A1C but not serum glycated albumin is elevated because of iron deficiency in late pregnancy in diabetic women.

OBJECTIVE We have already reported that A1C is elevated because of iron deficiency in late pregnancy among nondiabetic pregnant women. This report examined whether the same phenomenon is observed in pregnant women with diabetes. RESEARCH DESIGN AND METHODS This longitudinal study was conducted in 17 pregnant women with diabetes (20-35 weeks of pregnancy). A1C, serum glycated albumin, erythrocyte indexes, and iron metabolism indexes were measured. RESULTS A1C levels were significantly increased in late pregnancy, whereas serum glycated albumin showed no significant changes. Glycated albumin/A1C ratio, mean corpuscular hemoglobin, serum transferrin saturation, and serum ferritin were significantly decreased in late pregnancy. Serum transferrin saturation showed a significant positive correlation with glycated albumin/A1C ratio. CONCLUSIONS A1C levels, but not serum glycated albumin levels, are elevated in late pregnancy because of iron deficiency in diabetic women. Serum glycated albumin may offer an adequate marker for glycemic control during pregnancy.

A1C but not serum glycated albumin is elevated in late pregnancy owing to iron deficiency.

OBJECTIVE: A1C levels have been shown to be elevated in relation to glycemia in late pregnancy, although the precise mechanisms remain undetermined. We hypothesized that iron deficiency is involved in the A1C increase in late pregnancy. RESEARCH DESIGN AND METHODS: In study 1, A1C, serum glycated albumin, erythrocyte indexes, and iron metabolism indexes were determined in 47 nondiabetic pregnant women not receiving iron supplementation who were divided into four groups according to gestational period (group I, 21-24 weeks; group II, 25-28 weeks; group III, 29-32 weeks; and group IV, 33-36 weeks). In study 2, these determinants were obtained at two gestational periods (20-23 weeks and 32-33 weeks) in 17 nondiabetic pregnant women. RESULTS: In study 1, A1C levels were higher in groups III and IV than those in groups I and II, whereas serum glycated albumin levels were not different among these four groups. Hemoglobin, mean corpuscular hemoglobin (MCH), serum transferrin saturation, and serum ferritin were lower in groups III and IV. A1C levels were negatively correlated with MCH, serum transferrin saturation, and serum ferritin. In study 2, A1C levels were significantly increased at gestational weeks 32-33 from those at weeks 20-23, whereas serum glycated albumin levels did not differ between the two gestational periods. MCH, serum transferrin saturation, and serum ferritin were decreased at gestational weeks 32-33. A1C levels showed a negative correlation with MCH, serum transferrin saturation, and serum ferritin. CONCLUSIONS: A1C levels were elevated in late pregnancy owing to iron deficiency. Serum glycated albumin may offer a better index for monitoring glycemic control in pregnancy.

A pilot study of combination therapy with initial high-dose interferon and amantadine hydrochloride for patients with chronic hepatitis C with the genotype 1b virus.

BACKGROUND/AIMS: Interferon monotherapy for patients with chronic hepatitis C has been suboptimal. We studied the effect of the combination therapy of an initial high-dose of interferon and amantadine. METHODOLOGY: We investigated the virological response of 20 patients with naive chronic hepatitis C with a high viral load of the genotype 1b virus. Seven patients were administered 6MU of interferon-beta once daily for 6 weeks and then thrice weekly for 20 weeks, and 13 were administered 6 MU of interferon-beta daily for 4 or 6 weeks and then 10 MU of natural interferon-alpha thrice weekly for 22 or 20 weeks. All patients were treated with amantadine hydrochloride (100 mg/day) for 26 weeks during interferon administration. RESULTS: The complete response, transient response and no response rate were 15.0%, 60.0%, and 25%, respectively. After daily administration of interferon-beta intravenously, 19 patients (95.0%) showed negative tests for serum HCV-RNA by the polymerase chain reaction method. At the end of treatment, the serum HCV-RNA was not detected in any patients treated with daily interferon-beta and intermittent interferon-alpha with amantadine. At 6-month follow-up, three patients had eradicated HCV-RNA, who were in the group of daily interferon-beta and intermittent interferon-alpha with amantadine. In the patients treated with daily interferon-beta and intermittent interferon-alpha with amantadine, the complete response, transient response and no response rates were 23.1%,-76.9% and 0%, respectively. CONCLUSIONS: These findings suggest that the combination of an initial high-dose interferon and amantadine shows promising effects on the eradication of HCV-RNA in the chronic hepatitis C patients with a high viral load of the genotype 1b virus.

The combination therapy of interferon and amantadine hydrochloride for patients with chronic hepatitis C.

BACKGROUND/AIMS: The effect of interferon treatment for chronic hepatitis C patients with genotype 1b virus has been suboptimal. We studied the effect of the combination therapy of interferon and amantadine on patients with a high serum viral load of genotype 1b virus. METHODOLOGY: We studied the virological response of naive chronic hepatitis C patients with a high viral load of genotype 1b virus (4.5 log copies/50 microL or 100 kcopies/mL and higher) during interferon and amantadine administration for 6 months and 6 months after the end of treatment. Twenty patients were treated with interferon alone (natural interferon-beta 6 MU daily for 6 weeks and thrice-a-week for 20 weeks) for 26 weeks. Eleven patients were treated with the combination therapy of interferon and amantadine hydrochloride (100 mg orally daily) for 26 weeks. RESULTS: After daily administration of interferon-beta intravenously once a day for 6 weeks, all patients showed the negative tests of serum HCV-RNA by polymerase-chain-reaction methods by the combination therapy, while 13 patients (65.0%) showed the negative tests by interferon alone (p = 0.0257). At the end of treatment, serum HCV-RNA were not detected in 54.5% of patients treated with interferon and amantadine, while it was detected in 50.0% of patients treated with interferon alone. At 6 months follow-up, only one patient (9.1%) could eradicate HCV-RNA in patients with interferon and amantadine, while no patient could with interferon monotherapy (not significantly). CONCLUSIONS: Amantadine hydrochloride has the additive effects to interferon treatment on the virological responses of serum HCV-RNA during a co-administration, although the combination therapy has not shown a significantly promising effect on the eradication of HCV-RNA in the patients with chronic hepatitis C with a high viral load of genotype 1b virus.

Interferon treatment for patients with chronic hepatitis C infected with high viral load of genotype 2 virus.

BACKGROUND/AIMS: Interferon treatment is more effective in patients with chronic hepatitis C infected with genotype 2a virus than those with genotype 1b virus. We analyzed patients with chronic hepatitis C treated by interferon in our clinics to develop a more effective regimen of interferon treatment for patients with genotype 2 virus infection. METHODOLOGY: We retrospectively analyzed the virological response of 36 patients with chronic hepatitis C with a high viral load, including 28 cases infected with the genotype 2a virus and 8 cases with the genotype 2b virus. The serum viral load of these patients were 6.0 log copies/mL and higher by the competitive polymerase chain reaction assay method. All patients could be treated with interferon-alpha or -beta for 6 months. Eleven patients were administered 6 million units of interferon-beta once daily for 6 weeks and then thrice weekly (group A). Twelve patients were administered 6 million units of interferon-alpha daily initially for 2 weeks and then thrice weekly (group B), and 10 patients were treated with the same dose of interferon-alpha thrice weekly from the first administration (group C). We decided the criteria of complete remission as the absence of serum HCV-RNA at both points of the end of interferon treatment and 6 months later. RESULTS: For all patients with genotype 2a virus infection, the complete remission, transient response and no response rates were 46.4%, 39.3% and 14.3%, respectively. The complete remission rates in group A, B and C were 100%, 41.7% and 20%, respectively. The transient remission rates in group B and C were 41.7% and 60%, respectively. The no response rates in group B and C were 16.7% and 20%, respectively. All patients with a high viral load of genotype 2a virus showed eradicated serum HCV-RNA virus in group A. The eradication rate of serum HCV-RNA in patients infected with the genotype 2a virus in group A was significantly higher than that of group B (p < 0.02) or group C (p < 0.01). For all patients with genotype 2b virus infection, complete remission, transient remission and no response rates were 12.5%, 50.0% and 37.5%, respectively. The complete remission rate of patients with the genotype 2b virus in group A and group B plus C was 0% and 25.0%, respectively. The eradication rate of patients with the genotype 2a virus in group A was significantly higher than that of patients with the genotype 2b virus (p < 0.01). CONCLUSIONS: These findings suggest that the initial sufficient dose of interferon administration is effective to eradicate serum HCV-RNA in patients with a high viral load of genotype 2a virus in chronic hepatitis C.

PTHrP-producing tumor: squamous cell carcinoma of the liver accompanied by humoral hypercalcemia of malignancy, increased IL-6 and leukocytosis.

A 77-year-old man was admitted to our hospital showing symptoms of general fatigue and appetite loss. He had leukocytosis, thrombocytosis and hypercalcemia with elevated serum levels of parathyroid hormone related peptide (PTHrP) and interleukin-6 (IL-6). An increase in tumor markers SCC and CYFURA21-1 was observed. The liver contained a huge tumor, which was proved to be PTHrP producing squamous cell carcinoma by immuno-histochemical analysis. Since the tumor did not express IL-6, it was assumed to be induced by PTHrP in osteoblasts. This is the first report of PTHrP producing squamous cell carcinoma of the liver.