PubMed Health⌕ Search

Biomedical subjects

R Gemma

Publications and source records attributed to R Gemma.

9 recordsLinked to original sources
PubMed2001

Histological changes of thyroid tissues in patients with liver cirrhosis.

Alterations in thyroid hormone regulation and metabolism, such as low serum T3 and T4 with normal TSH, are frequently noted in liver cirrhosis, but few morphological studies have ever been done on thyroid tissue in liver cirrhosis. In this study we analyzed the histological changes of thyroid tissue in the patients with liver cirrhosis. Specimens of thyroid gland obtained from autopsies in 16 cirrhotic patients were examined, and compared with those of two control groups. Control group I consisted of 7 patients with diabetes mellitus and control group II, 12 patients who died from sudden onset of cardiovascular problems. We measured follicular diameter and epithelial width on light micrographs of the central portion of thyroid specimens. We graded the degree of colloid vacuole, lipofuscin deposition in follicular epithelia, regenerative reaction and perivascular fibrosis in 10 consecutive light microscopic fields of the specimen. In the cirrhotic group, mean follicular diameter and epithelial width were significantly shorter and thinner, respectively, than those in the two control groups. Perivascular fibrosis was more prominent in the cirrhosis group than in the controls. These findings suggest that thyroid glands in patients with liver cirrhosis have the characteristic features of hypoactivity.

Cardiovascular Diseases↗
PubMed1999

[Immunoregulatory genes in autoimmune thyroid disease].

Autoimmune thyroid diseases (AITD) has a strong genetic basis. Although several candidate genes have been studied, the AITD causing genes are still unknown. Major candidate immune regulatory genes include human leukocyte antigen (HLA) gene, Ig heavy chain genes, T cell receptor genes, IL-1 receptor antagonist gene, IL-1 alpha gene and cytotoxic T lymphocyte antigen-4 (CTLA-4) gene. The relation between HLA and AITD has extensively been studied. In addition, polymorphism of the 3'-untranslated region and codon 17 of the CTLA-4 gene has been reported to associate positively with AITD. However, no linkage analyses have showed positive relation between AITD and these candidate genes except for HLA.

Abatacept↗
PubMed1996

The change in 123I-uptake between 3- and 24-hours is useful in predicting early response to methimazole in patients with Graves' disease.

Some patients with Graves' disease respond well to anti-thyroid drug treatment but others do not. Factors determining the patient's responsiveness to the medical treatment are unclear, but the intrathyroidal iodine pool is believed one of the important factors. In this study, we found that delta radioactive iodine uptake (RAIU) (RAIU at 24 h-RAIU at 3 h) is useful in predicting early response to treatment with methimazole (MMI). Among 32 patients with Graves' disease, who were given 30 mg MMI as an initial dose, 11 patients responded quickly to MMI-treatment. Within one month, serum free T4 levels decreased to below the normal range in 6 patients (< 10.3 pmol/L) or decreased from beyond the highest level of the assay (> 125 pmol/L) to the normal range in 5 patients. When these rapid responders (group A) were compared with the remaining 21 patients who showed a more gradual response to MMI-treatment (group B), a different pattern of 123I-thyroid uptake was noted. RAIU at 3 h was significantly higher in group A than in group B, while RAIU at 24 h was similar in the two groups. As a result, rapid responders had a significantly lower delta RAIU value than gradual responders (-0.7 +/- 8.4% in group A, 14.2 +/- 8.2 in group B, P < 0.01). No significant difference was found between the two groups in various pre-treatment parameters such as severity and duration of thyrotoxicosis, the titer of TSH receptor antibodies (TRAb), frequency of positive antithyroglobulin antibodies (TGHA), urinary excretion of iodine and thyroid volume. The incidence of positive antithyroid microsomal antibodies (MCHA) was higher in group A than in group B, and thyroid ultrasonography showed a tendency to low echogenicity in group A. delta RAIU was negatively correlated with the reduction in the serum free T4 level during the first two weeks after MMI-treatment was initiated (r = -0.60, P < 0.01). Moreover, delta RAIU correlated positively with the biological half-life of the intrathyroidal iodine, calculated in a different series of 24 patients with Graves' disease who received radioisotope treatment (r = 0.54, P < 0.01). The low delta RAIU value is considered to reflect the rapid turnover of the intrathyroidal iodine, and may be related to the small intrathyroidal iodine pool. delta RAIU is useful in predicting early responsiveness of patients with Graves' disease to MMI-treatment.

Adult↗
PubMed1994

[The mechanism of thyroid hormone abnormalities in patients with diabetes mellitus].

In order to clarify the mechanism of impaired thyroid hormone levels in patients with diabetes mellitus, thyroid hormone, thyroid hormone binding inhibitor (THBI), inhibitor of extrathyroidal conversion of T4 to T3 (IEC) and free fatty acid (FFA) were examined. In addition, TRH test was performed on 9 diabetic patients showing poor control of plasma glucose before and after glycemic control. Before glycemic control, fasting plasma glucose and HbA1c were significantly higher than after glycemic control (P < 0.05). T3 and the T3/T4 ratio significantly increased and rT3 significantly decreased after glycemic control (P < 0.05). THBI index and plasma FFA level significantly decreased and %T3 production (IEC) significantly increased after glycemic control (P < 0.05). The response of TSH to TRH significantly increased after glycemic control. In conclusion, (1) the presence of THBI, (2) the presence of IEC, and (3) dysfunction of the hypothalamo-hypophysial-thyroid axis are considered to be involved in abnormal thyroid function in diabetic patients.

Blood Glucose↗
PubMed1994

[Regulation of thyroid hormone binding protein/protein disulfide isomerase (T3BP/PDI) gene expression].

PDI catalyzes the formation of disulfide bonds and plays a central role in the correct folding of nascent polypeptides. In addition, it is multifunctional and may participate in more complex enzyme systems, catalyzing other protein modification. PDI is also known to bind T3. The human T3BP/PDI gene, located in the chromosome 17, consists of a transcribed part of 16.5 kb and the protein coding sequence is divided into 11 exons. The analysis of the 5'-flanking region revealed several putative transcriptional elements, including a TATA box, 6 CCAAT elements and 5 GC-rich regions, each of which is related to the promoter activity. The mechanism of T3BP/PDI gene expression is, however, unknown. Treatment with T4, PTU, insulin and fasting-refeeding induced different responses in T3BP/PDI mRNA and protein levels among various tissues. Recent studies revealed that the unfolded proteins, accumulated in the ER lumen, might stimulate the gene expression of a set of protein including BiP, GRp94 and PDI, which is required for proper protein folding and assembling. The meaning of T3-binding activity of PDI is open for further study.

Animals↗
PubMed1992

Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses.

In order to clarify the role of free fatty acid (FFA) in thyroid hormone abnormalities in patients with nonthyroidal illness, thyroid function, FFA, inhibitor of extrathyroidal conversion of T4 to T3 (IEC) and thyroid hormone binding inhibitor (THBI) were studied in 99 patients with various nonthyroidal illnesses including diabetes mellitus (DM) (n = 35), liver cirrhosis (LC) (n = 33), chronic obstructive pulmonary disease (COPD) (n = 17) and chronic heart failure (CHF) (n = 14). Patients were divided into three groups based on the level of serum T3: Group I (T3 < 50 ng/dl), Group II (50 < or = T3 < 80) and Group III (80 < or = T3). Serum T4, FT3 and the T3/T4 ratio decreased significantly in the order Group III, Group II and Group I (Group III > II > I). The plasma FFA level was 0.91 +/- 0.12 mmol/l in Group I (P < 0.05, vs. Group III), 0.65 +/- 0.06 in Group II and 0.54 +/- 0.04 in Group III, respectively. The incidence of positive IEC was 80.0% in Group I (P < 0.05, vs. Group III), 53.7% in Group II (P < 0.05, vs. Group III) and 34.2% in Group III. However, IEC was not correlated with the serum T3 concentration. The incidence of positive THBI was 80% in Group I (P < 0.05, vs. Group III), 68.3% in Group II and 47.4% in Group III, but THBI was not correlated with the serum T4 level. Positive correlations were observed among FFA, IEC and THBI (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Lactate dehydrogenase (LDH)-linked immunoglobulin in a patient with Graves' disease treated with methimazole.

A 26-year-old woman who received methimazole treatment for Graves' disease is discussed. Two months following treatment, her serum GOT level rose to 45 K.U, her GPT to 60 K.U, and her lactate dehydrogenase (LDH) to 645 W.U; a hepatic disorder was then suspected. Later, the serum GOT and GPT concentrations decreased to a normal range, but her serum LDH continued to maintain a high level. An LDH isoenzyme analysis showed an abnormally broad LDH. The IgG that was linked to the LDH is suspected to have been the result of her underlying autoimmunity, the methimazole treatment, and the development of her hepatic disorder. Thus, this IgG was thought to be the autoantibody to LDH.

Adult↗
PubMed1988

[An inhibitor of extrathyroidal conversion of thyroxine to 3,5,3'-triiodothyronine (IEC) in plasma of patients with various nonthyroidal illnesses].

To evaluate the role of a circulating inhibitor of extrathyroidal conversion of T4 to T3 (IEC) in the causation of low T3 states in patients with various nonthyroidal illnesses (NTI), we measured the in vitro T3 production in the presence of ether extract of plasma. Blood samples were obtained from 22 normal subjects and 140 patients with various NTI; liver cirrhosis (LC) 37, diabetes mellitus (DM) 48, respiratory failure (RF) 15, chronic renal failure (CRF) 10 and others 30. The assay procedure of in vitro T3 production was as follows. Rat liver homogenate was incubated with 2.5 microM T4 in the presence of evaporated ether extract of plasma and the amount of T3 produced was quantified by RIA. In each assay, control plasma extracts taken from the two normal subjects were used. The results were expressed as a percentage of the control value (%T3 production), and estimated as positive IEC when %T3 production was under 72.7%, that was 2SD below the mean value of normal controls. Patients were divided into three groups; Group I (T3 greater than or equal to 80 ng/dl), Group II (80 greater than T3 greater than or equal to 50) and Group III (50 greater than T3). The %T3 productions were 88.5 +/- 22.0 in Group I, 84.9 +/- 31.5 in Group II and 78.9 +/- 34.0 in Group III respectively. The %T3 productions of each group were significantly lower than that of normal control, 101.9 +/- 14.6. IEC was positive 23.4% in Group I, 41.9% in Group II and 43.8% in Group III. There were eight nonsurvivors, and they all belonged to Group III, in which both serum T3 and T4 were subnormal. In nonsurvivors, serum concentrations of T3 (20 +/- 11 ng/dl) and TSH (1.2 +/- 1.1 microU/ml) were significantly lower than that of survivors in Group III (T3; 38 +/- 10 ng/dl p less than 0.005, TSH; 2.8 +/- 1.4 microU/ml p less than 0.05). The %T3 productions were 83.8 +/- 32.1 in survivors and 64.8 +/- 37.9 in nonsurvivors, and the incidences of positive IEC were 37.5% in survivors and 62.5% in nonsurvivors. From the standpoint of the underlying illnesses, serum concentrations of T3 (mean +/- SD ng/dl) were 49 +/- 21 in LC, 64 +/- 11 in DM, 40 +/- 22 in RF and 63 +/- 15 in CRF, and %T3 productions were 60.6 +/- 26.5 in LC, 82.5 +/- 25.8 in DM, 109.6 +/- 32.1 in RF and 97.6 +/- 24.3 in CRF.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗