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K Akamatsu

Publications and source records attributed to K Akamatsu.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Two cases of anti-neutrophil cytoplasmic antibody-negative generalized Wegener's granulomatosis with alveolar hemorrhage].

Anti-neutrophil cytoplasmic antibody (ANCA) is a distinct marker for Wegener's granulomatosis. We report two cases of ANCA-negative Wegener's granulomatosis. A 70-year-old woman (case 1) and a 27-year-old woman (case 2), who had sinus symptoms and renal disorders, were admitted to our hospital with alveolar hemorrhage. Wegener's granulomatosis was diagnosed on biopsy of the nasal mucosa. Case 1 responded well to the combination therapy with cyclophosphamide and prednisolone, while case 2 responded well to pulse therapy with methyl-prednisolone. These findings suggest that patients with ANCA-negative Wegener's granulomatosis may respond well to chemotherapy. This might lead to an improved prognosis in even severe cases, even though the prognosis of generalized Wegener's granulomatosis with alveolar hemorrhage is usually poor.

Adult↗
PubMed1997

New xenograft model of multiple myeloma and efficacy of a humanized antibody against human interleukin-6 receptor.

A new xenograft model of multiple myeloma (MM), where growth is strongly regulated by interleukin-6 (IL-6), was established in severe combined immunodeficiency (SCID) mice. In this model, endogenous IL-6 from SCID mice was ineffective at eliciting growth of the established human MM cell line KPMM2; these cells achieved autonomous growth through their autocrine secretion of IL-6. The etiopathology in this disease model is consistent with that of human MM. When greater than 3 x 10(6) KPMM2 cells were injected intravenously (IV), tumors developed in all mice and were predominantly localized in their bone marrow. Tumors were also apparent in the lymph nodes, but absent from other organs. Immunostaining of cell surface antigen (CD38) showed that more than 40% of bone marrow cells in femur were of myeloma origin in the advanced stage of tumor progression (day 37). Histologic analysis of these mice show that bone marrow was largely occupied by plasmablastic cells and bones had developed osteolytic lesions at multiple sites. Concurrently, there was a decrease in bone density throughout the body and a significant increase in ionized plasma calcium. M-protein was detected in the serum within 10 days after transplantation, which correlated with the tumor progression. Between 30 and 40 days after the transplantation, mice presented with a rapid and severe loss of body weight, hind leg paralysis, and fatigue. Subsequently, the mice died within a week. A single IV injection of 0.2 mg humanized anti-IL-6 receptor antibody (hPM1) into mice on the day after tumor transplantation substantially suppressed the elevation of serum M-protein and development of the tumor-associated abnormalities and significantly increased in the life span of tumor-bearing mice. Our data show the usefulness of this model to analyze the pathologic role of IL-6 in MM and the efficacy of targeting the IL-6 receptor in IL-6-dependent KPMM2 cells.

Animals↗
PubMed1997

Physicochemical and disposition characteristics of antisense oligonucleotides complexed with glycosylated poly(L-lysine).

The disposition characteristics of a 20 mer antisense phosphodiester oligonucleotide (PO) and its fully phosphorothioated derivative (PS) alone or complexed with glycosylated poly(L-lysine) (galactosylated polylysine, Gal-PLL; mannosylated polylysine, Man-PLL) were studied in mice in relation to their physicochemical characteristics. Good complex formation was obtained at a ratio of 1:0.6, w/w [oligonucleotides (ODNs)/carrier]. The 1:0.6 weight ratio of ODNs/Gal-PLL and ODNs/Man-PLL complexes had zeta potentials of -27 to -31 mV and mean particle size of 100 to 160 nm. After intravenous injection, 35S-labeled ODNs were eliminated rapidly from the circulation; however, their organ disposition characteristics depended on their type. Complex formation with glycosylated PLL increased the hepatic uptake and decreased the urinary clearance of these ODNs to a great extent. These complexes were taken up by both liver parenchymal cells (PC) and nonparenchymal cells (NPC). However, ODNs/Gal-PLL complexes showed a fairly high PC concentration, whereas ODNs/Man-PLL complexes distributed equally to both PC and NPC. The hepatic uptakes of PS/Gal-PLL and PS/Man-PLL complexes were partially inhibited by prior administration of Gal-BSA and Man-BSA, respectively, suggesting their hepatic uptake via the respective receptor-mediated endocytosis. However, uptake by galactose receptors of Kupffer cells, zeta potential, particle size, and Kupffer cell phagocytosis also seem to influence their uptake process. In conclusion, this study illustrates that ODNs can be delivered to hepatocytes and macrophages via galactose and mannose receptors, respectively.

Animals↗
PubMed1996

Anti-interleukin-6 receptor antibody prevents muscle atrophy in colon-26 adenocarcinoma-bearing mice with modulation of lysosomal and ATP-ubiquitin-dependent proteolytic pathways.

Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients. Interleukin-6 (IL-6) has been reported to be responsible for the loss of lean body mass during cancer cachexia in colon-26 adenocarcinoma (C-26)-bearing mice. This study was carried out to elucidate the intracellular proteolytic pathways operating in skeletal muscle in C-26-bearing mice, and to examine the effect of anti IL-6 receptor antibody on muscle atrophy. On day 17 after tumor inoculation, the gastrocnemius muscle weight of C-26-bearing mice had significantly decreased to 69% of that of the pair-fed control mice. This weight loss occurred in association with increases in the mRNA levels of cathepsins B and L, poly-ubiquitin (Ub) and the subunits of proteasomes in the muscles. Furthermore, enzymatic activity of cathepsin B+L in the muscles also increased to 119% of the control. The administration of anti-murine IL-6 receptor antibody to C-26-bearing mice reduced the weight loss of the gastrocnemius muscles to 84% of that of the control mice, whose enzymatic activity of cathepsin B+L and mRNA levels of cathepsin L and poly-Ub were significantly suppressed compared with those of the C-26-bearing mice. Our data indicate that both the lysosomal cathepsin pathway and the ATP-dependent proteolytic pathway might be involved in the muscle atrophy of C-26-bearing mice. The results also suggest that anti IL-6 receptor antibody could be a potential therapeutic agent against muscle atrophy in cancer cachexia by inhibiting these proteolytic systems.

Adenocarcinoma↗
PubMed1996

Down-regulation of telomerase activity is an early event in the differentiation of HL60 cells.

Telomerase has been shown to be essential for unlimited cell proliferation and has been linked to immortality. However, still very little is known about the mechanism by which this enzyme is activated or inactivated. To investigate its regulation, we closely monitored telomerase activity during HL60 cell differentiation induced by either 1 alpha,25-dihydroxyvitamin D3 or all-trans retinoic acid. To that effect, we used a new combination of TRAP assay and SPA, which provides reproducible data for the quantitation and detection of variations in enzyme activity. We thereby observed that the decrease in telomerase activity after induction of differentiation by either of these agents is an early event of the differentiation process rather than its consequence, and that it is independent of the growth arrest pathway. It is neither due to a reduced expression of its RNA component nor to the appearance of a telomerase inhibitor in differentiating cells but is parallel to an increase in p21 and Rb mRNA expression.

Base Sequence↗
PubMed1996

Humanization of an anti-human IL-6 mouse monoclonal antibody glycosylated in its heavy chain variable region.

Interleukin-6 (IL-6) inhibitors are good potential therapeutic agents in human patients, and anti-IL-6 antibodies are among the best candidates. Here, we have successfully humanized mouse monoclonal antibody SK2, which specifically binds to IL-6 and strongly inhibits IL-6 functions. Since this antibody possesses N-linked carbohydrates on Asn-30 of VH region, which seems to be very close to an antigen-binding site, influence of these carbohydrates on antigen-binding was investigated. A biosensor study showed that the mouse SK2 Fab and its deglycosylated fragments had almost equal Kd (Kon/Koff), 26.8 nM (1.05 x 10(6)/2.81 x 10(-2)) and 24.7 nM (1.28 x 10(6)/3.15 x 10(-2)), respectively. Furthermore, a mutant chimeric SK2 antibody, in which the N-glycosylation site was removed from the VH region, showed a Kd of 11 nM, almost similar to that of the original chimeric SK2 antibody, determined by Scatchard analysis with 125I-IL-6. These data indicate the carbohydrates of mouse SK2 VH region do not significantly influence antigen-binding activity. In the next step, two versions of each humanized SK2 VL and VH regions were carefully designed based on the amino acid sequences of human REI and DAW, respectively. Only one alteration, Tyr to Phe, was made at position 71 in the two light chains, according to the canonical residue for LI. A N-glycosylation site was introduced on the two heavy chains, by changing Ser to Asn at position 30. All four combinations of humanized light and heavy chains could bind to IL-6 as well as the chimeric SK2 antibody. The light chain first version, however, could not efficiently inhibit IL-6 binding to its receptor, indicating the importance of the LI loop conformation for the inhibitory activity of SK2 antibody. In contrast, both versions of the heavy chains were comparable, in yielding good humanized SK2 antibodies, suggesting that the glycosylation of the SK2 VH region has no influence in recreating a functional antigen-binding site in this humanization.

Amino Acid Sequence↗
PubMed1996

Effects of all-trans retinoic acid and antireceptor antibodies on growth and programmed cell death of human myeloma cells.

In contrast to cytotoxic agents inducing rapid cell death, biological agents such as hormones, vitamins (e.g., retinoids), cytokines, and antireceptor antibodies act slowly and may alter ratios between cell growth and programmed cell death (apoptosis). We showed previously that anti-interleukin 6 (IL-6) and antitransferrin (Tf) receptor antibodies inhibited in vitro growth and induced death of myeloma cells. Retinoids also inhibit in vitro growth of human cancer cells and decrease IL-6 receptor display and autosecretion by some myeloma cells. Retinoids may also antagonize in vitro growth-promoting effects of iron and transferrin. To develop a novel strategy for treating myeloma, we examined antiproliferative and cytotoxic effects of retinoids in combination with anti-Tf or anti-IL-6 receptor antibodies. Myeloma cell lines were cultured with retinoids with or without anti-growth factor receptor monoclonal antibodies. Both all-trans retinoic acid (ATRA) and 13-cis-retinoic acid showed variable, dose-dependent inhibition of myeloma cell line growth. ATRA also induced significant down-regulation of myeloma IL-6 receptors and inhibited IL-6 autosecretion by myeloma cells. Antiproliferative effects of ATRA were increased by coculture with anti-Tf but not anti-IL-6 receptor antibodies. Colony-forming assays showed that antiproliferative effects of anti-Tf receptor antibodies were largely reversible, but 1 microM ATRA was cytotoxic to myeloma cells. To assess apoptosis, a flow cytometry assay detecting DNA damage was used. Using previously studied cell line models, flow cytometry detected programmed cell death induced by transforming growth factor beta1 in leukemia cells and by anti-growth factor receptor antibody treatment of IL-6-dependent myeloma cells, treatments which caused only modest increases in the percentage of cells undergoing morphological apoptosis and increased internucleosomal DNA degradation. Flow cytometry analysis of ATRA and anti-Tf antibody-treated myeloma cells also showed evidence for apoptosis induced by ATRA, but not with anti-Tf receptor antibodies. These changes were apparent several days before detection of internucleosomal DNA degradation on agarose gels in 8226 cells but were not detected at any time in U266 cells, which underwent cell death but showed no DNA damage using flow cytometry or degradation on agarose gels. Retinoids merit further study as possible maintenance or chemoprevention therapies for clonal plasma cell disorders and for treating paraneoplastic disorders such as Castleman's disease. Flow cytometry rapidly detects apoptosis induced by biological agents and may be useful for in vitro screening of novel biological therapies.

Antibodies, Monoclonal↗
PubMed1995

Hepatitis B virus strains with mutations in the core promoter in patients with fulminant hepatitis.

OBJECTIVE: Fulminant hepatitis B can be induced by hepatitis B virus (HBV) strains with mutations in the precore region that cannot encode hepatitis B e antigen (HBeAg). Such mutations are rarely seen in HBV DNA clones from patients with fulminant hepatitis B in the United States and France. Thus, the other mutations in HBV strains causing fulminant hepatitis B need to be identified. DESIGN: Retrospective clinical, serologic, and molecular biological studies of patients with fulminant hepatitis B. SETTING: University and city hospitals in Japan. PATIENTS: 43 patients with fulminant hepatitis B. MEASUREMENTS: The precore region coding for a part of the HBeAg precursor and the core promoter regulating the transcription of precore messenger RNA were sequenced in HBV DNA clones. RESULTS: A point mutation from G to A at nucleotide 1896 in the precore region was detected in 519 (98%) of 529 HBV DNA clones from 38 patients. Two point mutations in the core promoter, from A to T at nucleotide 1762 and from G to A at nucleotide 1764, were detected in all 130 clones from the remaining 5 patients, who did not have mutations in the precore region, and in 20 (63%) of 32 clones from a patient with chronic hepatitis B who had transmitted HBV to 1 of these other 5 patients. Mutations in the core promoter were also detected in clones from 26 (68%) of the 38 patients with the precore mutation at nucleotide 1896. Neither HBeAg nor antibody to HBeAg was detected in 37 (90%) of the 41 patients tested. CONCLUSIONS: In Japan, fulminant hepatitis B is closely associated with HBV strains that do not produce HBeAg because of mutations in the precore region, which affect translation of HBeAg, or because of mutations in the core promoter, which affect transcription of the HBeAg coding region.

Acute Disease↗
PubMed1995

Sensitization of human renal cell carcinoma cells to cis-diamminedichloroplatinum(II) by anti-interleukin 6 monoclonal antibody or anti-interleukin 6 receptor monoclonal antibody.

Cytotoxic chemotherapy has shown little antitumor activity against renal cell carcinoma (RCC). It has been demonstrated that RCC cells secrete interleukin 6 (IL-6) and express IL-6 receptors (IL-6Rs). IL-6 inhibits apoptosis and enhances manganese superoxide dismutase expression. Several anticancer chemotherapeutic agents exert their cytotoxic activity in part through the induction of apoptosis and the production of free radicals. Thus, the resistance of RCC cells to the anticancer agents might correlate with IL-6 expression. The present study tested this hypothesis by examining the effect of anti-IL-6 mAb and anti-IL-6R mAb on the sensitivity of human RCC cells to anticancer chemotherapeutic agents. Treatment of Caki-1 cells with anti-IL-6 mAb or anti-IL-6R mAb in combination with cis-diamminedichloroplatinum(II) (CDDP) or mitomycin C overcame their resistance to CDDP or mitomycin C. However, treatment of Caki-1 cells with anti-IL-6 mAb or anti-IL-6R mAb in combination with Adriamycin, vinblastine or 5-fluorouracil did not overcome their resistance to these anticancer agents. Treatment of CDDP-resistant Caki-1 cells (Caki-1/DDP), two other RCC cell lines (ACHN and A704), and three freshly derived RCC cells with CDDP in combination with anti-IL-6 mAb or anti-IL-6R mAb reversed the resistance to CDDP in all these tumors. We then studied the effectiveness of other platinum derivatives. Treatment of Caki-1 cells with anti-IL-6 mAb or anti-IL-6R mAb enhanced their sensitivity to carboplatin, but not to trans-diamminedichloroplatinum(II). Several experiments investigated the mechanism of the antibody-mediated sensitization of RCC cells to CDDP. Incubation of Caki-1 cells with anti-IL-6 mAb or anti-IL-6R mAb did not change the intracellular accumulation of CDDP. The expressions of the multidrug resistant phenotype (gp170) and c-myc oncogene were not affected by the antibody-mediated sensitization. Treatment of Caki-1 cells with the anti-IL-6 mAb or anti-IL-6R mAb down-regulated the expression of glutathione S-transferase pi mRNA. This study demonstrates that treatment of RCC cells with CDDP in combination with anti-IL-6 mAb or anti-IL-6R mAb can overcome their CDDP-resistance and that the down-regulation of glutathione S-transferase pi expression by anti-IL-6 mAb or anti-IL-6R mAb might play a role in the enhanced cytotoxicity obtained.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1995

Humanization of mouse ONS-M21 antibody with the aid of hybrid variable regions.

Mouse monoclonal antibody, ONS-M21, directed against human medulloblastoma cells, has been humanized by complementarity determining region (CDR) grafting. A humanized ONS-M21 VH region, comparable to the original mouse ONS-M21 VH region, was easily constructed based on framework regions (FRs) 1, 2 and 3 from human EU antibody and on FR4 from human ND antibody. Five alterations in the FRs were made at amino acids 27, 28, 29, 30 and 94 which are all part of the canonical structure for CDR1 (H1). The humanized ONS-M21 VL regions were constructed based on the FRs from human REI antibody. We first identified five amino acid residues in the FRs at positions 20, 21, 71, 73 and 87 as having a possible adverse influences on antigen binding. None of the versions with a variety of combinations at these five positions showed any bindings to antigen. In order to identify the mouse residues that must be retained in the human FRs, hybrid VL regions were constructed by joining the mouse ONS-M21 VL region and the first humanized version within CDR2. The hybrid VL regions revealed that residues in FR1 and/or FR2 were critical in creating a functional antigen binding site. Redesigning several versions with alterations in FR1 and FR2 revealed that the Pro-46 residue was the only critical residue for creating an antigen binding site. This approach should be helpful in identifying key residues in difficult cases of antibody humanization.

Amino Acid Sequence↗
PubMed1995

Endogenous ET-1 contributes to liver injury induced by galactosamine and endotoxin in isolated perfused rat liver.

Injury to hepatocytes most likely occurs via disturbances in the microcirculation. The role of vasoconstriction due to the effect of endogenous endothelin-1 (ET-1) in the development of galactosamine (GalN)- and lipopolysaccharide (LPS)-induced liver injury was investigated. Using the multiple indicator dilution technique, we measured the volume of the hepatic sinusoids and the apparent Disse space as indicators of overall hepatic microcirculation. Serum purine nucleoside phosphorylase activity as a marker of damage to nonparenchymal cells increased and the volume of the sinusoids and the Disse space decreased prior to hepatocyte damage in rats treated intraperitoneally with GalN and LPS. Moreover, the amount of ET-1 release was elevated. When livers from untreated rats were perfused with ET-1 in a recirculating system, hepatocyte damage was observed similar to experiments with GalN and LPS. A monoclonal anti-endothelin antibody, AwETN40, diminished the extent of liver injury caused by GalN and LPS in isolated perfused rat liver. The present study suggests that vasoconstriction is an early event in GalN- and LPS-induced liver injury and that the development of hepatocyte damage is mediated via microcirculatory disturbances due to endogenous ET-1.

Alanine Transaminase↗
PubMed1995

Clinical significance of antiphospholipid antibodies in fulminant hepatic failure.

We examined the incidence of antiphospholipid antibodies (APA) in patients with fulminant hepatic failure (FHF) and various liver diseases using the enzyme-linked immunosorbent assay (ELISA), and assessed possible correlations with the pathophysiology of these diseases. The APA assay employed cardiolipin (CL), phosphatidylserine (PS), and phosphatidylinositol (PI) as antigens. Anti-CL IgA antibody was detected in 13/14 (92.9%) patients with FHF. The incidence of anti-CL-IgG, anti-CL-IgM, anti-PS-IgG, and anti-PI-IgG was 14.3%, 35.7%, 64.3%, and 71.4%, respectively. Despite the high incidence of APA in FHF, these antibodies were not detected in most patients with acute or chronic hepatitis. There was a negative correlation between anti-CL-IgA and the platelet count, and a negative correlation between anti-PI-IgG and the amount of residual liver parenchyma. Our results suggest that APA develop secondarily to hepatocyte or sinusoidal cell damage and may aggravate both thrombocytopenia and liver failure.

Adult↗
PubMed1995

Well-differentiated hepatocellular carcinoma: clinicopathological features and results of hepatic resection.

OBJECTIVES: To clarify clinicopathological features and surgical results in patients with well-differentiated hepatocellular carcinoma (wd-HCC) corresponding to Edmondson's cell grading I/I-II. METHODS: The clinicopathological characteristics, diagnosis, and results of surgery were studied in 14 wd-HCC patients who underwent limited hepatic resection. RESULTS: All patients had liver cirrhosis and solitary tumors. The tumor sizes ranged from 10 to 25 mm. Serum alpha-fetoprotein levels were normal in 13 patients. The detection rates of sonography, computed tomography (CT), angiography, CT during arterial portography, 1-wk lipiodol CT, and 3-wk lipiodol CT were 100%, 43%, 36%, 69%, 57%, and 0%, respectively. High echoic pattern on sonography and disappearance of lipiodol 3 wk after injection were characteristic findings. There was no operative death. Although seven patients developed intrahepatic tumor recurrence, early treatment including ethanol injection therapy and arterial embolization/infusion therapy controlled the recurrences in five patients. Eleven patients are surviving 25-83 mo after surgery (mean, 44 mo); the remaining three died of pneumonia or hepatic insufficiency 44-62 mo after surgery. Eight patients received successful direct interruption surgery for concurrent esophagocardia varices. Pathological features of wd-HCCs included lack of tumor invasiveness or capsule, nuclear crowding, microacinar formation, fat deposition, presence of portal tracts, and surrounding adenomatous hyperplasia. CONCLUSION: Wd-HCCs present atypical findings in various imagings and histology because of the earlier developmental stage of HCCs. Hepatic resection for wd-HCCs provides excellent patient survival.

Carcinoma, Hepatocellular↗
PubMed1993

Synthesis and damage specificity of a novel probe for the detection of abasic sites in DNA.

The abasic site (apurinic/apyrimidinic site) is the most common lesion in DNA and is suggested to be an important intermediate in mutagenesis and carcinogenesis. We have recently reported a novel assay for the detection and quantitation of abasic sites in DNA [Kubo, K., Ide, H., Wallace, S. S., & Kow, Y. W. (1992) Biochemistry 31, 3703-3708]. In this assay, the aldehyde group in an abasic site is first modified by a probe bearing a biotin residue, called the Aldehyde Reactive Probe (ARP) and then the tagged biotin is quantified by an ELISA-like assay. However, in the previous study, ARP was prepared only in a crude form, and no solid chemical data concerning the structure and specificity of ARP were reported. In this study, an improved method for the preparative synthesis of ARP has been established, and its structure has been unambiguously characterized using spectroscopic means. In order to elucidate the specificity of ARP to DNA damages, ARP was incubated with a variety of damaged bases or nucleosides and the reaction mixtures were analyzed by HPLC. Of the 14 compounds tested for their reactivity to ARP, 2-deoxyribose (a model compound for an abasic site) and 5-formyluracil reacted with ARP. Interestingly, compounds bearing a formamide group such as formamidopyrimidine and deoxyribosylformamide did not react with ARP, indicating that ARP is specific to damages having an alkyl or allyl aldehyde group. Furthermore, the ability of ARP synthesized by the defined chemical route to detect abasic sites has been substantiated using natural DNA containing abasic sites. Potential applications and limitations of the ARP assay are discussed.

Animals↗
PubMed1993

Effect of chronic alcohol intake on rat liver microcirculation assessed by the multiple indicator dilution technique.

To study the hepatic microcirculatory disturbance in alcoholic liver injury, rats were chronically (8-12 weeks) fed with alcohol via a gastric fistula according to the method of Tsukamoto and French (1986). The hepatic microcirculation was studied by measuring the sinusoidal volume (SV) and the apparent space of Disse (DS) volume using a multiple-indicator dilution technique. Both the SV and the DS volume were significantly decreased in the alcohol-fed rats at 8-12 weeks despite the absence of microscopically detectable hepatic fibrosis. Similar changes were noted in the alcohol-fed and control rats regarding expansion of the SV and the DS volume with alterations in portal pressure. However, since the volumes in the alcohol-fed group increased with the increase of portal pressure, they maintained a steady difference from the control values. These results suggested that the decrease of the SV and the DS volume may have been secondary to compression caused by steatosis and/or hepatocyte enlargement, although a possible role for microscopically undetectable hepatic fibrosis could not be ruled out.

Alcoholism↗
PubMed1993

Development and evaluation of a needle for percutaneous ethanol injection therapy.

To avoid the disadvantages associated with use of the traditional percutaneous transhepatic cholangiography (PTC) needle in ultrasonically guided percutaneous ethanol injection therapy (PEIT) for hepatocellular carcinoma, the authors developed a needle with a three-sided tip and three holes within 3 mm of the tip. In comparison with a PTC needle, the PEIT needle passed into the liver along a straighter line with less resistance and reflected a higher echo from the tip.

Ethanol↗
PubMed1993

Alcoholic hypertriglyceridemia with decreased activity of lipoprotein lipase and hepatic triglyceride lipase.

A 35-year-old male with alcoholic hypertriglyceridemia due to decreased lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities is reported. The patient had been drinking about 180 ml of whiskey (equivalent to 80 g of 100% ethanol) every day for the last 17 years, and the highest levels of serum triglyceride (TG) and cholesterol were 5,120 mg/dl and 506 mg/dl, respectively. Serum TG level returned to normal levels after complete alcohol abstinence. Further intake of ethanol resulted in an increase in serum TG to 326 mg/dl with a concomitant decrease in the serum levels of LPL and HTGL activities.

Adult↗