Unusual radioiodine uptake in a patient with thyroid cancer and cranial metallic clips.
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Biomedical subjects
Publications and source records attributed to A Campenni.
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Old studies in animals and unblinded studies in a few hyperthyroid patients suggested that L -carnitine is a periferal antagonist of thyroid hormone action at least in some tissues. This conclusion was substantiated by our recent observation that carnitine inhibits thyroid hormone entry into the nucleus of hepatocytes, neurons, and fibroblasts. In the randomized, double-blind, placebo-controlled 6-month trial reported here, we assessed whether 2 or 4 g/d oral L-carnitine were able to both reverse and prevent/minimize nine hyperthyroidism- related symptoms. We also evaluated changes on nine thyroid hormone-sensitive biochemical parameters and on vertebral and hip mineral density (bone mineral density). Fifty women under a fixed TSH-suppressive dose of L -T(4) for all 6 months were randomly allocated to five groups of 10 subjects each. Group 0 associated placebo for 6 months; groups A2 and A4 started associating placebo (first bimester), substituted placebo with 2 or 4 g/d carnitine (second bimester), and then returned to the association with placebo. Groups B2 and B4 started associating 2 and 4 g/d carnitine for the first two bimesters, and then substituted carnitine with placebo (third bimester). Symptoms and biochemical parameters worsened in group 0. In group A, symptoms and biochemical parameters worsened during the first bimester, returned to baseline or increased minimally during the second bimester (except osteocalcin and urinary OH-proline), and worsened again in the third bimester. In group B, symptoms and biochemical parameters (except osteocalcin and urinary OH-proline) did not worsen or even improved over the first 4 months; they tended to worsen in the third bimester. In both the A and B groups, the two doses of carnitine were similarly effective. At the end of the trial, bone mineral density tended to increase in groups B and A (B > A). In conclusion, L-carnitine is effective in both reversing and preventing symptoms of hyperthyroidism and has a beneficial effect on bone mineralization. Because hyperthyroidism depletes the body deposits of carnitine and since carnitine has no toxicity, teratogenicity, contraindications and interactions with drugs, carnitine can be of clinical use.
We are currently interested in a group of proteins associated with the dementias characterized by amyloid deposition in the brain: amyloid beta protein precursor (A beta PP) of Alzheimer's disease (AD) and the abnormal isoform of prion protein (PrP) of spongiform encephalopathies such as kuru, Creutzfeldt-Jacob disease (CJD) and Gerstmann-Straussler-Scheinker disease (GSSD). Here we show that both A beta PP and prion protein (PrP) consist of peculiar internal repeats and share regions of sequence similarity. Further analysis revealed that local homology is also shared with the other proteins involved in specific forms of amyloidosis--i.e., the amyloid related proteins (ARP).
A very small proportion of hypopituitarism is due to head trauma, which may have occurred from days to years earlier. In the literature we found only three cases (two males, one female) of post-traumatic hypopituitarism in whom the hormone deficiency was claimed to be restricted to the gonadotrophs and considered to be permanent after a period of follow-up ranging from less than one year to four years. Here we describe a 26 yr-old male patient who, eight years after a motorcycle accident, was evaluated for hypogonadism and followed-up for three years. Serum testosterone, basal and GnRH-stimulated FSH and LH remained undetectable over the first 22 months of follow-up. Then, basal and GnRH-stimulated gonadotropins moved progressively into the normal range. Basal and dynamic evaluation of the other anterior pituitary hormones was persistently normal. At the 15th month of follow-up there was a change in the pituitary CT scan, presumably due to pituitary revascularization. Therefore, our patient disproves that post-traumatic isolated gonadotropin deficiency is irreversible.