Biomedical subjects

H Kohno

Publications and source records attributed to H Kohno.

At least 19 recordsLinked to original sources

PubMed1997

Resection of the caudate lobe of the liver for primary and recurrent hepatocellular carcinomas.

BACKGROUND: Resection of the caudate lobe of the liver to treat malignancies has recently received attention, but long-term results after such resection for hepatocellular carcinoma have not been reported for an acceptable number of patients. This study analyzed the short- and long-term results after resection of the caudate lobe for primary and recurrent hepatocellular carcinoma in 19 patients. STUDY DESIGN: Complete or partial resection of the caudate lobe was performed for the treatment of primary (n = 13) and recurrent (n = 6) hepatocellular carcinoma. Eleven patients had a solitary tumor only in the caudate lobe, but eight patients had tumors in other segments of the liver as well. There were 16 men and 3 women. Age ranged from 35 to 79 years, averaging 63 years. Clinicopathologic features of these cases were evaluated from various viewpoints. RESULTS: The duration of the operation ranged from 80 to 250 minutes (mean plus or minus standard deviation; 149 +/- 47) and blood loss from 200 to 2,400 g (836 +/- 651). Four patients (21.8 percent) had postoperative complications and one (5.3 percent) died of postoperative variceal bleeding. Tumor size ranged from 1.0 to 6.0 cm, averaging 3.7 +/- 1.4. A capsule was seen around the tumor in 68.4 percent, daughter nodules in 5.3 percent, and vascular invasion in 31.2 percent. Hepatic cirrhosis was present in 15 patients and chronic hepatitis in four. The 5-year survival rate in all patients was 31.3 percent. The survival rate was significantly better in patients with primary hepatocellular carcinoma than in those with recurrent tumors (49.2 percent compared with none) because of frequent recurrence in the latter group. CONCLUSIONS: Resection of the caudate lobe of the liver for hepatocellular carcinoma associated with chronic hepatic disease can be performed safely with a satisfactory long-term result, particularly in patients with primary tumors in this lobe.

Aged↗

PubMed1996

Bni1p implicated in cytoskeletal control is a putative target of Rho1p small GTP binding protein in Saccharomyces cerevisiae.

The RHO1 gene encodes a homolog of mammalian RhoA small GTP binding protein in the yeast Saccharomyces cerevisiae. Rho1p is localized at the growth sites, including the bud tip and the cytokinesis site, and is required for bud formation. We have recently shown that Pkc1p, a yeast homolog of mammalian protein kinase C, and glucan synthase are targets of Rho1p. Using the two-hybrid screening system, we cloned a gene encoding a protein which interacted with the GTP-bound form of Rho1p. This gene was identified as BNI1, known to be implicated in cytokinesis or establishment of cell polarity in S.cerevisiae. Bni1p shares homologous domains (FH1 and FH2 domains) with proteins involved in cytokinesis or establishment of cell polarity, including formin of mouse, capu and dia of Drosophila and FigA of Aspergillus. A temperature-sensitive mutation in which the RHO1 gene was replaced by the mammalian RhoA gene showed a synthetically lethal interaction with the bni1 mutation and the RhoA bni1 mutant accumulated cells with a deficiency in cytokinesis. Furthermore, this synthetic lethality was caused by the incapability of RhoA to activate Pkc1p, but not glucan synthase. These results suggest that Rho1p regulates cytoskeletal reorganization at least through Bni1p and Pkc1p.

Base Sequence↗

PubMed1996

Interaction of the Rho family small G proteins with kinectin, an anchoring protein of kinesin motor.

The Rho family small G proteins are implicated in various cell functions, such as cell morphological change, cell motility, and cytokinesis. However, their modes of action in regulating these cell functions remain to be clarified. In the present study, we have isolated a cDNA encoding a protein which interacts with the GTP-bound form, but not with the GDP-bound form, of the Rho family members, including RhoA, Racl, and Cdc42, by the yeast two-hybrid method. This protein is kinectin, known to be a vesicle membrane anchoring protein of kinesin, which is an ATPase motor transporting vesicles along microtubules.

Binding Sites↗

PubMed1996

Human colorectal carcinomas specifically accumulate Mr 42,000 ubiquitin-conjugated cytokeratin 8 fragments.

Recent studies have shown that various tumor cells accumulate ubiquitin (Ub)-conjugated proteins, the profiles of which differ from those of normal cells. To identify the Ub-conjugated proteins accumulated specifically by human carcinoma cells, a two-dimensional immunoblot analysis of 31 surgically resected human primary colorectal carcinoma tissues was performed using an anti-Ub monoclonal antibody, KM691. Two distinct Mr 42,000 and 45,000 proteins in the Triton X-insoluble fractions of carcinoma tissues reacted with this antibody, whereas only one Mr 45,000 protein reacted in normal tissues. The Mr 42,000 Ub-conjugated proteins were specific to carcinoma tissues from 25 patients (80.6%). One of the purified Mr 42,000 proteins was digested with Achromobacter protease I. This protein was identified as a cytokeratin 8 (CK 8) fragment based on both molecular mass determination and molecular mass searching of Achromobacter protease I-digested fragments of proteins registered in a protein sequence data base. Two-dimensional immunoblot analysis with an anti-CK 8 antibody confirmed that all of the Mr 42,000 proteins were CK 8 degradation products. These results demonstrate that human colorectal carcinomas specifically accumulate Mr 42,000 Ub-conjugated CK 8 fragments. This accumulation was observed frequently not only in advanced (18/22, 81.8%), but also in early stage cases (7/9, 77.8%), suggesting that it occurs even in the early stages of colorectal carcinoma progression.

Adult↗

PubMed1996

An intensive chemotherapy of adult T-cell leukemia/lymphoma: CHOP followed by etoposide, vindesine, ranimustine, and mitoxantrone with granulocyte colony-stimulating factor support.

SUMMARY: An intensive combination chemotherapy regimen supported by granulocyte colony-stimulating factor (G-CSF) was evaluated in adult T-cell leukemia/lymphoma (ATLL) patients in a multiinstitutional, cooperative study. Vincristine 1 mg/m2 i.v. day 1, Adriamycin 40 mg/m2 i.v. day 1, cyclophosphamide 400 mg/m2 i.v. day 1, prednisolone 40 mg/m2 i.v. days 1 to 3 and 8 to 10, etoposide 35 mg/m2 i.v. days 1 to 8, vindesine 2 mg/m2 i.v. day 8, ranimustine 50 mg/m2 i.v. day 8, mitoxantrone 7 mg/m2 i.v. day 8, and G-CSF 50 mg/m2 s.c. days 9 to 21 were given for 2 to 4 courses every 3 weeks to 83 patients with ATLL. Complete remission (CR) and partial remission (PR) were achieved in 35.8 and 38.3 percent, respectively, of 81 evaluable patients. The median survival of all patients was 8.5 months, with a predicted 3-year survival of 13.5 percent by the Kaplan-Meier method. The median duration of response was 7.6 months (range 0.2-42.7), and 13 patients were alive. Their median survival time was 29.1 months (range 19.2-44.7). In 67.6 percent of courses, white blood cell (WBC) nadirs were < 1.0 x 10(9)/L. Days required for the recovery of WBC from the nadir to > 1.0 x 10(9)/L were <5 days in 71.4 percent of the treatment courses. The G-CSF supported an intensified chemotherapy regimen for ATLL and yielded better response rate and longer survival compared to previous reports in Japan. Because duration of remission is still short, further studies of postremission therapy or other strategies are warranted.

Adult↗

PubMed1996

Molecular characterization of Euglena ascorbate peroxidase using monoclonal antibody.

Ascorbate peroxidase (EC 1.11.1.11) has been purified to electrophoretic homogeneity from Euglena gracilis Z. The enzyme showed a molecular mass of 58 kDa on SDS-PAGE and gel filtration, indicating that Euglena ascorbate peroxidase exists as a monomeric form. The substrate specificity for an electron donor and the stability of the purified enzyme were similar to those of cytosolic isozymes from higher plants. One of the characteristic properties was that Euglena ascorbate peroxidase reduces organic hydroperoxides as well as hydrogen peroxide. The N-terminal amino-acid sequence showed no significant similarity to any other ascorbate peroxidase from higher plants. However, the sequence of the peptides from the purified enzyme exhibited a high degree of homology to sequences of cytosolic and chloroplastic ascorbate peroxidases. Monoclonal antibodies against the purified Euglena ascorbate peroxidase were prepared. Two monoclonal antibodies (EAP1 and EAP2) showed high homology to cytosolic ascorbate peroxidases of higher plants, as judged by Western blot analysis. The EAP1 was also specific for chloroplastic ascorbate peroxidase from spinach. These findings indicate that Euglena ascorbate peroxidase exists in highly homologous regions with the ascorbate peroxidases of higher plants.

Amino Acid Sequence↗

PubMed1996

Requirement of multiple DNA-protein interactions for inducible expression of RNR3 gene in Saccharomyces cerevisiae in response to DNA damage.

The RNR3 gene encodes the large subunit of ribonucleotide reductase. Transcription of this gene is induced 12-fold in response to DNA damage or by a DNA replication blocker. To investigate cis-acting regulation, deletion analysis of the promoter region of the RNR3 gene was performed and we identified two upstream-repressing sequences in the RNR3 regulatory region. An 18-base-pairs fragment, termed DNA-damage responsive element 1 (DRE1) located between -212 and -194 in this region was found to be essential for the induction of RNR3. This fragment contained a negatively acting sequence where a protein factor bound to the region during normal growth but disappeared by exposure to 4-nitroquinoline-1-oxide. The other repressive element homologue to DRE1 was located at -263 to -254. One possible upstream-activating sequence which regulates the basal expression of RNR3 was also found. These results show that at least three potential cis-elements are necessary for the inducible expression of yeast expression of yeast RNR3 in response to DNA damage.

4-Nitroquinoline-1-oxide↗

PubMed1996

Hepatocyte growth factor induces transglutaminase activity that negatively regulates the growth signal in primary cultured hepatocytes.

Transglutaminase (TGase) activity increased 2.5-fold at 6 h after treatment of rat hepatocytes with 117 nM hepatocyte growth factor (HGF). In the same manner, putrescine incorporation into proteins of cells occurred in HGF-treated cells but did not in those pretreated with monodansylcadaverine (MDC), a TGase inhibitor, even in the presence of HGF. These results suggest that HGF-induced TGase was active and catalyzed some cross-linkage reaction. Cycloheximide completely blocked the increase in TGase activity induced by HGF, suggesting that HGF stimulated de novo synthesis of TGase within 6 h. Both [35S]methionine incorporation and Northern blotting analyses supported this possibility. Pretreatment of cells with MDC additionally increased HGF-induced DNA synthesis and the ratio of cells in S-phase. Similarly, TGase antisense oligonucleotide inhibited de novo synthesis of TGase, resulting in increase in the ratio of S-phase cells in the presence of HGF. Analyses of cross-linking of HGF to the receptor indicated that the antisense oligonucleotide inhibited the downregulation of HGF receptor subsequent to HGF-addition. These results provide the first evidence for inducibility of de novo synthesis of TGase by HGF and suggest that TGase negatively regulates the growth signal of HGF through the downregulation of receptor.

Animals↗

PubMed1996

Mouse coproporphyrinogen oxidase is a copper-containing enzyme: expression in Escherichia coli and site-directed mutagenesis.

We previously isolated cDNA for mouse coproporphyrinogen oxidase (CPO) and provided evidence for the induction of mRNA during differentiation of murine erythroleukemia cells (Kohno et al. (1993) J. Biol. Chem. 268, 21359-21363). To better understand the structure and the mechanisms of reaction of the enzyme, we expressed mouse CPO in Escherichia. coli and purified it to a homogeneity. Analysis of the metal content revealed that the recombinant mouse CPO contains one copper atom per polypeptide chain. When the bacterial cells were treated with D-penicillamine, a copper chelator, formation of the active CPO was partially reduced. Addition of Cu2+ in minimal medium resulted in 6-fold higher level of CPO activity. These results suggest that expression of active mouse CPO in E. coli depended on the presence of Cu2+ in the culture medium. To elucidate the apparent involvement of Cu2+ in enzyme function, a series of mutant enzymes, whose highly conserved histidine and cysteine residues were individually converted to alanine residue, were prepared by site-directed mutagenesis. Mutant enzymes were expressed in E. coli and their activities examined. Mutation at histidine 158 resulted in a complete loss of enzyme activity, yet the enzyme protein was expressed at a comparable level. Concomitantly, only a trace amount of Cu2+ was detected in the purified H158A enzyme. We propose that mouse CPO is copper-containing enzyme and Cu2+ interacts with a conserved histidine residue.

Amino Acid Sequence↗

PubMed1996

Transglutaminase induced by epidermal growth factor negatively regulates the growth signal in primary cultured hepatocytes.

Transglutaminase (TGase) activity increased 2.5-fold at 6 h after treatment of rat hepatocytes with 17 nM epidermal growth factor (EGF). In the same manner, putrescine incorporation into the proteins of cells occurred in EGF-treated cells, but not in those pretreated with monodansylcadaverine (MDC), a TGase inhibitor, even in the presence of EGF. These results suggest that EGF-induced TGase was active and catalysed some cross-linkage reaction. Cycloheximide completely blocked the increase in TGase activity induced by EGF, suggesting that EGF stimulated de novo synthesis of TGase within 6 h. Furthermore, Northern blotting analysis indicated that EGF increased the expression of TGase mRNA. Pretreatment of cells with MDC additionally increased EGF-induced DNA-synthesis and the ratio of cells in S-phase. TGase antisense oligonucleotide inhibited de novo synthesis of TGase, resulting in increases in the ratios of S- and G2/M-phase cells in the presence of EGF. This effect was the result of inhibition of EGF-induced down-regulation of high-affinity receptor expression. These results suggest that the EGF-induced increase in TGase activity is a negative regulator of a growth signal in rat hepatocytes.

Animals↗

PubMed1996

Repeat hepatectomy for recurrent hepatocellular carcinoma.

This study evaluated the results of repeat hepatectomy for recurrent hepatocellular carcinoma (HCC) and delineated the limitations of such a treatment strategy. Of 290 patients who had radical hepatic resection, 167 had intrahepatic tumour recurrence. Fifty patients underwent a second hepatectomy. Third and fourth hepatectomies were carried out on six and two patients respectively. There were 36 men and 14 women. Age ranged from 32 to 77 years (mean 59.1 years). Liver cirrhosis was present in 38 and chronic hepatitis in 12 patients. Operative death occurred in four patients (8 per cent) after a second and in one of six after a third hepatectomy, compared with 4.5 per cent after first hepatectomy. The five postoperative deaths were attributed to either Child grade B or C liver disease, or severe intraoperative bleeding. The 5-year survival rate was better in these 50 patients (41 per cent) than in 117 patients who were treated otherwise (7 per cent). The present study indicates that repeat hepatectomy may be useful for recurrent HCC. It is indicated principally for patients with a solitary tumour and Child grade A liver disease.

Adult↗

PubMed1996

1 alpha,25-dihydroxyvitamin D3 inhibits cell growth and chondrogenesis of a clonal mouse EC cell line, ATDC5.

Here we report the effects of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] in vitro on the growth and chondrogenesis of a chondroprogenitor-like clonal mouse EC cell line, 10(-10) to 10(-7) M ATDC5. 1,25(OH)2D3 inhibited [3H]thymidine incorporation in undifferentiated chondroprogenitor-like ATDC5 cells in time- and dose-dependent manners. 1,25(OH)2D3 suppressed cartilage-nodule formation and the accumulation of cartilage-specific proteoglycan in ATDC5 cells in a dose-dependent manner. The 1,25(OH)2D3-induced inhibition of cartilage-nodule formation was reversible and direct, unrelated to the antiproliferative action of the hormone on the undifferentiated ATDC5 cells. ATDC5 cells even in the precartilaginous stage expressed 4.4 kb vitamin D receptor (VDR) mRNA as assessed by northern blot analysis. The equilibrium saturation binding experiment revealed the presence of a single class of saturable and high-affinity binding sites for 1,25(OH)2D3 in the cytosols. These results provide evidence for the hypothesis that both recruitment and chondrogenesis of chondroprogenitors are negatively regulated by 1,25(OH)2D3 via a VDR-mediated process in vivo.

Animals↗

PubMed1996

Estimation of coronary flow reserve with the instantaneous coronary flow velocity versus pressure relation: a new index of coronary flow reserve independent of perfusion pressure.

Our goal was to develop a new method to evaluate coronary flow reserve independent of perfusion pressure by equipping dogs with a Doppler flow probe in the left anterior descending artery. The slope of the linear portion of the velocity-pressure loop in the late diastolic phase was defined as VP slope; the hyperemic:basal ratio of the VP slope was defined as VP slope ratio, and the hyperemic:basal ratio of the mean coronary blood flow velocity was defined as coronary flow reserve (CFR). We measured VP slope ratio and CFR, altering aortic pressure by aortic banding and inferior vena cava occlusion. VP slope ratio was independent of aortic pressure, but CFR increased with increments in aortic pressure. The VP slope ratio and CFR decreased in the presence of coronary stenoses. In conclusion, VP slope ratio is considered to be a physiologic index of the severity of coronary stenosis, which is independent of perfusion pressure. This measure is easily applicable in clinical practice.

Angioplasty, Balloon, Coronary↗

PubMed1996

Inhibition of growth and induction of TGF-beta 1 in human hepatocellular carcinoma with androgen receptor by cyproterone acetate in male nude mice.

BACKGROUND/AIMS: Hepatocellular carcinoma possesses androgen receptor but its true role is not known. This study aimed to investigate the effect of an anti-androgen cyproterone acetate on the growth of androgen receptor-positive hepatocellular carcinoma. METHODS: Androgen receptor-positive human hepatocellular carcinoma cells (KYN-1/SM-10) were subcutaneously transplanted into male nude mice. When the tumor size was about 10 mm, animals were subcutaneously administered cyproterone acetate (0.1 mg/day and 0.8 mg/day) or solvent alone for 21 days. Animals were serially sacrificed for measurements of testicular weight, tumor size, and cytosolic and nuclear androgen receptor levels in tumor. Proliferating cell nuclear antigen, transforming growth factor-alpha, and transforming growth factor-beta 1 in tumor were investigated immunohistochemically, using monoclonal antibodies. Apoptotic activity was also studied by the in situ DNA nick end labeling method. RESULTS: Cyproterone acetate depressed testicular weight, suppressed tumor growth, and decreased both cytosolic-androgen receptor and nuclear-androgen receptor levels dose-dependently. Numbers of proliferating cell nuclear antigen-positive cells were decreased transiently with the low dose but continuously with the high dose of cyproterone acetate. Transforming growth factor-alpha expression was not influenced by cyproterone acetate, but the high dose of cyproterone acetate induced higher expression of transforming growth factor-beta 1, associated with increased numbers of apoptotic tumor cells, peaking on day 3. CONCLUSIONS: The inhibition of growth of androgen receptor-positive hepatocellular carcinoma with cyproterone acetate in male nude mice could be due to G1-phase cell cycle arrest, and to some extent apoptosis induced by increased synthesis of transforming growth factor-beta 1 in tumor, caused by the direct action of cyproterone acetate through androgen receptors, as well as decreased testosterone levels in blood due to cyproterone acetate-induced testicular atrophy.

Androgen Antagonists↗

PubMed1996

Mutations in the envelope gene of hepatitis B virus variants co-occurring with antibody to surface antigen in sera from patients with chronic hepatitis B.

Three clones of hepatitis B virus (HBV) DNA were propagated from sera of each of five patients with chronic hepatitis B who possessed hepatitis B surface antigen (HBsAg) and antibody to HBsAg in their serum. The clones were sequenced within the envelope gene (the preS1, preS2 regions and the S gene). Clones from four patients had various missense mutations involving codons 124-147 of the S-gene which encode amino acids in the loop structures that form the conformational, common antigenic determinant of HBsAg. Clones from three patients had Asn-130 (Gly in the wild-type), which generated a potential N-glycosylation site, Asn-Thr-Ser, spanning amino acids 130-132 of the S-gene product. In addition, clones from one patient had Arg-145 (Gly in the wild-type), which has been reported in escape mutants of HBV. One of the three clones from another patient had Ser-126 in place of lle or Thr in wild-type HBV, but the remaining two had no mutations known to affect expression of the common determinant of HBsAg. The remaining patient possessed HBsAg of subtype adr and anti-HBs specific for the w determinant. Clones from this patient did not reveal any mutations which are known to affect the common antigenic determinant of HBsAg.

Amino Acid Sequence↗

PubMed1996

Effectiveness and limitations of the fallback I algorithm for transient supraventricular tachyarrhythmias in DDD pacing.

To examine the function of the fallback I algorithm (Chorus I, Ela Medical Inc., Montrouge, France), which automatically changes the DDD mode to VDI during transient supraventricular tachyarrhythmias to prevent high-rate tracking of the venticule, a total of 45 patients who were preoperatively diagnosed with sick-sinus syndrome (SSS) (Group 1; n = 19) or with advanced or complete atrioventricular block (AVB) (Group 2; n = 26) were followed up and analyzed. Mean follow-up times (mean +/- SD) were 22.4 +/- 9.7 and 12.4 +/- 10.9 months, respectively. Each of the groups was further divided into subgroups according to the preoperative existence of of paroxysmal atrial fibrillation (PAF) or paroxysmal supraventricular tachyarrhythmia (PSVT). During follow-up, the fallback started through a given cycle of ventricular pacing at a upper-rate limit (URL) to avoid a continuous high-rate tracking during the arrhythmias specifically in the patients with PSVT (0/4) (p = 0.0004). The fallback, however, sometimes started in the patients who had AVB not associated with either PAF or PSVT (4/21) during normal exercise because the fallback algorithm did not distinguish a normal P wave from the abnormal atrial waves. To further clarify the behavior of the fallback, a treadmill test was conducted in 25 of the 45 patients. The fallback start was observed in 12 of the 17 patients with AVB (Group 2). In such patients, the use of a long fallback delay and/or a high URL setting prevented the fallback starts during normal exercise. These results suggest that, in DDD pacing, the algorithm in Chorus I is useful in patients with SSS or AVB to avoid highrate tracking of the ventricle during transient supraventricular tachyarrhythmias, but special care must be taken to avoid the fallback starts during the normal exercise in AVB patients.

Adult↗

PubMed1996

Use of automatic mode change between DDD and AAI to facilitate native atrioventricular conduction in patients with sick sinus syndrome or transient atrioventricular block.

The benefits of the automatic DDD (DDD/AMC) mode in the Chorus II pacemaker (Chorus 6234; Ela Medical Inc.), which automatically switches the modes between DDD and AAI to respect spontaneous AV conduction as much as possible in AAI while preserving safety pacing in DDD during paroxysmal AV block (AVB) only, remain unproven. This study examined the functions of the DDD/AMC mode in 12 patients with sick sinus syndrome (SSS; n = 10) or paroxysmal complete AVB (n = 2). A short-term (24 hours) comparative study between simple DDD mode and the DDD/AMC mode was performed in 8 of the 12 patients, and a medium-term (55.2 +/- 54.6 days) follow-up of the DDD/AMC mode was completed in all 12 patients. A comparative pair of 24-hour surface Holter ECGs was obtained in 6 of the 8 patients in the short-term study. Telemetry and built-in Holter histograms were collected in the outpatient clinic in all 12 patients. Although the percentage atrial pacing of the telemetry increased from 59.2 +/- 35.4 in DDD to 70.4 +/- 31.8 in DDD/AMC (P < 0.009; n = 8), the percentage ventricular pacing decreased from 64.6 +/- 37.7 in DDD to 36.2 +/- 43.1 in DDD/AMC (P < 0.027) in the short-term study. In particular, the reduction of percentage ventricular pacing to < 10% was observed in four patients with SSS not associated with > or = first-degree (1 degree) AVB on preoperative ECGs. Between the two modes a significant difference in arrhythmic events was not observed by the 24-hour surface Holter ECGS taken from the six patients in the short-term study. AAI-DDD switching associated with automatic modulation of AV delay and AV hysteresis occurred in all patients in the medium-term study. From the medium-term study, the total AV delay (AV delay plus AV hysteresis) exceeded 300 ms in 6 of the 12 patients in DDD/AMC, and usually became longest during nighttime. From the short- or medium-term study in the 12 patients, two patients preferred the DDD/AMC mode while one preferred the DDD mode. These results suggest that the DDD/AMC mode is useful, at least in SSS patients without > or = 1 degree AVB, by reducing the percentage ventricular pacing.

Adult↗

PubMed1996

Body composition, atherogenic risk factors and apolipoproteins following growth hormone treatment.

We studied the change in atherogenic risk factors in 27 children, 21 boys and 6 girls, 6 to 14 years of age, with growth hormone deficiency during 12 months of growth hormone replacement therapy. Changes in body composition and lipid profile during growth hormone treatment were evaluated. The atherogenic index was calculated using the equation [(total cholesterol- high-density lipoprotein cholesterol)(apolipoprotein B)]/[(apolipoprotein AI)(high-density lipoprotein cholesterol)]. Body fat decreased (p < 0.01), associated with an increase in lean body mass (p < 0.01). Total cholesterol and high-density lipoprotein cholesterol showed no significant changes. The atherogenic index significantly decreased from 1.44 +/- 0.60 to 1.09 +/- 0.52 (p < 0.01) after 12 months. Apolipoproteins CII and CIII increased throughout the study period (p < 0.01). Lipoprotein(a) and apolipoproteins AI, B and B/AI ratio did not change significantly. In conclusion, growth hormone treatment improved body composition and reduced atherogenic risk factors in children with growth hormone deficiency.

Adolescent↗