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H Y Fung

Publications and source records attributed to H Y Fung.

7 recordsLinked to original sources
PubMed1992

Postpartum thyroid dysfunction.

Postpartum thyroid dysfunction (PPTD) refers to the syndromes of transient hyperthyroidism, transient hypothyroidism, or both, occurring sequentially in the first 12 months postpartum. Approximately 5 to 9% of women develop the disorder in this period. PPTD is most often subclinical but some women will experience symptoms such as lack of energy and depression in the hypothyroid phase. The thyroid gland, which normally enlarges during pregnancy, will remain enlarged or enlarge further in the postpartum period in a significant number of affected women, instead of returning to the prepregnancy size as in unaffected women. The gland is painless and histologically demonstrates lymphocytic infiltration. PPTD is strongly associated with the presence of antimicrosomal and/or antithyroglobulin antibodies, which occur in up to 76% of cases. Antibody activity tends to increase in the postpartum period and to peak at the time of onset of the disorder. TSH receptor antibodies are not seen and the gland has low radioiodine uptake, distinguishing PPTD from Graves' disease. The HLA associations are controversial, as is the role of dietary iodine. The etiology of PPTD is almost certainly immunological, reflecting the phenomenon of rebound from the relative immune tolerance of pregnancy. Detection of the disorder is important in order to reassure or treat those who are symptomatic and because PPTD may recur in subsequent pregnancies. In addition, up to one third of affected women will go on to develop permanent hypothyroidism 2 to 4 years later. The role of screening for PPTD remains to be clarified.

Autoantibodies↗
PubMed1990

IgG subclass distribution and relative functional affinity of thyroid microsomal antibodies in postpartum thyroiditis.

An association between the development of postpartum hypothyroidism and high levels of IgG1 subclass microsomal (M) antibodies has been reported. Using an assay designed to detect reasonable levels of all the four IgG subclasses, we found no differences in the proportion of each IgG subclass in M antibodies of patients with postpartum hyperthyroidism or hypothyroidism compared with control postpartum patients with M antibodies but no thyroid dysfunction. However the total amount of M antibody of each IgG subclass was elevated above the controls in the patients with thyroid dysfunction. The relative functional affinity of M antibodies did not differ between controls and patients with hypothyroidism but declined 5 and 10-12 months after delivery compared to values at 2 months. These results do not support the suggestion that the amount of IgG1 subclass M antibodies particularly determines the course of postpartum thyroiditis. Rather, the total M antibody level, in all four subclasses, is associated with clinical outcome. Resolution of the disease, despite persisting M antibodies, may occur in part because the relative functional affinity of these antibodies declines after delivery.

Antibody Affinity↗
PubMed1988

Postpartum thyroid dysfunction in Mid Glamorgan.

A high prevalence of postpartum thyroid dysfunction has been reported in several countries, but there have been no systematic studies of its prevalence in Britain. Among a group of 901 consecutive, unselected pregnant women thyroid autoantibodies were detected in 117 (13%) at booking. The clinical course of postpartum thyroid dysfunction, factors associated with its development, and its likely prevalence were defined in 100 of these women with thyroid antibodies and 120 women with no such antibodies who were matched for age. None of the women had a history of autoimmune thyroid disease. Normal reference ranges for thyroid function during pregnancy and post partum were established in the 120 women negative for thyroid antibodies. On the basis of these observations postpartum thyroid dysfunction was observed in 49 (22%) of the 220 women studied, and the prevalence in the total group of 901 women was estimated to be 16.7%. Thyroid dysfunction, mainly occurring in the first six months post partum, was usually transient and included both destruction induced hyperthyroidism and hypothyroidism. The development of the syndrome was significantly related to smoking more than 20 cigarettes a day and the presence of thyroid microsomal autoantibodies at booking. Of the 16 women with a family history of thyroid disease in whom thyroid microsomal autoantibody activity was detectable at booking, 11 developed thyroid dysfunction. Age, parity, presence of goitre at presentation, duration of breast feeding, and the sex and birth weight of the infant were not associated with the development of postpartum thyroid dysfunction. The mood changes experienced by women post partum may in part be associated with altered thyroid function during this time.

Adult↗
PubMed1979

A model of cardiac arrhythmias and sudden death: cantharidin-induced toxic cardiomyopathy.

Toxic cardiomyopathy may result in fatal arrhythmias. To develop a model to study ventricular fibrillation and asystole, we investigated the effect of cantharidin in the production of cardiac arrhythmias and myocardial damage. Conscious albino rabbits, weighing between 1.8 to 2.8 kg received an intravenous bolus injection of cantharidin ranging from 0.6 to 1.9 mg/kg or a control injection of solvent. The electrocardiogram was continuously monitored on tape before and after injection for extended periods of time. Dose-related effects were observed with the following: 1) presence, magnitude and duration of ST depression after injection; 2) occurrence of fatal arrhythmias; 3) survival time (high doses were usually fatal within 3 hr); and 4) electron microscopic evidence of mitochondrial swelling, intramitochondrial granules and myofibrillar degeneration. The most common arrhythmias associated with the high doses of cantharidin were frequent ventricular ectopics, ventricular tachycardia, ventricular fibrillation or asytole. The arrhythmias could not be explained by alterations in blood pressure, electrolytes or blood gases. These findings show the cardiotoxic properties of cantharidin and its ability to produce fatal cardiac arrhythmias. Thus, it may serve as a model to study sudden death and the efficacy of antiarrhythmic drugs.

Animals↗
PubMed1976

Assessment of intrarenal perfusion with radioxenon: a critical review of analytical factors and their implications in man.

Radioxenon has achieved wide use for assessing tissue perfusion. Here we review its application to the kidney for assessing mean blood flow and intrarenal perfusion rates. Correlation with alternative methods in animals suggests that the initial disappearance slope provides an adequate measure of mean renal blood flow despite the theoretical limitations of this approach. The stochastic method and compartmental analysis can also provide an acceptable measure fo mean renal blood flow, but only after the slowest flow components have been removed. Compartmental analysis does, however, provide an index of cortical perfusion not available from other methods. The evidence that the rapid component of xenon washout provides an index of cortical perfusion in man is reviewed, along with insights gained from the application of this approach to human disease.

Acute Kidney Injury↗
PubMed1975

Porcine malignant hyperthermia: effects of halothane on mitochondrial respiration and calcium accumulation.

Vastus lateralis muscle was excised from normal pigs and from pigs susceptible to malignant hyperthermia. Anesthesia consisted of diazepam, N2O:O2, and a lidocaine field block. In the susceptible (MHS) pigs, respiratory control in mitochondria of excised muscle was normal, while electron transport was accelerated. Glutamate log Q3's and log Q4's were in inverse linear relationship to porcine weights. In the presence of glutamate, state 3 respiration was 3.5 times, and state 4 respiration 3.2 times, higher in MHS than in normal mitochondria (independent of weight or halothane dose). Thus, the MHS mitochondria were able to produce ATP more efficiently than normal mitochondria. In vitro, halothane inhibited glutamate Q3's and R.C.I.'s, slightly increased succinate Q3's and R.C.I.'s, had no significant effect on glutamate or succinate Q4's, and, moderately lowered glutamate and succinate P/O ratios. These changes were similar to those observed in normal pigs. Calcium uptake into MHS mitochondria was markedly less than normal but was not significantly altered by in-vitro halothane. These results suggest a mitochondrial membrane component for the defect of procine malignant hyperthermia since calcium is normally associated with the formation of the phospholipid lattice of this membrane. (Key words: Hyperthermia, malignant; Metabolism, mitochondrial; Muscle, skeletal, mitochondria; Anesthetics, volatile, halotbane; Ions, calcium.)

Adenosine Diphosphate↗