Fumitoshi Ohno

Influence of serum amyloid A protein on high-density lipoprotein in chronic inflammatory disease.

We determined the concentration of serum amyloid A protein (SAA) in plasma and each lipoprotein fraction from patients with inflammatory disease (n = 62) and healthy subjects (n = 35). The mean SAA concentration in the patients with inflammatory disease (396 mg/L) significantly exceeded that in healthy subjects (1.4 mg/L). In the patients with acute inflammatory disease SAA was distributed mainly in the high-density lipoprotein (HDL) fraction. HDL-cholesterol (HDL-C) showed an initial increase followed by an immediate decrease, and gradually returned to the baseline. Plasma concentrations of apoA-I and apoA-II (apolipoprotein, apo) were decreased, and gradually returned to normal along with HDL-C. In patients with rheumatic disease the concentration of HDL-C, apoA-I, or apoA-II was lower than in healthy subjects, and was inversely correlated with the concentration of plasma SAA (r = -0.409, r = -0.642, r = 0.545, respectively). These results are in keeping with the suggested mechanism of SAA displacing apoA-I and apoA-II, which may result in increased catabolism of HDL.

ANTITHYROID ANTIBODIES IN ALPORT'S SYNDROME

Two families in which more than two members had Alports syndrome were examined. Serum-antithyroid-antibodies were found in all those with Alports syndrome and some of their relatives. These included three cases of Alports syndrome with nephritis and/or nerve deafness and two normal people who can be regarded as carriers of Alports syndrome from one family, and one case of the syndrome with nephritis and deafness from the other family. One case of Alports syndrome had symptoms of hypothyroidism, and biopsy specimens from another case were characteristic of chronic thyroiditis. The results indicate that serum-anti-thyroidantibodies, together with nephritis and deafness, are a sign of Alports syndrome. The results accord with transmission of the syndrome as an autosomal dominant trait and suggest that Alports syndrome may be caused by an immunological abnormality.

A case of vasculitic cholecystitis associated with Schönlein-Henoch Purpura in an adult

SummaryA case of Schönlein-Henoch Purpura (SHP) in a 32 year-old female, showing gastrointestinal manifestations including acute vasculitic cholecystitis was reported. In the course of hospitalization urgent laparotomy was performed because of the severe abdominal pain. The gallbladder was inflamed with a brownish-red edematous wall and subserosal hemorrhage, and was resected. Histological examination of the resected gallbladder specimen revealed leucocytoclastic vasculitis. The patient was treated with prednisolone postoperatively, and symptoms abated over two weeks. Acute cholecystitis with SHP is extremely rare, and as far as the authors know this is the second case of this disorder documented by histological examination. Patients with acute abdomen associated with SHP should be managed with consideration of the complications of acute cholecystitis.

Plasma apolipoprotein H (β2-glycoprotein I) phenotype frequencies in a Japanese population

SummaryWe determined plasma apolipoprotein H (β2-glycoprotein I) levels in 300 healthy adult individuals and evaluated the frequencies of the BgN and BgD alleles in a Japanese population. These results were then compared with the previous reports. The plasma apo H levels in the subjects showed bimodal distribution: 274 subjects were in the range 15.6–33.2 mg/dl and were considered to be homozygous for BgN (phenotype NN), and 26 subjects were found in the range 9.6–14.8 mg/dl and were presumably heterozygous for BgN and BgD (phenotype ND). In this study, no sample below 5 mg/dl (phenotype DD) was found. Mean plasma apo H levels in NN and ND groups were 22.1±1.6 mg/dl and 12.5±1.6 mg/dl, respectively. The gene frequencies of BgN and BgD in a Japanese population were 0.957 and 0.043, respectively. These results were similar to gene frequencies of BgN and BgD in Caucasoids.

A Five-year Follow-up Study of Fasting Plasma Glucose Levels in 3,604 Subjects Undergoing Health Screening.

1992年4月から1995年3月までに, 当センターで健診を受け, 5年後にも当センターを受診した3, 604名 (平均年齢50.9歳) を対象として, 非糖尿病 (空腹時血糖 (FPG) が125mg/dl/以下かつ糖尿病としての治療を受けていない) から糖尿病 (本論文では, FPG 126mg/dl/以上をもって糖尿病型とし, 糖尿病治療中である者と合わせて糖尿病と診断) への悪化する率を検討した。スターティングポイントのBody Mass Index (BMI) およびFPGにより対象を区分し, 5年の前後でBMIおよびFPGの変化量の平均と5年後に糖尿病を示した率を算出したところ, 以下の結果が得られた。 (1) スターティングポイントで糖尿病を示した率は4.1% (147/3, 604) であったのに対し, 5年後に糖尿病を示した率は7.1% (257/3, 604) であった。 (2) スターティングポイントのFPGが100mg/dl～104mg/dlの2.0%, FPGが105mg/dl～109mg/dlの7.7%, FPGが110mg/dl/～114mg/dlの18.3%, FPGが115mg/d/l～119mg/dlの37.7%, FPGが120mg/dl～125mg/dlの68.4%が, 5年後に糖尿病を示した。 (3) FPGが100mg/dl～119mg/dlの場合には, 5年後に糖尿病を示す率にBMIの各層間で有意差は認められなかった。一方, FPGが120mg/dl～125mg/dlの場合には, BMIが24未満の層では5年後に糖尿病を示した率が46.2%であったのに対し, BMIが24以上の層では5年後に糖尿病を示した率は87.1%を示し, この差はマン・ホイットニ検定にて有意なものであった。したがって, FPGが120mg/d/～125mg/dlでBMIが24以上の場合には, 糖尿病に準じる厳重な管理が必要であると考えられる。