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Results for “PROPYLTHIOURACIL”

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PubMed1988

Propylthiouracil, but not other antithyroid treatments, lengthens hamster circadian period.

Two experiments were performed to evaluate the role of the thyroid gland as a mediator of circadian rhythms in the hamster. In experiment 1, the antithyroid drug propylthiouracil (PTU) lengthened the circadian period (tau), increased thyroid weight, and eliminated detectable thyroxine (T4) and triiodothyronine (T3) from blood. A low-iodine diet greatly reduced T4 levels but had no effect on T3 or tau. Treatment with 500 microCi of 131I failed to alter any parameter of physiology or rhythmicity measured. In this experiment, some animals in the low-iodine and PTU groups had greatly reduced testes sizes, and testes size was inversely correlated with change in tau. In experiment 2, T4 and T3 levels detected 11 wk after surgical thyroidectomy were significantly less than those found in sham-operated animals, but concentrations of the two hormones varied widely across the thyroidectomized group. Thyroidectomy did not increase tau either 4 or 11 wk after surgery, nor was there evidence from individuals that level of thyroid function was associated with change in tau. The results from these experiments suggest that diminished thyroid function is not causal of lengthened circadian period.

Animals↗

PubMed2005

Epitope analysis of myeloperoxidase-specific antineutrophil cytoplasmic autoantibodies (MPO-ANCA) in childhood onset Graves' disease treated with propylthiouracil.

AIM: This study aimed to elucidate the relationship between epitope profiles and clinical manifestations of patients with myeloperoxidase antineutrophil cytoplasmic autoantibodies-(MPO-ANCA) positive childhood onset Graves' disease treated with propylthiouracil (PTU). METHODS: Sixteen patients were studied. The patients were grouped into ten without clinical vasculitis and nephritis (non-vasculitis group) and six with biopsy-proven pauci-immune necrotizing crescentic glomerulonephritis (vasculitis group). Epitope analysis was performed on serum samples by an enzyme-linked immunosorbent assay (ELISA) using a panel of recombinant deletion mutants of MPO. RESULTS: The high frequency sites were region upstream of Met341 (Ha region) near the N-terminus of the heavy chain, and regions downstream of Gly598 (Hf and Hg regions) near the C-terminus. Most patients in the non-vasculitis group had polyclonal MPO-ANCA recognizing both the above linear sites and other epitope sites of the heavy chain of MPO. Only one of ten patients in the non-vasculitis group, and four of six patients in the vasculitis group had MPO-ANCA recognizing only the linear sites of the heavy chain of the MPO molecule (Ha, Hf and/or Hg). Of the four patients in the vasculitis group, two had nephritis, like rapidly progressive glomerulonephritis and one had alveolar hemorrhage. CONCLUSION: These findings suggest that most patients with childhood onset Graves' disease treated with PTU who manifest no vasculitis have polyclonal MPO-ANCA recognizing both the linear and other epitope sites of the heavy chain of MPO. However, some patients who develop nephritis have MPO-ANCA recognizing only the linear sites of the heavy chain of MPO. This clonality of MPO-ANCA may be a risk factor that induces clinical vasculitis and nephritis in patients treated with PTU. Therefore, patients exposed to PTU should be monitored for MPO-ANCA level and epitopes.

Adolescent↗

PubMed1999

Influence of hypovolemic and hypertonic treatments on plasma vasopressin levels and fluid balance in the propylthiouracil-induced hypothyroid rat.

This study was undertaken to investigate the effects of hypovolemic and hypertonic treatments on plasma vasopressin (AVP) levels and fluid balance in propylthiouracil (PTU)-induced hypothyroidism in the rat. The influence of hypothyroidism on AVP responsiveness to hypertonic and hypovolemic stimuli were compared. Adult male rats were divided into two groups. Groups I and II were intraperitoneally (i.p.) injected with saline (1ml/250g) and PTU (10mg/kg/day), respectively, for a period of two weeks. These groups were further divided in three subgroups each containing six rats. The first subgroup consisted of unchallenged rats. I.P. 700 mg polyethylene glycol was used for hypovolemic treatment. The third subgroup consisted of hypertonic (1.5 M NaCl; 1ml/100 g) stimulated animals. All rats were decapitated and trunk blood collected in hep-arinized tubes. Plasma samples were stored at -20 degrees C until assayed. Plasma AVP, T3 and T4 levels were measured by radioimmunassay. Hematocrit values and plasma Na concentrations were also determined. In the PTU-induced hypothyroid rats, hypertonic treatment caused lower increase in plasma AVP levels (p<0.05) compared to the respective control animals. In the hypovolemic group, decreases in AVP responses were not found to be statistically significant. In conclusion, although hypothyroidism does not statistically change basal AVP levels, it may affect AVP response to hypertonic stimulus. It is not clear whether changes in fluid-electrolyte balance cause disturbance in AVP release in hypothyroidism or vice versa. Therefore, these preliminary findings need to be confirmed by further investigations.

Journal Article↗

PubMed1984

Obligatory role of thyroid hormones in development of peripheral sympathetic and central nervous system catecholaminergic neurons: effects of propylthiouracil-induced hypothyroidism on transmitter levels, turnover and release.

Thyroid status is thought to play a major role in establishing the time course of development of sympathetic nerve pathways. Hypothyroidism induced by perinatal administration of propylthiouracil to developing rats resulted in substantial deficits in cardiac norepinephrine levels that persisted into adulthood. This shortfall was not accompanied by compensatory receptor supersensitivity or by increased utilization of remaining transmitter. Indeed neonatal hypothyroidism is known to result in end-organ subsensitivity and the norepinephrine turnover rate, an index of spontaneous activity of the neuron, was found to be markedly subnormal. The ability of cardiac sympathetic neurons to release transmitter upon pharmacological challenge was also compromised by hypothyroidism: in control neonates, administration of tyramine resulted in displacement of norepinephrine from nerve terminals, a response which was present very early in development. Hypothyroid rats did not develop the ability to release transmitter in response to tyramine until 10 days postnatally and a fully mature response was not apparent until weeks later. Ontogeny of the capability to release norepinephrine in response to hypotension (baroreflex) also was assessed through administration of hydralazine, a direct arteriolar vasodilator; control rats showed a characteristic development of this response at the end of the 2nd postnatal week, whereas hypothyroid rats did not show any potential for norepinephrine release until young adulthood (41 days). In comparison to cardiac sympathetic neurons, an overall evaluation of central catecholaminergic pathways in whole brain indicated a much smaller effect of hypothyroidism, with no (norepinephrine) or only minor (dopamine) deficits in transmitter content and smaller, transient reductions in turnover.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1963