregnancies complicated with liver dysfunction may tend to have a low platelet count; 2) liver dysfunction and thrombocytopenia are more likely to become complicated in preeclamptic pregnancies with a male fetus; 3) closer observations would be needed for preeclamptic pregnancy with liver dysfunction and thrombocytopenia.
Ultracytochemical localizations of cyclic nucleotide-metabolizing enzymes, namely adenylate cyclase (AC), guanylate cyclase (GC) and cyclic 3',5'-nucleotide phosphodiesterase (PDE), have been demonstrated in the human term placenta. AC activity was found positive on the basal plasma membrane of the syncytiotrophoblast and on the pinocytotic vesicle of the fetal capillary endothelial cell. GC activity was observed to be strong on the plasma membrane of the microvilli of the syncytiotrophoblast. The cAMP PDE activity was shown positive both on the basal plasma membrane and on the microvillous membrane, while cGMP PDE activity was exclusively confined to the microvilli of the syncytiotrophoblast. These observations suggest that the syncytiotrophoblast plays an important role in the cyclic nucleotide metabolism in the human term placenta and that there might be significant functional differences between its basal plasma membrane and its microvillous membrane.
The degree of follicular development was examined in a patient with 17 alpha-hydroxylase deficiency that accounted for impairment of estrogen and androgen biosynthesis. The ovarian content of P was markedly higher than those of any other steroids requiring 17 alpha-hydroxylation for synthesis. The morphologic analysis of the ovaries demonstrated that normal follicles could not develop to more than 2.2 mm in diameter, and most follicles with diameters of 1.0 mm or more yielded to atresia. It is known that estrogen and FSH act synergistically on the growth of the follicles. Our data suggest that the follicles can develop up to the size of 2.2 mm in diameter at most with the sole stimulation of gonadotropin.
The portal hemodynamics were studied in ten patients with portal hypertension, including three patients who had interposition mesocaval shunt (IMCS), three patients who had distal splenorenal shunt (DSRS), one patient who had gastrocaval shunt (GCS), and three patients who had splenectomy. Portal blood flow was measured by an ultrasonic Doppler duplex system, and portal venous pressure was measured by portal catheterization before, during, and after operation. The portal blood flow, and especially the splenic venous blood flow, was less during operation than before operation. Blood flow through the IMCS was greater than that through the DSRS, and the shunt flow had a tendency to increase after operation. The portal venous pressure measured during operation was slightly higher than that measured percutaneously before operation. In the patients who had the shunt operation, the portal venous pressure tended to decrease after operation. Study of portal hemodynamics, especially with the ultrasonic Doppler method, is useful in analysis and follow-up of patients who have shunt operations since the same method can be used before, during, and after operation.
This study was designed to investigate the effects of progesterone on the gonadotrophin rise after bilateral salpingo-oophorectomy (BSO). Twenty-eight regularly menstruating women underwent hysterectomy and BSO during the follicular phase of the menstrual cycle. They were divided into 5 groups depending on the treatment after BSO. Plasma LH and FSH were studied serially for 14 days after BSO and the patterns of LH and FSH rises were contrasted to those observed in the control group which received neither progesterone nor estrogen. LH and FSH levels in the group which were given low dose progesterone only, rose consistently after BSO and these patterns were similar to those seen in the control group. However, the addition of estrogen reduced gonadotrophin rises significantly more than estrogen did alone. Further, the luteal phase level of progesterone solely has a suppressive effect on the gonadotrophin rises after BSO. Our observations suggest that synergism of progesterone with estrogen may exist in suppressing gonadotrophin secretion in the normal luteal phase and should help in understanding why gonadotrophin levels in the luteal phase are lower than those in the follicular phase of the menstrual cycle.
Reports have so far accumulated suggesting that cyclic nucleotide may play an important role in the regulation of placental function. Cyclic 3',5'-nucleotide phosphodiesterase (PDE) is the enzyme which degrades cyclic nucleotide to nucleotide monophosphate. The presence of this enzyme in the human placenta has been speculated on biochemical grounds, but direct cytochemical evidence has been lacking. Therefore, ultracytochemical localization of PDE activity was demonstrated in the human term placenta directly by electron microscopical enzymecytochemistry. Both cyclic AMP PDE and cyclic GMP PDE activity was observed on the syncytiotrophoblast, but subcellular localization differed in detail. Cyclic AMP PDE activity was positive both on the microvillous membrane and on the basal plasma membrane, while cyclic GMP PDE activity was confined to the microvillous membrane of the syncytiotrophoblast. These observations suggest that the syncytiotrophoblast may play an important role in cyclic nucleotide metabolism and that PDE may regulate nascent cyclic nucleotide in the syncytiotrophoblast.
Reports have so far accumulated suggesting that cyclic nucleotide may play an important role in the regulation of placental function, including fetal growth. However, only biochemical data are available on the localization of adenylate cyclase (AC) and guanylate cyclase (GC) and direct histochemical evidence is lacking. Therefore, to understand the cyclic nucleotide metabolism in human term placenta, ultracytochemical localization of AC and GC activity was studied. The AC activity was mainly positive on the basal plasma membrane of syncytiotrophoblast and on the pinocytotic vesicle of fetal capillary endothelial cell. GC activity was observed to be strong on the plasma membrane of microvilli of syncytiotrophoblast. All the cytochemical control studies confirmed the specificities of each enzyme activity. These observations suggest that syncytiotrophoblast may play an important role in cyclic nucleotide metabolism and that AC may receive information from fetal circulation, whereas GC may receive regulation from maternal circulation.