[Cyclosporin A reverses steroid-resistance induced by P-glycoprotein in patients with SLE].
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ATP Binding Cassette Transporter, Subfamily B, Mem↗
Biomedical subjects
S Eto
Publications and source records attributed to S Eto.
[Hashimoto disease].
Hashimoto disease is a representative organ-specific autoimmune disease. It occurs very frequently in middle-aged women. Generally, the symptom is only diffuse and elastic hard goiters detected by careful plpation. Immunological tests frequently reveal anti-thyroglobulin antibody and anti-TPO antibody. Hypothyroidism develops in some patient along with progression of the disease. In some patient, on the other hand, a condition called destructive thyroiditis may develop during the course of the disease, in which the thyroid gland is transiently destroyed, accompanied by thyrotoxic state. In this state, namely painless thyroiditis, 123I-uptake ratio is extremely low and TSH-receptor antibody is generally not observed. The thyroid hormone is administered to patient with large goiter or hypothyroidism, and antiphlogistic analgesics or adrenocortical hormone with beta-blockers in case of destructive thyroiditis.
Female↗
Crosslinking of CD44 on rheumatoid synovial cells augment interleukin 6 production.
CD44 is a ubiquitous molecule also known as hyaluronic acid or homing receptor. However, its cellular functions and its role in inflammation, for example rheumatoid synovitis, are currently unknown. Here we propose a novel function for CD44. Using synovial cells from patients with rheumatoid arthritis (RA), we demonstrated that CD44 crosslinking and binding to hyaluronan augmented IL-6 production. Briefly, we found that (a) rheumatoid synovial cells highly expressed CD44; (b) crosslinking of CD44 augmented IL-6 production and its mRNA transcription; (c) hyaluronan, especially when fragmented, also increased IL-6 production; and (d) CD44 activated the transcription factor activator protein-1 and CAMP-responsive element binding protein. These results indicate that the adhesion of RA synovial cells to matrices such as hyaluronic acid through CD44 could activate transcription factor, resulting in cytokine production. We therefore propose that the function of adhesion molecules as a signaling molecule may be pivotal in the pathogenesis of inflammation, including RA synovitis.
Arthritis, Rheumatoid↗
Constitutive up-regulation of integrin-mediated adhesion of tumor-infiltrating lymphocytes to osteoblasts and bone marrow-derived stromal cells.
Tumor-reactive T cells, known as tumor-infiltrating lymphocyte(TIL)s are known to infiltrate various tumors. Although TILs exert cytotoxic activities against tumor cells, only a small percentage of tumors usually contain TILs that specifically react to tumor antigens. Because the exact role of these lymphocytes is unclear, we investigated the mechanisms of migration and adhesion of TILs to bone metastatic tumors, particularly to osteoblasts and bone marrow-derived stromal cell(BMSC)s. Histopathological examination showed that most TILs in secondary bone metastatic tumors (from primary tumors in the lung or breast) were found in the supporting tissue stroma between the bone and tumor mass. Cultured TILs (obtained from breast tumors) adhered spontaneously to osteoblasts and BMSCs (obtained from patients with osteoarthritis) without exogenous stimulation. Adhesion was further enhanced by chemokines macrophage inflammatory protein (MIP)-1alpha and MIP-1beta. TILs highly expressed activation antigens CD25 and CD69. A spontaneous activation of an integrin, lymphocyte function-associated antigen-1 (LFA-1), was also detected on TILs. TILs produced high concentrations of MIP-1alpha and MIP-1beta and spontaneous polymerization of cytoskeletal F-actin was observed in these cells. Adhesion of TILs to osteoblasts and BMSCs via LFA-1 and very late antigen-4 was associated with the production of osteoclastogen interleukin 6 by the latter cells. Our results indicate that integrins on TILs are activated in an autocrine manner by MIP-1alpha and MIP-1beta, and that treatment with the chemokines increases the binding of TILs on osteoblasts and stromal cells via a mechanism involving intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 as targets for the integrin. Our data also indicated that interactions between TILs and osteoblasts/stromal cells lead to the secretion by the latter of the osteoclastogenic cytokine interleukin 6.
Actins↗
Constitutive chemokine production results in activation of leukocyte function-associated antigen-1 on adult T-cell leukemia cells.
Adult T-cell leukemia (ATL) is characterized by massive infiltration of circulating ATL cells into a variety of tissues, a finding often associated with poor prognosis. Leukocyte migration from circulation into tissue depends on integrin-mediated adhesion to endothelium, and integrins are tightly regulated by several stimuli, such as inflammatory chemokines. However, the exact mechanisms that enhance adherence of leukemic cells to the endothelium and infiltration into tissues remain to be fully understood. We investigated the mechanisms of extravasation of leukemic cells using ATL cells and report the following novel features of endogenous chemokine-induced adhesion of ATL cells to the endothelium. ATL cells spontaneously adhered to endothelial cells without exogenous stimulation. Integrin leukocyte function-associated antigen-1 (LFA-1) on ATL cells was spontaneously activated. ATL cells produced high amounts of chemokines, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta. Adhesion of ATL cells to endothelial cells and the expression of activated form of LFA-1 were reduced by pretreatment with pertussis toxin, wortmannin, or anti-MIP-1alpha and MIP-1beta antibodies or transfection with antisense of MIP-1alpha or MIP-1beta. Spontaneous polymerization of cytoskeletal F-actin was observed in ATL cells, which was also inhibited by pertussis toxin and wortmannin. We propose that ATL cells adhere to endothelial cells through an adhesion cascade similar to normal leukocytes and that the chemokines produced by ATL cells are involved in triggering integrin LFA-1 through cytoskeletal rearrangement induced by G-protein-dependent activation of phosphoinositide 3-kinases in an autocrine manner. These events result in a strong adhesion of ATL cells to the endothelium and spontaneous transendothelial migration.
3-Phosphoinositide-Dependent Protein Kinases↗
Induction of expression of MHC-class-II antigen on human thyroid carcinoma by wild-type p53.
Mutation of the tumor-suppressor gene p53 is involved in carcinogenetics. We investigated the role of p53 in the induction of anti-tumor immune responses by establishing a thyroid carcinoma cell line (1F3) prepared by transfection of wild-type human p53 gene into a p53-deficient cell line (FRO). Our results showed for the first time the involvement of p53 in the induction of anti-tumor immune responses, as demonstrated by: (i) expression of the major-histocompatibility-complex(MHC)-class-II antigen on 1F3, but not FRO; (ii) mRNA of class-II gene was expressed both in 1F3 and in FRO, but was stable at post-transcriptional level in FRO, which restrained protein synthesis; (iii) 1F3 induced MHC-class-II-specific CD4+ cytotoxic-T-cell activity through allo-antigen presentation and co-stimulation. Although our novel results are limited to the wild-type-p53-expressing clone from a p53-deficient cell line, we suggest that the absence of p53 in carcinoma cells may reduce the induction of CD4+ cytotoxic-T-cell activity against carcinoma cells by diminishing the expression of class-II antigen.
Blotting, Western↗
Heparan sulfate proteoglycan on endothelium efficiently induces integrin-mediated T cell adhesion by immobilizing chemokines in patients with rheumatoid synovitis.
OBJECTIVE: To clarify the role of heparan sulfate proteoglycan (HSPG) and chemokines in integrin-mediated T cell adhesion to endothelial cells in the synovium of patients with rheumatoid arthritis (RA). METHODS: Endothelial cells were purified from RA synovium. Expression of heparan sulfate, chemokines, and adhesion molecules on the endothelium was assessed by immunohistochemical analysis or flow cytometry. The effects of chemokines and heparan sulfate on T cell adhesion to RA endothelium were estimated with relevant antibodies and signaling inhibitors. Production of chemokines from synovial T cells was detected by Northern blotting and enzyme-linked immunosorbent assay. RESULTS: The endothelium in RA synovium highly expressed HSPG. The soluble form of chemokines, macrophage inflammatory protein 1beta (MIP-1beta), induced T cell adhesion to the endothelial cells. When MIP-lalpha and MIP-1beta were immobilized on RA endothelial cells, a more efficient integrin-mediated adhesion of T cells was induced compared with their soluble form. The induced T cell adhesion was reduced by pretreatment with either heparitinase, anti-MIP-lalpha antibody, or anti-MIP-lbeta antibody, indicating that these chemokines were bound to heparan sulfate on the cells. T cell adhesion was also inhibited by pertussis toxin, wortmannin, and cytochalasin B. MIP-lalpha and MIP-1beta were found on vessels in RA synovium in vivo, which were spontaneously produced from T cells purified from RA synovium. CONCLUSION: Endothelial cells in RA synovium characteristically express HSPG, which is involved in T cell integrin triggering by "posting" chemokines, which are produced by synovial T cells, and by "relaying" them to their receptors on T cells, which activate G protein-dependent phosphoinositide 3-kinase and actin-dependent integrin triggering.
Arthritis, Rheumatoid↗
Renal hemodynamics in rats with cadmium-induced nephropathy.
Glomerular filtration rate (GFR) is known to decline in patients with cadmium (Cd)-induced nephropathy. However renal hemodynamics in Cd-induced nephropathy remain unknown. We investigated renal hemodynamics in experimental Cd-induced nephropathy. Male Sprague-Dawley rats were given 0.18 mg/rat of cadmium chloride i.p. three times a week for 3 and 16 months. Age-matched control rats were given physiological saline. Mean arterial pressures after 3 and 16 months were identical among the groups. In comparison with age-matched control rats, significant decreases in GFR associated with a significantly lower filtration fraction (FF) were demonstrated in both groups of Cd-treated rats, but the changes were more prominent in the 16-month Cd-treated rats. Renal plasma flow was significantly decreased in the 3-month Cd-treated rats whereas it was preserved in the 16-month Cd-treated rats because of anemia. Urinary sodium excretions in both groups of Cd-treated rats were significantly greater than those in the respective control rats. On light microscopic examination, only mild degeneration of tubular cells and interstitial edema in limited areas of the proximal tubules were observed in the 3-month Cd-treated rats. In the 16-month Cd-treated rats multifocal tubular atrophy and interstitial fibrosis in the outer cortex were noted. Electron microscopic examinations revealed conspicuous degenerative changes in the proximal tubular epithelial cells, diffuse thickening of glomerular basement membranes, and foot process fusions in 16-month Cd-treated rats. These data suggested that the decline in GFR in the Cd-treated rats resulted mainly from the decline in FF, which might be functional rather than structural in origin and might be associated with proximal tubular dysfunctions.
Animals↗
Short-term treatment of recombinant murine interleukin-4 rapidly inhibits bone formation in normal and ovariectomized mice.
Estrogen deficiency contributes to an increase in bone resorption and bone formation characterized by a high rate of bone turnover. Interleukin-4 (IL-4) is a rapid and potent inhibitor of bone resorption. We examined the short term in vivo effects of recombinant murine IL-4 (rmIL-4) on bone remodeling in normal and ovariectomized mice. Eight-week-old mice were randomized into the following five groups: (1) sham-operated mice (sham); (2) sham-operated mice infused with rmIL-4; (3) ovariectomized mice (ovx); (4) ovx infused with rmIL-4; and (5) ovx replaced by 10 or 20 microg of 17beta-estradiol (E2) for 14 or 28 days after ovariectomy, respectively. rmIL-4 at a dose of 5 microg/day was infused into ovx and sham for 3 days prior to sacrifice. Analyses were performed 14 and 28 days after operation. An increase in serum alkaline phosphatase and urinary deoxypyridinoline levels induced by ovariectomy was inhibited by the 3-day infusion of rmIL-4. In ovx, serum and urinary IL-6 levels were also increased significantly 14 days after ovariectomy, which were restored by E2 but not by rmIL-4. Histomorphometrical analysis of trabecular bone revealed that the 3-day infusion of rmIL-4 inhibited the high rate of bone turnover induced by ovariectomy, such as an increase in the osteoclastic surface (Oc.S/BS), number of osteoclasts per mm bone surface (N.Oc/BS), mineralized surface per mm bone surface (MS/BS), and bone mineral apposition rate (MAR). A significant decrease in the bone volume (BV/TV) observed in ovx was not modulated by a 3-day infusion of rmIL-4 prior to sacrifice. In sham, rmIL-4 also caused a significant decrease in the Oc.S/BS, N.Oc/BS, MS/BS, and MAR, but the BV/TV was not modulated by rmIL-4. We conclude that short term infusion of rmIL-4 in vivo rapidly inhibits not only bone resorption but also its formation in both sham-operated and ovariectomized growing mice, resulting in a low rate of bone turnover without modulating bone volume.
Alkaline Phosphatase↗
Centrally administered parathyroid hormone (PTH)-related protein(1-34) but not PTH(1-34) stimulates arginine-vasopressin secretion and its messenger ribonucleic acid expression in supraoptic nucleus of the conscious rats.
It has been suggested that PTH-related protein (PTHrP) is an endogenous modulator of cardiovascular systems. We have reported that PTHrP(1-34), but not PTH(1-34), causes the release of arginine-vasopressin (AVP) from the supraoptic nucleus (SON) of the hypothalamus in vitro through a novel receptor distinct from the PTH/PTHrP receptors (type I or type II) described previously. In this study, we have investigated the in vivo effects of PTHrP(1-34) on AVP secretion and its, messenger RNA (mRNA) expression in the SON in conscious rats. Intracerebroventricular (i.c.v.) administration of PTHrP(1-34) resulted in an increase in plasma AVP concentration in a dose-dependent manner (0-400 pmol/rat). The maximal effect was obtained at 15 min after i.c.v. administration of PTHrP(1-34). Neither PTHrP(7-34) nor PTH(1-34) had any effect on plasma AVP levels. PTHrP(1-34)-induced AVP secretion was antagonized by pretreatment with PTHrP(7-34) but not by that with PTH(1-34). In addition, in situ hybridization study revealed that AVP mRNA expression in the SON and paraventricular nucleus was significantly increased 30 min after i.c.v. administration of PTHrP(1-34) and reached a maximum at 180 min. Furthermore, in Northern blot analyses, AVP mRNA expression in the SON was increased to approximately a 2-fold of basal level by PTHrP(1-34). On the other hand, neither PTHrP(7-34) or PTH(1-34) had any effect on the mRNA expression. The PTHrP(1-34)-stimulated AVP mRNA expression was eliminated by pretreatment with PTHrP(7-34) but not with PTH(1-34). These results suggest that, in the central nervous system, PTHrP(1-34) is involved in AVP secretion through a novel receptor distinct from the PTH/PTHrP receptors reported previously, playing a role in the body water and electrolyte homeostasis.
Animals↗
Hepatocyte growth factor is a potent trigger of neutrophil adhesion through rapid activation of lymphocyte function-associated antigen-1.
Recruitment of neutrophils into tissue occurs in several pathologic processes such as inflammation, atherosclerosis, thrombosis, and ischemia. In inflammation, the adherence of neutrophils to the endothelium depends on neutrophil integrins. Integrin-mediated adhesion is tightly regulated, ie, integrins do not function if neutrophils are not triggered by certain activation stimuli. We investigated the role of hepatocyte growth factor (HGF) in the adhesion of neutrophils to endothelial cells in inflammation. Our results showed that (a) HGF induced not only lymphocyte function-associated antigen-1 (LFA-1)-mediated adhesion of neutrophils to endothelial cells but also transmigration of neutrophils in a concentration-dependent manner; (b) HGF functionally transformed neutrophil integrin LFA-1 to active form and reduced surface L-selectin expression level; (c) HGF induced F-actin polymerization and cytoskeletal rearrangement within seconds; (d) genistein, a tyrosine kinase inhibitor, as well as wortmannin, a phosphoinositide 3 (PI 3)-kinase inhibitor, inhibited both F-actin polymerization and LFA-1-mediated adhesion of neutrophils to endothelial cells; and (e) neutrophils in cutaneous inflamed tissue highly expressed HGF and serum levels of HGF were elevated in patients with Behçet's disease, which is associated with neutrophilic vasculitis and marked neutrophil accumulation. Our results indicate that HGF plays a pivotal role in integrin-mediated adhesion and transmigration of neutrophils to sites of acute inflammation through cytoskeletal rearrangement activated by tyrosine kinase and PI 3-kinase signaling.
Actins↗
Human T-cell leukemia virus type I Tax transactivates the promoter of human prointerleukin-1beta gene through association with two transcription factors, nuclear factor-interleukin-6 and Spi-1.
The human T-cell leukemia virus type I (HTLV-I), which infects a wide variety of mammalian cells including monocytes and macrophages, encodes a transactivating protein designated as Tax. We now report that Tax induces the human prointerleukin-1beta (IL1B) gene promoter in monocytic cells. In our transient transfection assays using human THP-1 monocytic cells, a chloramphenicol acetyltransferase (CAT) construct containing the IL1B promoter sequence between positions -131 and +12 showed an approximately 90-fold increase in activity following cotransfection of a Tax expression vector. Moreover, Tax synergized with lipopolysaccharide (LPS) to induce the IL1B promoter activity. Analyses of specific nucleotide substitutions further indicated that the Tax-induced transcriptional activation requires two transcription factor binding motifs within the IL1B promoter; one is a binding site for nuclear factor (NF)-IL6 (CCAAT/enhancer binding protein beta, C/EBP beta), which belongs to the basic region-leucine zipper (bZIP) family and the other for Spi-1 (PU.1), which is an Ets family protein found principally in monocytes, macrophages, and B lymphocytes. In electrophoretic mobility shift assays (EMSA) using in vivo THP-1 nuclear extracts, Tax expression in THP-1 monocytic cells significantly increased binding of the two factors to their target IL1B promoter sequences. However, in contrast to NF-IL6 and Spi-1, DNA binding activity of Oct-1, an ubiquitously expressed octamer-binding protein was not affected by Tax. Additional EMSA using in vitro translated proteins also showed that recombinant Tax enhances DNA binding of both of recombinant NF-IL6 and Spi-1 proteins. These data were supported by our glutathione S-transferase (GST)-pull-down data, which indicated that Tax physically interacts with the two proteins. Based on the results obtained from the present study, we conclude that the IL1B promoter is a Tax-responsive sequence as a result of ability of Tax to induce binding of NF-IL6 and Spi-1 to the IL1B promoter sequence through protein-protein interaction.
Binding Sites↗
[Nephrotic syndrome and the thrombolytic therapy].
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Anticoagulants↗
C-type natriuretic peptide suppresses arginine-vasopressin secretion from dissociated magnocellular neurons in newborn rat supraoptic nucleus.
Central administration of C-type natriuretic peptide (CNP) affects various neuroendocrine systems. In the present study, we examined whether CNP acts directly on arginine-vasopressin (AVP) secretion from rat supraoptic nucleus (SON) neurons, using acute dissociated cell preparations. CNP inhibited the basal secretion of AVP in a dose-dependent manner (10(-11)-10(-6) M). A- type natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) also suppressed the basal secretion of AVP, however, the effects were two-orders of magnitude less potent than CNP. CNP also suppressed All-induced AVP secretion, however, the inhibitory effect of CNP was less than that of ANP or BNP. These findings suggest that CNP inhibits the basal secretion of AVP through natriuretic peptide receptor (NPR)-B and has a role in the body water and electrolyte homeostasis in the central nervous system.
Animals↗
Distinct phenotype of leukemic T cells with various tissue tropisms.
There is an emerging concept, the validity of which remains to be proven, that preferential expression of selective adhesion molecules on particular T cell subsets may result in tissue-specific migration. L-selectin, cutaneous lymphocyte-associated Ag (CLA), and integrin alpha4beta7 are proposed to be involved in selective migration of T cell subsets into peripheral lymph nodes, skin, and gastrointestinal mucosa, respectively. Adult T cell leukemia (ATL) is associated with lymphoid infiltration of tissues and secondary lymphoid organs. To clarify the role of these putative homing molecules in vivo, we assessed their expression on circulating ATL cells from patients with lymph node, skin, and gut involvement. L-selectin expression was significantly higher on peripheral ATL cells in patients with lymphadenopathy than in patients without it. CLA was highly expressed on peripheral ATL cells compared with normal T cells: its expression was also significantly higher on peripheral ATL cells from patients with skin involvement compared with cells from patients without it. beta7 was particularly highly expressed on peripheral ATL cells from patients with gastrointestinal involvement. In summary, the differential expression of beta7 and beta1 on peripheral ATL cells correlates with the presence of gastrointestinal involvement. Similarly, the presence of skin involvement is associated with the expression of CLA(high)beta7low on peripheral ATL cells. These results, which are consistent with the molecules CLA and alpha4beta7 mediating preferential T cell migration to the skin and gastrointestinal mucosa, respectively, may allow for a refinement of the classification of lymphoid neoplasms on the basis of differential expression of homing molecules.
Adult↗
Parathyroid hormone-related peptide-(1-34) [PTHrP-(1-34)] induces vasopressin release from the rat supraoptic nucleus in vitro through a novel receptor distinct from a type I or type II PTH/PTHrP receptor.
PTH and PTH-related peptide (PTHrP) bind to a type I PTH/PTHrP receptor expressed in bone and kidney or a type II receptor in nonclassical target tissue with equal affinity and similar bioactivities. PTHrP is abundant in the central nervous system, but its physiological role remains unknown. Herein, we examined the role of PTHrP-(1-34) on arginine vasopressin (AVP) release from the rat supraoptic nucleus (SON). Application of PTHrP-(1-34) to SON slices caused an increase in AVP release in a concentration-dependent manner. Neither PTHrP-(7-34) nor PTH-(1-34) had any effect on AVP release from the SON. PTHrP-(1-34)-induced AVP release was antagonized by a large excess of PTHrP-(7-34) and by H89, an inhibitor of cAMP-dependent protein kinase (A kinase), but not by PTH-(1-34) or PTH-(13-34). PTHrP-(1-34), but not PTH-(1-34), also dose-dependently increased the levels of cAMP in the SON. 125I-Labeled PTHrP-(1-34) bound specifically to crude membranes isolated from the SON. Scatchard analysis showed a single class of binding sites for PTHrP-(1-34) with a Kd of 36.4 nM and a maximum binding capacity of 3.94 pmol/mg protein. No specific binding for 125I-labeled PTH-(1-34) was noted. The binding of 125I-labeled PTHrP-(1-34) was displaced by unlabeled PTHrP-(1-34) and unlabeled PTHrP-(7-34), but not by unlabeled PTH-(1-34). These findings suggest that PTHrP-(1-34), but not PTH-(1-34), causes the release of AVP from the SON through a novel receptor distinct from type I or II PTH/PTHrP receptors.
Animals↗
Chondrocytes are regulated by cellular adhesion through CD44 and hyaluronic acid pathway.
The articular cartilage consists of resident chondrocytes embedded within the extracellular matrix which contains several components such as collagen and hyaluronic acids (HA). CD44 is a major cell surface receptor for HA and is homologous to cartilage-link proteins. Although CD44 is present in cartilage, it is not clear if chondrocytes adhere to HA through CD44 or whether such adhesion changes the function of chondrocytes. We studied the molecular mechanisms of CD44-related chondrocyte adhesion to HA and the effects of such adhesion on chondrocyte function. Experiments were performed using the human chondrosarcoma-derived chondrocyte-like cell line HCS-2/8. Our results showed that (a) HCS-2/8 cells highly expressed CD44; (b) HCS-2/8 cells efficiently adhered to HA without any stimuli; (c) monoclonal antibody (mAb)-blocking studies indicated that adhesion of HCS-2/8 cells to HA was mainly mediated by the CD44/HA pathway; (d) cellular adhesion to HA increased the proliferation of HCS-2/8 cells, independent of transforming growth factor-beta (TGF-beta), but this was inhibited by CD44 mAb; (e) the adhesion of chondrocytes to HA also induced c-myc mRNA expression and this was also inhibited by CD44 mAb; and (f) the adhesion of cells to HA augmented TGF-beta mRNA expression, a process also reduced by CD44 mAb. Thus, HCS-2/8 cells effectively adhered to HA through cell surface CD44. The adhesion was also involved in cellular signaling which induced cellular proliferation and expression of c-myc mRNA as well as TGF-beta mRNA expression within the cells. Our results indicate that CD44 on chondrocytes plays an important role in normal and abnormal functions of cartilage through its adhesion to HA, which induces a variety of stimulatory signals to regulate chondrocyte proliferation as well as matrix synthesis in cartilage microenvironment.
Antibodies, Monoclonal↗
A case of active acromegalic woman with a marked increase in serum insulin-like growth factor-1 levels after delivery.
Pregnancy in a woman with active acromegaly is very rare, because amenorrhea, due to hyperprolactinemia and disturbed pituitary gonadotropin secretion may cause infertility. We report a 28-year-old pregnant woman with untreated acromegaly, who was followed up from early pregnancy to delivery. Her pregnancy was uneventful, and she went into spontaneous labor at 38 weeks and delivered a normal infant. Her serum GH levels were further increased in late pregnancy, followed by decreased in postpartum periods, which may be associated with enlargement of pituitary adenoma during pregnancy. In contrast with serum GH, her serum insulin-like growth factor-1 (IGF-1) levels were dissociated with her serum GH levels during late pregnant and postpartum period. Her serum GH and IGF-1 levels in late pregnancy were different from the levels in pregnant women with acromegaly reported previously.
Acromegaly↗