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At least 19 recordsLinked to original sources
PubMed1977

T and B lymphocytes in patients with chronic active hepatitis (CAH).

Absolute numbers of T and B lymphocytes as well as active E rosette-forming cells were measured in twenty-seven patients with chronic active hepatitis (CAH), and in thirty control patients. In patients with CAH without cirrhosis, active E rosette-forming cells (a subpopulation of T lymphocytes considered to be actively involved in cell-mediated immune reactions) as well as lymphocytes with surface markers for IgA, IgM and IgG were increased. In patients with CAH and cirrhosis, total T lymphocytes were decreased. These results emphasize the significance of lymphocytes in CAH, and suggest the importance of monitoring T- and B-cell populations in patients with this disease.

Adult↗
PubMed1979

Comparison of two tests for heterozygosity in congenital adrenal hyperplasia (CAH).

The increase of plasma cortisol (F), androstenedione (A), 17 alpha-hydroxy-progesterone (17-OH-P) and testosterone (T) was measured after iv administration of ACTH in heterozygotes for CAH and in controls under two different conditions: Test 1: ACTH stimulation was performed without any particular preparation. Test 2: 1.5 mg of dexamethasone (dex.) was given the evening before the ACTH stimulation. Plasma F, A, 17-OH-P and T were measured by specific radioimmunoassays (RIA). Following ACTH stimulation, the increase of 17-OH-P was significantly higher in CAH-heterozygotes than in controls in both tests (P less than 0.0005). Heterozygotes were characterized by a 17-OH-P increase after ACTH stimulation exceeding the + 2 SD limit of the 17-OH-P increase found in controls. The detection of female heterozygotes was considerably improved by the administration of dex. before testing (test 2). In males, however, a better identification of heterozygotes was obtained without previous administration of dex. (test 1). By these tests, 100% of female (test 2) and 79% of male (test 1) CAH heterozygotes could be correctly identified. There were no significant differences in the levels of F, A and T between heterozygotes and controls except for decreased T levels in test 1 (2P less than 0.01) in most male heterozygotes after ACTH stimulation.

Adrenal Cortex Function Tests↗
PubMed1977

[The frequency of congenital adrenal hyperplasia (cah) in Munich (author's transl)].

In Munich the frequency of homozygotes of CAH (with and without salt losing syndrome) in the years 1963-1972 was 1; 9831. The CAH gen frequency was 1:99 and the frequency of heterozygote carriers was 1: 50. From these observations it was concluded that the number of undiagnosed boys suffering from CAH without salt losing syndrome must be very high. Assuming a sex ration of 1:1 for the children without salt losing syndrome the frequency of homozygotes (with and without salt losing syndrome) can be calculated to 1:7520. The statistical comparison of the frequency for Munich and for Zürich (Prader 1958) does not show a significant difference.

Adrenal Hyperplasia, Congenital↗
PubMed1977

HLA and chronic active hepatitis (CAH).

A family study of 2 parents and 5 SD identical (HLA-A1, A3, B7, B8) siblings, one of whom has 'classic CAH' has been used to demonstrate that in this family the maternally ingerited HLA-B8 antigen is not solely serving to mark genetic predisposition to this disease. The patient's lymphocytes both responded to, and stimulated those of her 4 siblings in MLR indicating the possible involvement of an HLA-D antigen in CAH. This HLA-D antigen could have been of paternal orgin, or could have been a result of a recombination event involving an HLA-D antigen liked to the maternal HLA-A2, B12 haplotype. The lymphocytes of the four helthy siblings were mutually unresponsive in MLR.

Chronic Disease↗
PubMed1979

Antibody-dependent cell-mediated cytotoxicity (ADCC) and cell-mediated cytotoxicity (CMC) to HBsAg-coated target cells in patients with hepatitis B and chronic hepatitis (CAH).

A new technique using HBsAg-coated Chang cells as target cells was developed in order to measure cell-mediated immune reactions to HBsAg. The specificity of cytotoxic reactions was tested in experiments using Chang cells conjugated with human serum albumin. Antibody-dependent cell-mediated cytotoxicity (ADCC) specific for the HBsAg-coated target cells was demonstrated up to dilutions of anti-HBsAg serum of 10,000 : 1, when lymphocytes from the peripheral blood of normal individuals were added to the target cells. Spontaneous cell-mediated cytotoxicity (CMC) to HBsAg-coated target cells was demonstrated for lymphocytes from patients with hepatitis B and from patients with chronic active hepatitis (CAH), but not for lymphocytes from healthy controls. The CMC of hepatitis B lymphocytes to HBsAg-coated target cells was inhibited in the presence of antiserum to HBsAg. In experiments using purified lymphocyte populations evidence is presented that the CMC is T-cell dependent. HLA-restriction of the CMC was not observed. The described cytotoxicity test system has the advantage that target cells conjugated with defined antigens are used and that relevant control target cells are available.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1991

[Preliminary results of the treatment of patients with chronic active hepatitis (CAH) HBsAg+,HBeAg+ with low oral doses of human interferon-alpha].

The treatment conception was based on the theory of immunocorrective activity function of low doses of human interferon alpha (HuIFN alpha) multi-played by logistic amplifier system included in oral cavity. Twelve patients with chronic hepatitis, HBV infected, aged 7-59, were randomly chosen for treatment. Previously they underwent immunosuppression without success. All of them revealed clinical and biochemical symptoms of steel active disease with morphological progression including active cirrhosis (3 cases). HuIFN alpha therapy was started just after withdrawal of immunosuppression (steroids, steroids and azathioprine). Effects of 50-100 U/d dose of HUIFN alpha were monitored by examination of hematological, biochemical parametres and indicators of humoral and cellular immune response and HBV markers in control liver biopsy specimens too. The HBVDNA serum level was measured besides, using the method of molecular hybridisation. Observation period is from 5 to 17 month, now. Among all patients during 1-2 months from the treatment beginning, transient increase of biochemical parametres of liver function (f. ex: 2-3 times ALAT increase) were observed without any clinical signs of disease exacerbation. All patients revealed immune system activation that lasted longer than incipiens intensive stimulation. Four from twelve patients that finished therapy, eliminated HBVDNA from blood serum. One of them eliminated HBsAg too. Three further confirmed decrease of HBsAg with e system seroconversion. Three from 8 patients treated 6-9 months reveal decrease of HBVDNA concentration in blood serum.

Administration, Oral↗
PubMed1992

Inherited congenital adrenal hyperplasia in the rabbit: absent cholesterol side-chain cleavage cytochrome P450 gene expression.

We investigated adrenal steroidogenic enzymes, their activity and mRNA expression, and in vitro biosynthesis of an enzyme in rabbits with congenital adrenal hyperplasia (CAH; weight: CAH, 19 +/- 5 mg/adrenal; normal, 2.7 +/- 1.0 mg/adrenal). Serum pregnenolone (delta 5-P) levels in CAH newborn rabbits (12-36 h) were normal (mean/range, 438/51-2191 ng/dl), but corticosterone levels were low [0.05 +/- 0.05 microgram/dl; P less than 0.001 vs. normal (0.66 +/- 0.57)]. Serum Na+ levels in CAH newborn rabbits were in the normal range (143 +/- 30 meq/liter), but K+ levels were elevated [7 +/- 1.1 meq/liter; P less than 0.05 vs. normal (5.9 +/- 0.6 meq/liter)]. Minced normal adrenal tissue incubated with [3H] cholesterol (30-100 pmol/flask) and ACTH (100 mU/flask) produced [3H]delta 5-P (newborn, 21 and 45 fmol/100 mg; adult, 3 and 5 fmol/100 mg) and [3H]corticosterone (newborn, 23 fmol/100 mg; adult, 11.3 fmol/100 mg), but CAH adrenals produced no product (less than 1.3 fmol/100 mg). Adrenal mitochondria from normal newborn rabbits produced delta 5-P (4.4-7 nmol/mg protein), but CAH adrenals did not, while CAH adrenal mitochondria demonstrated over 4 times greater 11 beta-hydroxylase activity. A Western blot of adrenal homogenate from normal newborn rabbits revealed a cholesterol side-chain cleavage cytochrome P450 (P450scc)-immunoreactive species (mol wt, 53 x 10(3), but this species was absent in CAH adrenals; CAH adrenals had a normal adrenodoxin and intensified 17 alpha-hydroxylase cytochrome P450 (P450(17)alpha) band compared to normal adrenals. In vitro translation of RNA in a cell-free rabbit reticulocyte lysate system containing [35S] methionine yielded a precursor P450scc protein (mol wt, 58.5 x 10(3)) with normal adrenal RNA, but not with CAH adrenal RNA. P450scc mRNA was detected in all normal adrenals, but was not detected in all CAH adrenals. 21-Hydroxylase cytochrome P450 mRNA expression was detected at a similar level in both normal and CAH adrenals. We conclude that CAH in the rabbit is caused by inherited absent P450scc gene expression. The clinical, pathological, and biochemical manifestations of P450scc deficiency in the rabbit are nearly identical to the human disorder. Increased 11 beta-hydroxylase activity and increased P450(17)alpha on Western blot of CAH adrenals indicate altered gene expression of other steroidogenic enzymes due to CAH. Further molecular analysis of the P450scc gene in this animal CAH model will facilitate understanding of P450scc deficiency CAH.

Adrenal Glands↗
PubMed1992

Histologic study of chronic active hepatitis C; comparison with chronic active hepatitis B.

Reports on the histologic findings of chronic active hepatitis C (CAH-C) have been rare, and the characteristic histologic findings of CAH-C have been not yet determined. To compare the differences in the histologic findings between CAH-C and chronic active hepatitis B (CAH-B) group, we analyzed the histologic findings of 19 patients with CAH-C, who had positive tests for HCV-antibody by EIA, and 19 patients with CAH-B who had negative tests for HCV-antibody but positive tests for HBsAg by RIA. Histologic features were analyzed between the CAH-C and CAH-B groups using a scoring system which is modified from Knodell's histologic activity index-looking at portal inflammation, periportal necroinflammation, portal fibrosis, focal necrosis, regeneration, polyploid nuclear change, sinusoidal lymphocytic reaction and fatty change. Portal inflammatory cell infiltrations with prominent lymphocytes and follicular arrangement were more frequent in the CAH-C group (10 of 19 cases) than in the CAH-B group (5 of 19 cases). Severe sinusoidal lymphocytic reactions were also more prominent in the CAH-C group (11 of 19 cases) than in the CAH-B group (6 of 19 cases). However, periportal necroinflammation, portal fibrosis, focal hepatic necrosis, regeneration and polyploid nuclear changes were more prominent in the CAH-B group than in the CAH-C group. In conclusion, follicular portal inflammation and severe sinusoidal lymphocytic reactions were common histologic findings in serologically proven CAH-C when compared to CAH-B.

Adult↗
PubMed1991

Is the inappropriate gonadotropin secretion of patients with polycystic ovary syndrome similar to that of patients with adult-onset congenital adrenal hyperplasia?

OBJECTIVE: To assess gonadotropin alterations in adult-onset congenital adrenal hyperplasia (CAH) and to compare these findings with those of patients with polycystic ovary syndrome (PCOS) in an effort to better understand the pathophysiology of these abnormalities. DESIGN: Prospective study of 9 newly diagnosed patients with CAH, 10 with PCOS, and 10 ovulatory controls. INTERVENTIONS: Baseline measurements of serum androgens, progestins, estradiol (E2), estrone (E1), unbound E2, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Serum LH and FSH were measured after intravenous gonadotropin-releasing hormone (GnRH) and in 15-minute blood samples for 6 hours to determine LH pulsatility. RESULTS: Serum androgens were elevated but comparable in the two patient groups. Serum LH was also elevated (P less than 0.05) but was higher in PCOS than CAH. Serum LH:FSH ratios were similar as were the responses to GnRH. Serum E1 was elevated only in PCOS, but unbound E2 was elevated to the same degree in both PCOS and CAH (P less than 0.05). Patients with PCOS had a decreased LH interpulse interval compared with controls and CAH (P less than 0.05), but LH pulse amplitude was increased in both PCOS and CAH (P less than 0.05). Serum E2 and unbound E2 correlated significantly with LH (P less than 0.05), LH responses to GnRH as well as to LH pulse amplitude in CAH (P less than 0.05). The LH interpulse interval did not correlate with estrogen in any group. None of the LH parameters correlated with serum progestin levels in CAH. CONCLUSIONS: The gonadotropin abnormalities of CAH appear to be intermediate between those of controls and PCOS. Although elevated estrogen may explain these abnormalities in CAH, additional factors may be operative in PCOS.

Adolescent↗
PubMed1976

Effects of cadmium on carbonic anhydrase activity and hemoglobin content of rat testes.

The cadmilm-induced (Cd) damage of mammalian testes is thought to be correlated with an inhibition of carbonic anhydrase (CAH) by Cd. Since Cd causes dose-dependent changes in blood flow of the testes, an inhibition of CAH in the testes could be simulated by a decrease of CAH-rich erythrocytes. Therefore, CAH activities and hemoglobin (Hb) content were determined in blood and testes of untreated and Cd-treated Sprague-Dawley rats as well as in testes perfused via the testicular artery. Cd was intraperitoneally applied as CdCl2 in single doses of 1.5, 3.0, and 5.0 mg Cd2+/kg b.w., respectively. 1. The experiments on perfused testes clearly demonstrated that the CAH activities originate from erythrocytes rather than from a tissue located enzyme. 2. The alterations in blood circulation occurring shortly (0.25-1.0 h) after the Cd administration were characterized by a dose-dependent, transient decrease (1.5 mg Cd2+/kg) as well as an increase (3.0 and 5.0 mg Ck2+, respectively) of the Hb content in the testes. 3. Independent of these minor alterations in a later state (14-24 h after 1.5 mg Ck2+/kg, 7-14 h after 3.0 mg Cd2+/kg, and 1-3 after 5.0 mg Cd2+/kg), Cd induced the well known hemorrhagic alterations of the testes with a high increase of Hb content and CAH activity. 4. By means of the correlations between CAH activities and Hb content in blood and testes an inhibition of the CAH by Cd as the primary cause for the tissue damage of the testes could largely be excluded.

Animals↗