Biomedical subjects

R T Liu

Publications and source records attributed to R T Liu.

At least 19 recordsLinked to original sources

PubMed2006

Two-stage Turing model for generating pigment patterns on the leopard and the jaguar.

Based on the results of phylogenetic analysis, which showed that flecks are the primitive pattern of the felid family and all other patterns including rosettes and blotches develop from it, we construct a Turing reaction-diffusion model which generates spot patterns initially. Starting from this spotted pattern, we successfully generate patterns of adult leopards and jaguars by tuning parameters of the model in the subsequent phase of patterning.

Animals↗

PubMed2001

Turing model for the patterns of lady beetles.

We simulate the patterns on the hard wings of lady beetles using a reaction-diffusion equation based on the Turing model. A part of a spherical surface is used to approximate the geometry of the hard wings. Various patterns common to lady beetles in Taiwan can be produced on this curved surface by adjusting the parameters of the model.

Animals↗

PubMed2000

The prediction of late rectal complications following the treatment of uterine cervical cancer by high-dose-rate brachytherapy.

PURPOSE: This study aimed to correlate patient, treatment, and dosimetric factors with the risk of late rectal sequelae in patients with uterine cervical cancer treated with external beam radiation therapy (EBRT) and high dose rate intracavitary brachytherapy (HDRICB). METHODS AND MATERIALS: From September 1992 to December 1995, a total of 128 patients with uterine cervical cancer, who were treated and survived more than 12 months, were evaluated. After EBRT with 40-44 Gy/20-22 Fr/4-5 weeks to the whole pelvis, the dose was boosted up to 54-58 Gy with central shielding for patients with bilateral parametria of Stage IIb or greater. HDRICB consisted of three to four insertions at doses of 5-7.2 Gy (to Point A) at intervals of 1 week. Patient and treatment factors were analyzed using logistic regression analysis and the cumulative rectal biologic equivalent dose (CRBED) was calculated. RESULTS: After 30-75 months of follow-up (median, 43 months), 38 patients (29.7%) had late rectal sequelae. Patients who had Stage IIb-IVa disease, cumulative rectal dose (external RT + total ICRU rectal dose) greeater than 65 Gy, or age greater than 70 years had a high risk of developing late rectal sequelae. When 110 Gy was used as the cut-off value, 19.6% (10 of 51) of patients whose CRBED was less than 110 Gy had rectal complications, while 36.4% (28/77) of patients whose CRBED was greater than 110 Gy developed rectal complications. CONCLUSION: Risk factors of late rectal complications were advanced stage, age greater than 70 years, and cumulative rectal dose of greater than 65 Gy.

Adult↗

PubMed1999

DNA binding affinity of hTRbeta1 mutants as heterodimers with traps from different tissues.

Patients with generalized resistance to thyroid hormone (GRTH) show various organ-specific features, for example mental retardation, growth abnormalities, liver damage, delayed bone age or cardiac disorders. Could this reflect aberrant mutant thyroid hormone receptor beta1 (TRbeta1) heterodimerization with specific TR auxiliary proteins (TRAPs) from different tissues, altering the mutant's ability to transactivate tissue-specific genes? To answer this question, we examined the heterodimerization of TRbeta1 mutants and TRAPs of several rat tissues (cerebrum, cerebellum, liver, heart, lung, spleen, and kidney), and in vitro translated RXRalpha, beta and gamma by electrophoretic gel mobility shift assay (EMSA). Mutant TRbeta1 proteins, synthesized in reticulocyte lysate, were incubated with 32P rat malic enzyme (rME) thyroid hormone response elements (TRE) and nuclear extracts of rat tissues. The TRbeta1 mutants used were Mf (G345R), and GH (R316H). Both have non-detectable T3 binding affinity. GH has weak dominant negative effect and Mf has strong dominant negative effect. Two major bands were observed in EMSA. Cerebrum, cerebellum, lung and liver extracts formed a slower migrating band than a TR homodimer, while kidney extracts formed a faster migrating band, and heart and spleen extracts had both bands. There were no qualitative differences in heterodimerization between TRbeta1wt, and TRbeta1 mutants, when using tissue extracts and DNA in excess ratio to TR. We found that RXRalpha, beta, and gamma were differentially expressed in each rat tissue and formed heterodimer complexes with wild type (WT) TRbeta1. Scatchard analysis of affinity and capacity of the binding of TR-TRAP heterodimers to response elements was performed by competing with 2.5-, 5-, 10-, 25-, and 250-fold excess non-radiolabeled rME-TRE. When using kidney extract, the DNA binding affinity of heterodimers was significantly decreased both in wild type and mutant TRs, suggesting that the DNA binding affinity of the faster migrating band was lower than that of the slower migrating band. Mutant GH, which causes 'pituitary RTH' and shows weak dominant negative effect, tended to form heterodimers with lower DNA binding affinity than TRbeta1wt with all extracts. Mutant Mf, which has strong dominant negative effect, tended to show higher DNA binding affinity than TRbeta1WT. When the data were pooled for all tissues, GH and Mf were found to form heterodimers with significantly lower, or higher, affinity for TREs than TRbeta1wt. These results indicate that: 1) differences of DNA binding affinity of mutant TR-TRAP heterodimers to response elements in DNA play a part in its reduced or strong dominant negative effect; and 2) differences in formation of heterodimers with TRAPs present in tissues do not appear to explain the apparent tissue-specific and mutant-specific variations seen in RTH.

Animals↗

PubMed1999

Levothyroxine suppression of thyroglobulin in patients with differentiated thyroid carcinoma.

For patients with differentiated thyroid carcinoma, the appropriate degree of TSH suppression by levothyroxine (L-T4) is still unknown. To find the target level of TSH suppression, we analyzed the relationship between the degree of TSH suppression determined by third generation assay and thyroglobulin (Tg) response during the titration of the dosage of L-T4. Ninety-two patients with differentiated thyroid carcinoma (19 males and 73 females; age, 40.5+/-13.5, mean +/- SD) were included. All of the recruited patients had near-total thyroidectomy, 30-150 mCi 131I thyroid ablation, and negative Tg autoantibodies. They were classified into 3 groups. Group A was composed of 25 patients with local or distant relapse. Group B was composed of 12 patients without clinically detectable relapse, but Tg levels either above 2 ng/mL under L-T4 suppression or above 3 ng/mL off L-T4 therapy. Group C included 55 patients who had no active disease and Tg levels below 2 and 3 ng/mL during and off L-T4 suppression, respectively. Serum TSH and Tg were measured simultaneously at the end of 8-12 weeks of a certain dose of L-T4 therapy during dosage titration and also after withdrawal of L-T4 for 4-6 weeks for the total body scan. Wilcoxon signed ranks test was used to compare paired samples of Tg, and Spearman rank correlation was used to determine the correlation of relative changes in TSH to changes in Tg calculated by individual. The results showed that 1) Tg levels were significantly higher during the period off L-T4 therapy than on L-T4, therapy in all 3 groups (P < 0.01); 2) during L-T4, therapy, within the same treatment course, mean Tg levels were higher when TSH levels were normal than when TSH levels were suppressed, statistically significant in group A (P = 0.001), nonsignificant in group B (P = 0.09), and nonsignificant in group C (P = 0.30); and 3) when TSH was suppressed below normal, there was no correlation between the relative changes in TSH and Tg by individual in all 3 groups (P > 0.05). The data suggest a stratified postoperative thyroid hormone management of patients with differentiated thyroid carcinoma. TSH should be lowered to below normal in patients with active disease. If patients are clinically disease free with Tg levels below 2 ng/mL, TSH can be kept within the normal range. For the most controversial group B patients, it is recommended that the TSH be suppressed and be closely followed up.

Adult↗

PubMed1998

Outcome of Graves' disease after antithyroid drug treatment in Taiwan.

The outcome of Graves' disease after treatment with antithyroid drugs (ATDs) varies widely among countries, and large-scale studies in Asia are rare. We investigated the associations of various clinical and laboratory features with the outcome of ATD therapy for Graves' disease in Taiwan. A total of 210 patients (177 women, 33 men; mean +/- SD age, 41.7 +/- 15.1 yr) treated with ATD in Taiwan were included. ATD therapy started with methimazole 30 mg daily or propylthiouracil 300 mg daily and was continued until a euthyroid state was achieved. Afterwards, 154 patients received a maintenance dose of ATD alone, while 56 patients received a combination of an ATD and thyroxine (L-T4). Patients were considered to be in remission if they remained in a euthyroid state for more than 2 years after drug withdrawal. The mean follow-up periods were 45.0 +/- 20.9 months for patients with remission and 30.4 +/- 19.8 months for those with relapse. Relapse occurred in 126 (60%) patients during the follow-up period, within 3 months after drug withdrawal in 47 (37%), and within 6 months in 60 (46%). The relapse rate was 100% among patients with two or more previous relapses. Patients with a second occurrence had a higher relapse rate than those with a first occurrence (84% vs 43%). Past history of recurrence, goiter size, thyroid-stimulating hormone level and thyrotropin-binding inhibition immunoglobulin activity at the end of ATD treatment were independently associated with relapse. Prolonged duration of treatment did not yield better results in patients with larger goiters or a history of recurrence, or both. Combination therapy with L-T4 yielded similar results to those achieved with ATD treatment alone. In conclusion, the relapse rate of Graves' disease after ATD treatment in Taiwanese patients was high, especially in those with a history of recurrence. The treatment duration and drug regimen did not affect the outcome.

Adolescent↗

PubMed1996

An artificial thyroid hormone receptor mutant without DNA binding can have dominant negative effect.

The syndrome of resistance to thyroid hormone (RTH) encompasses a heterogeneous group of conditions which are caused by mutations of thyroid hormone receptor beta 1 (TR beta 1). Mutations usually cluster in two regions of the ligand-binding domain. The mutant receptors can inhibit normal receptor activity in a dominant negative manner, consistent with the dominant mode of inheritance of RTH. Recent evidence suggested that this dominant negative effect (DNE) of the RTH mutants involves competition for DNA binding and emphasized the essential role of intact DNA binding activity for mutants in order to exert DNE. However, we found that a Cys73Ser substitution in the DNA-binding domain (DBD) of wild-type produces a TR which can inhibit the transcriptional activation by TR alpha 1, either in the presence or absence of T3, on three different TRE-containing reporter genes, in transient co-transfection studies. Co-expression of TRv alpha 2, a TR alpha splicing variant, can enhance this DNE. However, DNE was not observed on the negatively-regulated TSH alpha Luc reporter gene when wild-type and DBD mutant were co-transfected at equimolar ratios. The DNE of DBD mutant is not reversed by co-transfection with excess retinoid X receptor alpha. DBD mutant alone can also inhibit the transactivation from a TK-luciferase reporter gene either linked with rat malic enzyme thyroid response element, or not. These observations parallel those we previously observed using TRv alpha 2. Our results indicate that a DBD mutant can have DNE, possibly through a mechanism similar to that of TRv alpha 2, which may involve interference with basal transcription factors. The clinical significance of these DBD mutants is currently unclear, but it is logical to expect such mutants do occur in nature.

Animals↗

PubMed1996

Ectopic parathyroid adenoma with severe hungry bone syndrome: a case report.

The presentation rate of ectopic mediastinal parathyroid adenoma is about 5 approximately 22%. Ectopic parathyroid adenoma is a common etiology of failed parathyroid surgery as well as a diagnostic challenge to clinicians. We reported a case of ectopic mediastinal parathyroid adenoma. A 20-year-old girl presented with arthralgia for 2 years before hyperparathyroidism was diagnosed. Parathyroid ultrasonography failed to find the lesion, but a vivid uptake in the superior mediastinum was discovered by thallium-201 (Tl-201) and technetium-99m-sestamibi (Tc-99m-MIBI) images. Removal of the ectopic adenoma resulted in severe Hungry bone syndrome, which required a large amount of calcium and phosphorous supply. Later, the patient suffered from bilateral femoral neck fracture due to marked osteoporosis. Bone mineral density study revealed marked increase of fracture risk. Although bone disorder is rare in cases of hyperparathyroidism nowadays, it still should be considered in patients with arthritis of unknown etiology like our case. Early diagnosis and treatment can reduce the morbidity.

Adenoma↗

PubMed1995

Functional analysis of a proline to serine mutation in codon 453 of the thyroid hormone receptor beta 1 gene.

Mutations in the gene encoding human thyroid hormone receptor beta (hTR beta) have been associated with generalized resistance to thyroid hormone (GRTH). This disorder is associated with significant behavioral abnormalities. We examined the hTR beta gene in a family with members who manifest inappropriately normal TSH, elevated free T4, and free and total T3. Sequence analysis showed a cytosine to thymine transition at nucleotide 1642 in one allele of the index patient's genomic DNA. This altered proline to serine at codon 453. The resulting mutant receptor when expressed in vitro bound DNA with high affinity, but the T3 affinity of the receptor was impaired. The mutant TR demonstrated a dominant negative effect when cotransfected with two isoforms of wild-type receptor and also in the presence of TR variant alpha 2 in COS-1 cells. Mutations of codon 453 occur more frequently than at other sites, and four different amino acid substitutions have been reported. Significant differences in phenotype occur among affected individuals, varying from normality to moderately severe GRTH. There is no clear correlation between Ka or in vitro function of the mutant receptor, and phenotype. This study extends the association between GRTH and illness, and indicates that early diagnosis and counseling are needed in families with TR beta 1 abnormalities.

Adult↗

PubMed1995

Triiodothyroacetic acid has unique potential for therapy of resistance to thyroid hormone.

3,5,3,'-Triiodothyroacetic acid (Triac) has been used in therapy of resistance to thyroid hormone on an empirical basis and appears beneficial in some studies. We observed that the T3 analogs, Triac and 3,5,3'-triiodothyropropionic acid (Triprop), have a higher affinity for the thyroid hormone receptor-beta 1 (TR beta 1) than does T3 (2.7- and 1.8-fold, respectively), whereas the affinities of the three compounds for TR alpha 1 are the same. To evaluate whether T3 analogs would have a differential effect on TR beta 1 and TR beta 1 mutants and thus be a specific treatment for patients with resistance to thyroid hormone, we examined the induction of the transcriptional activation of wild-type (wt) TR alpha 1, TR beta 1, and mutant TR beta 1s by T3, Triac, and Triprop. The dose response of transcriptional activation by T3 analogs was measured by transient cotransfections with TRs and a rat malic enzyme-TRE fused to thymidine kinase (TK)-chloramphenicol acetyltransferase (CAT) in COS-1 cells. For TR alpha 1 wt, induction of CAT activity by T3 and Triac occurred at the same concentration. For TR beta 1 wt, Triac and Triprop showed a higher maximal activity than T3 (Tripro > Triac > T3) and reached 50% induction at a lower concentration than T3 (Tripro < Triac < T3). Induction of CAT activity in five mutant TR beta 1s (kindreds Mh, Mc, CL, Mf, and GH) was also analyzed. Even high levels of T3 analogs could not restore CAT activity to that of TR beta 1wt for any mutant. A dominant negative effect was produced by Mh, Mc, and Mf. Mutants CL and GH had a mild dominant negative effect depending on T3 analog concentrations and TREs. Cotransfection studies were performed using a rat malic enzyme-TK-CAT reporter plasmid to analyze the effects of hormones at near-physiological concentrations of T3 and Triac. Triac had a significantly higher transcriptional activation than T3 in Mc, CL, and GH, suggesting that Triac would have a beneficial effect to different degrees for different mutant TR beta 1s. Using mutants Mc and GH, further studies were carried out using rat GH and double palindromic and inverted palindromic TREs in COS-1 cells. On each TRE, 10 nmol/L Triac induced higher transcriptional activation in TR beta 1wt, mutant TR beta 1s, and TR beta 1wt plus mutant TR beta 1s (1:1 ratio) than the same dose of T3.(ABSTRACT TRUNCATED AT 400 WORDS)

Base Sequence↗

PubMed1995

The dominant negative effect of thyroid hormone receptor splicing variant alpha 2 does not require binding to a thyroid response element.

The functionally inactive thyroid hormone receptor splicing variant-alpha 2 (TRv alpha 2) can inhibit transcriptional activation by TR alpha 1 or beta 1, demonstrating a dominant negative effect (DNE). We examine here the three commonly proposed mechanisms, namely, competition for binding to thyroid hormone response elements (TREs), formation of inactive heterodimers, and squelching. A mutation introduced into the DNA-binding domain (DBD) of the TRv alpha 2 was designed to prevent its binding to TREs. In transient cotransfection studies, the DBD mutant has nearly the same DNE as does TRv alpha 2 on three different TRE-containing reporter genes. The DNE of TRv alpha 2 is also not reversed by cotransfection with excess retinoid X receptor-alpha. Extracts of COS cells cotransfected with TR alpha 1 and either TRv alpha 2 or DBD mutant at different ratios were analyzed by gel shift assays. Neither TRv alpha 2 or the mutant altered binding of TR alpha 1 to four radiolabeled TREs. TRv alpha 2 itself can inhibit constitutive transactivation by a thymidine kinase promoter-driven reporter construct. Our results suggest that TRv alpha 2 can function in a dominant negative manner without binding to a TRE, at least for certain TREs. It is concluded that the DNE of TRv alpha 2 may occur through another unrecognized mechanism, perhaps by binding to basal transcription factors.

Animals↗

PubMed1995

Importance of the most proximal GC box for activity of the promoter of human thyroid hormone receptor beta 1.

We wish to localize the sequences required for transcriptional expression of the thyroid hormone receptor beta 1 (TR beta 1). Constitutive activity of the promoter of human thyroid hormone receptor beta 1 was assessed by transient transfection of deletion constructs attached to luciferase as reporter, into P19, GH3, HepG2, H19-7, and COS1 cells. A 40-base pair fragment of the beta 1 promoter including the TATA box induced minimal luciferase activity, which was considered basal activity. The activities of various lengths of the beta 1 promoter were estimated relative to the minimal promoter in five cell lines. The region between -130 and -40 was crucial for constitutive activity in all cell lines. Further deletion analysis in HepG2 cells showed that two regions mainly augmented the transcriptional activity of the minimal 40 base pair fragment. One region located at -115 to -93, which is highly GC-rich, included the most proximal of five putative GC boxes present in the whole 1325-base pair promoter. A second region contributing to expression of TR beta 1 in HepG2 cells is at -70 to -40. Mutation of the most proximal GC box strongly suppressed transactivity of the whole promoter in P19 and HepG2 cells. In contrast, mutations in the other GC boxes did not suppress transactivation in P19 cells and slightly suppress activation in HepG2 cells. In Schneider cells, which do not express Sp1, transactivity of the region distal to -40 is positively regulated by cotransfection with a vector expressing Sp1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Tc-99m pertechnetate trapping and thyroid function in Hashimoto's thyroiditis.

Tc-99m pertechnetate thyroid imaging was studied in 52 patients with Hashimoto's thyroiditis, with special reference to the thyroid functional state and Tc-99m trapping by the gland. The most common finding was diffusely increased trapping of radioactivity, a pattern similar to Graves' disease. On the other hand, the increased trapping in Hashimoto's thyroiditis was usually associated with hypothyroidism. The degree of Tc-99m trapping did not correlate with the degree of the endogenous TSH elevation. However, increased Tc-99m trapping could predict the reversibility of hypothyroidism in just 3 months.

Adult↗

PubMed1994

Serum thyroglobulin in the follow-up of patients with treated differentiated thyroid cancer.

To determine the significance of serum thyroglobulin (Tg) level in terms of presence or absence of thyroid cancer, we evaluated available serum Tg data on and off T4 therapy in 180 patients with differentiated thyroid cancer who have now been followed up to 18 yr. The presence of cancer was established by radioiodine scans, x-rays, and clinical examination. Thirty-two patients with detectable serum Tg autoantibodies were excluded from this analysis. Tg was measured by RIA with a sensitivity of 1 ng/mL. Patients who had all stages of cancer, but who had no evidence of active disease after treatment, were grouped according to operative and 131I ablative therapy. In patients with a partial thyroidectomy with or without ablation, the presence of Tg did not indicate the presence of cancer since levels were often above either a 5 ng/mL or a 10 ng/mL cutoff. The presence of residual normal thyroid tissue decreases the diagnostic value of serum Tg assay. In patients who underwent near total (NTT) or total thyroidectomy (TT) and 131I ablation, 3 of 55 (5.5%) patients had Tg greater than 5 ng/mL and 1 of 55 (1.8%) patients had Tg greater than 10 ng/mL during therapy, whereas off therapy 13 of 57 (22.8%) patients had Tg greater than 5 ng/mL and 6 of 57 (10.5%) patients had Tg levels greater than 10 ng/mL. In this group of patients, a Tg level less than 10 ng/mL during suppressive therapy indicated the absence of apparent tumor in 54 of 55 (98.2%) of patients. Whereas sensitivity of the assay was increased by withdrawal of hormone, "false positives" increased especially at lower (3-6 ng/mL) cut-off levels. No cut-off value properly categorized all patients. These data suggest, that even in patients who underwent 131I ablation and total thyroidectomy and were thought to be cured, small foci of thyroid tissue which are undetectable by standard 2 mCi 131I scans may exist and produce some Tg. However, these residual cells do not appear to cause an adverse prognosis in most patients. In patients with recurrent or continued disease, during T4 treatment, Tg levels ranged between 2-21,000 ng/mL and 5 of 11 patients had a Tg less than 5 ng/mL. Off treatment, Tg levels ranged between 6-10,700 ng/mL and 3 of 13 patients had a Tg less than 10 ng/mL. In 4 patients Tg levels were less than 10 ng/mL on treatment but greater than 10 ng/mL off therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1994

Ectopic ACTH syndrome with nocardiosis--a case report.

A 25-year-old man was admitted with chief complaints of multiple ecchymoses over face and both arms after a trivial trauma since one month before entry. Physically, he was thin without moon face, buffalo hump, or purple striae, while extensive fungus infection was present. Mild hyperglycemia, hypokalemic alkalosis were also found. Chest x-ray revealed multiple cavitary nodular lesions over bilateral lung fields. Needle biopsy from a rib lesion showed small cell carcinoma with strongly positive ACTH stain. The patient's basal cortisol level was greater than 62 micrograms/dl and failed to be suppressed by both low and high dose dexamethasone. The 24 hours urine free cortisol, 17 KS, and 17 OHCS were 8454 micrograms/24h, 49.8 mg/24h, and 50.8 mg/24h respectively. His plasma ACTH level was 725 pg/ml and remained high (1210 pg/ml) after high dose dexamethasone suppression. On the 10th day after admission, the patient's general condition got worse rapidly. Fever, dyspnea developed with progression of the lung lesions. Nocardia infection was proved. He expired three days later in spite of antibiotics and ketoconazole treatment.

ACTH Syndrome, Ectopic↗

PubMed1993

Limited joint mobility of the hand: prevalence and relation to chronic complications in non-insulin-dependent diabetes mellitus patients.

A total of 170 non-insulin-dependent diabetes mellitus (NIDDM) patients admitted to Kaohsiung Chang Gung Memorial Hospital during the period from January 1988 to December 1989 were examined for the presence of cheiroarthropathy. Fifty-four percent (92 patients) had limited joint mobility (LJM) of the hand, a prevalence significantly higher than that of non-diabetic controls (7%). Duration of diabetes was positively related to the severity of LJM (p = 0.03, chi-square contingency table). Chronic diabetic complications such as cataracts (p = 0.04) and overt proteinuria (p = 0.03) were also associated with the presence of LJM, and diabetic retinopathy (p = 0.007); vision-threatening retinopathy was strongly associated with the presence of LJM (p = 0.0002). The sex ratio, HbA1c and creatinine clearance rates did not show significant differences between patients with and without LJM. In conclusion, the occurrence of LJM of the hand in NIDDM patients observed at this hospital is common and is often accompanied by other chronic diabetic complications. Its presence should alert physicians to other associated diabetic complications with increased morbidity and mortality.

Adult↗

PubMed1992

Serum steroid hormonal profiles by reversed-phase liquid chromatography in patients with 17-hydroxylase deficiency and in an affected family.

We used an optimized isocratic reversed-phase high-performance liquid-chromatographic procedure to separate and measure 12 steroid hormones, and studied the steroid hormone profiles in sera from three patients with 17-hydroxylase deficiency (17-OHD). Two of the patients were sisters, one of whom (II-3), expressing normotension and primary amenorrhea, was diagnosed on the basis of chromatographic data and followed up for seven years. The untreated patients had obvious abnormalities on chromatograms of serum extracts, characterized by markedly increased corticosterone (B) and decreased or undetectable cortisol (F) and cortisone (E). The concentration of 11-deoxycorticosterone was much greater in the patient with classical symptoms than in the normotensive patient. In all three patients, concentrations of aldosterone were within the normal range, but concentrations of progesterone were much lower than in the patients with 21-hydroxylase deficiency. We evaluated the responses to corticotropin and dexamethasone. HPLC evaluation of the serum steroid profiles before and after corticotropin stimulation in the affected family showed that in the parents and one other sibling, concentrations of F before and after stimulation were within the normal ranges. The sums of the ratio of B to F before and the ratio of B to F after corticotropin stimulation (sigma B/F) in the parents and the other sibling were 0.292, 0.496, and 0.614, respectively, all much higher than the normal value (mean +/- SD: 0.164 +/- 0.038). Thus the sigma B/F value may be a hormonal marker of heterozygotes carrying this defect.

Adolescent↗

PubMed1991

Agranulocytosis associated with anti-thyroid drug in patients with Graves' thyrotoxicosis--report of 11 cases.

Retrospective analysis of 11 Chinese patients with Graves' thyrotoxicosis developing agranulocytosis during anti-thyroid treatment was done. Seven of them received methimazole and 4 received carbimazole. None of the 11 patients had taken propylthiouracil. The major chief complaints were high fever (100%), chillness (91%), and sore throat (73%). The duration of drug treatment prior to the detection of agranulocytosis ranged from 13 to 63 days (mean +/- 1SE: 33.1 +/- 16.1). At the time of agranulocytosis detected, the peripheral leukocyte counts were 0.5 to 2.1 X 1000/mm3 (mean +/- 1SE: 1.05 +/- 0.47 X 1000/mm3), absolute neutrophil counts 0 to 450/mm3 (mean +/- 1SE: 54.27 +/- 132.12/mm3), and hemoglobin 8.2 to 15.9 g/dl (mean +/- 1SE: 11.85 +/- 2.24 gm/dl). Three of the 11 patients had positive bacterial blood cultures. The recovery time of absolute neutrophil counts above 500/mm3 ranged from 3 to 25 days (mean +/- 1SE: 10.5 +/- 6.6) after discontinuation of antithyroid drugs. Mortality was found in 2 of them (18%).

Adolescent↗