Patient 14bis Goiter and low TSH
Patient 14: Morbo di Basedow - ipertrigliceridemia

Author: Gianpiero Pescarmona
Date: 14/01/2017


1) Definizione del paziente e della storia

Anno di nascita : 1988
Peso: 64 Statura: 1,70 BMI: 22,1

Anamnesi patologica prossima

gozzo che comprime la trachea, cisti liquide.
in terapia con cavitazione per ridurre la massa

transferrina 300 ferritina 15/30 (donatrice di sangue; il limite per donare e' a 25)

TSH 0,2/0,4

TSH basso pulsazioni 70 ipotiroidismo ipotalamico o ipertiroidismo??


metabolismo basale nella norma (kcal 1454/24h)

pH urine: 7 (non uso di diuretici ne' alcalinizzanti)

Anamnesi patologica remota

  • 21anni: Xanax

gozzo dopo cura dimagrante con erbe?? quali??

in tal modo la sequenza temporale degli eventi è chiara e il legame con l'età è istintivo.

Anamnesi familiare

madre con crisi di panico e Xanax da anni

2) Le basi molecolari degli eventi descritti, tenendo conto di tutti i sintomi ed utilizzando i link alle informazioni pertinenti

Goiter iron deficiency - Results from Quertle®

Dopamine receptors in the striatum of rats exposed to repeated restraint stress and alprazolam treatment. 1998

3) Eventuali proposte di terapia, volta al ripristino delle condizioni ottimali


Dopaminergic modulation of TSH and its subunits: in vivo and in vitro studies. 1983

We have studied the effects of dopamine on the secretion of TSH and its subunits in vivo and in vitro. Four normal controls, seven patients with primary hypothyroidism, two patients with peripheral resistance to thyroid hormone (PRTH), and two patients with alpha-secreting pituitary tumours underwent a 3-h dopamine infusion (4 micrograms/kg/min). Serial blood samples were drawn for TSH, PRL, alpha, and TSH-beta subunit. In normal subjects, TSH fell from 2.1 /- 0.9 (/- SE) to 0.7 +/- 0.1 microU/ml (P less than 0.05), and alpha declined from 1.5 +/- 0.4 to 1.0 +/- 0.1 ng/ml (P less than 0.01). TSH-beta was at or slightly above the detection limits of the assay before and after dopamine. In hypothyroidism, basal serum TSH was 81 +/- 14 microU/ml. With dopamine, TSH fell to 35 +/- 8 microU/ml (P less than 0.001), while alpha decreased from 3.2 +/- 0.4 to 2.0 +/- 0.3 ng/ml (P less than 0.01). Serum TSH-beta also declined from 0.97 +/- 0.06 to 0.57 +/- 0.05 ng/ml (P less than 0.001). A similar fall in TSH and alpha was seen in the two patients with PRTH. In normals and hypothyroid patients, the percentage change in alpha concentration was significantly less than that observed for intact TSH. This is due presumably to the contribution of the gonadotrophs to the circulating alpha pool. TSH and TSH-beta were undetectable in the two pituitary tumour patients, and alpha declined only slightly in each patient after dopamine. The in vitro effects of dopamine were studied using cultured bovine anterior pituitary cells. Dopamine (10(-4)-10(-8) mol/l) did not change basal TSH, alpha, or TSH-beta release. However, dopamine at all doses significantly blunted TRH (10(-7) mol/l)-stimulated TSH and TSH-beta release, and blunted TRH-mediated alpha release at the two highest dopamine doses. These data suggest that dopamine modulates both TSH and TSH subunit secretion. These effects may be exerted directly at the level of the thyrotroph.


Participation of serotonin in thyrotropin release. II. Evidence for the action of serotonin on the phasic release of thyrotropin. 1979

During a 12-h light 12-h dark schedule (lights off at 1900 h), male Sprague-Dawley rats show a circadian rhythm of plasma TSH with a zenith near midday. The participation of serotonin (5HT) in the phasic release of TSH was studied using both pharmacological and surgical-stereotaxical approaches. Animals treated with parachlorophenylalanine methyl ester (pCPA), an inhibitor of 5HT synthesis (one or two injections of 250 mg/kg each) showed a reduction or a disappearance of the diurnal peak of TSH, respectively. Additional treatment by 5-hydroxytryptophan, a precursor of 5HT, completely, restored the diurnal TSH peak. Treatment with 5,6-dihydroxytryptamine creatine sulfate, a neurotoxin which selectively destroys 5HT terminals, also induced alterations of the diurnal peak of TSH. There were no major modifications observed in the low nocturnal levels of TSH in rats treated with pCPA, 5-hydroxytryptophan, or 5,6-dihydroxytryptamine. The major serotoninergic innervation of the hypothalamus originates from the raphe dorsalis or centralis; destruction of these two nuclei caused a quasiabolition of the diurnal TSH peak (only a low amplitude TSH circadian rhythm persisted). Hypothalamic 5HT content was measured in the majority of these experiments; the greatest depletions (near 90%) were observed after two injections of pCPA or in rats bearing raphe lesions. We conclude that the diurnal peak of TSH, observed during the physiological circadian rhythm, is serotoninergic dependent.

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