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Biomedical subjects

I Saletnich

Publications and source records attributed to I Saletnich.

15 recordsLinked to original sources
PubMed1998

Severe thyrotoxicosis due to functioning pulmonary metastases of well-differentiated thyroid cancer.

We report two cases of thyrotoxicosis resulting from hyperfunctioning lung metastases from differentiated thyroid cancer. In both patients, a simultaneous diagnosis of thyrotoxicosis and metastatic thyroid cancer was made, based on thyroid function tests as well as 131I whole-body scans showing low thyroid uptake of radioiodine and multiple foci of intense 131I uptake in the lungs. After total thyroidectomy (performed in Patient 2 only) and 131I therapy (cumulative dose of 12.3 GBq in Patient 1 and 9.6 GBq in Patient 2), there was a rapid clinical improvement with significant reduction of the pulmonary metastatic disease in both patients: Patient 1 became euthyroid, while Patient 2 became hypothyroid. Analysis of the 54 cases reported in the literature, including the 2 cases described here, shows this to be a very rare cause of thyrotoxicosis and one that can pose serious problems for both the diagnostic evaluation and choice of therapeutic strategy when compared with the much more common nonhyperfunctioning metastases from thyroid cancer. Lesser degrees of thyroid hormone secretion by differentiated thyroid cancer may be detected and exploited diagnostically by the chromatographic analysis of serum for endogenously labeled thyroid hormones after 131I administration.

Adenocarcinoma, Follicular↗
PubMed1997

Unusual false-positive radioiodine whole-body scans in patients with differentiated thyroid carcinoma.

Radioiodine whole-body imaging is the most accurate method in the diagnosis of metastases from differentiated thyroid cancer. However, false-positive images rarely occur. The authors report unusual cases of thymic hyperplasia and post-traumatic skull changes mimicking mediastinal, skull, or cerebral metastases. Nonthyroidal causes were diagnosed by other radionuclide studies (bone and brain scintigraphy) and CT scans. Follow-up and undetectable thyroglobulin levels helped confirm the benign cause.

Adult↗
PubMed1996

Disseminated bone marrow metastases of insular thyroid carcinoma detected by radioiodine whole-body scintigraphy.

We present 131I scintigraphic findings in a patient with insular carcinoma of the thyroid showing diffuse abnormal uptake throughout the skeleton. The scintigraphy closely resembled the pattern of [131I]MIBG distribution in children with bone marrow metastases of neuroblastoma. The extent of involvement was underestimated by bone scintigraphy and radiography. Insular carcinoma of the thyroid in the bone marrow was subsequently demonstrated by biopsy. The patient was treated with 242 mCi 131I given in two courses, which led to severe myelosuppression and died as a result of progressive disease and severe pancytopenia 10 mo after initial therapy.

Biopsy↗
PubMed1995

Radiolabeled somatostatin analog scintigraphy in medullary thyroid carcinoma and carcinoid tumor.

The aim of this study was to evaluate the effectiveness of a recently developed radiolabelled somatostatin analog (111In-pentetreotide) for the detection and localization of both medullary thyroid carcinoma (MTC) and carcinoid tumors, and to compare the results obtained with the results of 99mTc(V)-DMSA, and radioiodinated MIBG imaging. 111In-pentetreotide scintigraphy was performed in 9 patients with MTC and in 9 patients with carcinoid tumor. Whole body and SPECT studies were performed at 4 and 24 hours post-injection. SMS scintigraphy gave a positive result in 5 out of 7 patients with proven MTC lesions, and in 7 out of 9 patients with known lesions of carcinoid tumor. It gave a negative result in 2 MTC patients with high levels of calcitonin but with no evidence of disease at conventional diagnostic modalities. The scintigraphic results were comparable with those obtained with 99mTc(V)-DMSA in MTC and were superior to those of radioiodinated MIBG in both MTC and carcinoid tumors. When compared with the modifications of calcitonin levels brought about by the acute administration of octreotide ("Octeotride test"), these correlated well in 8 out of 9 patients studied.

3-Iodobenzylguanidine↗
PubMed1993

Thyroid cancer in suppressed contralateral lobe of patients with hot thyroid nodule.

We studied 60 patients with thyrotoxicosis due to single toxic nodule. At surgery in 3 patients (5%) a papillary carcinoma has been detected in the contralateral suppressed lobe. Thyroid function tests and thyroid scan confirmed thyrotoxicosis. Thyroid stimulating hormone (TSH) was undetectable in all patients. It is common opinion that differentiated thyroid tumour growth is TSH dependent. On the basis of our study two hypotheses are possible: (1) the development of thyroid carcinoma precedes the adenoma and suppressed TSH levels inhibit tumour growth; (2) suppressed TSH levels do not protect patients from the occurrence of cancer. In the evaluation of hot thyroid nodule we suggest careful ultrasonographic control in order to look for nodules outside the adenoma. A complete surgical examination of the whole thyroid gland is required and intraoperative biopsies are advocated in abnormal areas.

Adenoma↗
PubMed1993

Thyrotoxicosis due to ectopic retrotracheal adenoma treated with radioiodine.

Ectopic thyroid tissue is rarely found in the cervical retrotracheal region and its functional autonomy with suppression of the normal gland can be considered unusual. We report a case of thyrotoxicosis in a patient who had no palpable goitre in the neck but was found to have a solitary toxic thyroid nodule behind the trachea. US and CT scanning confirmed that the nodule was retrotracheal and apparently was not continuous or contiguous with the normal thyroid gland. The toxic adenoma showed avid uptake of iodine-131 (131I), and using thallium-201-chloride (201Tl)-SPECT the normal thyroid gland together with the retrotracheal autonomous nodule was demonstrated. The patient underwent radiometabolic therapy with 666 MBq of 131I and a 131I scan performed 6 months later showed only the previously suppressed normal thyroid gland.

Adult↗
PubMed1989

[Naloxone doesn't determine the response of growth hormone to clonidine in obese patients].

The effect of naloxone (opioid receptor blocker) on the impairment of growth hormone (GH) release after clonidine (alfa 2-adrenergic agonist) was investigated in 10 volunteer obese subjects. The patients (4 males and 6 females, 16-22 year old) with fat excess (15 +/- 2 kg) estimated by bioelectrical impedance analysis (BIA) were studied repeatedly. The patients, were perfused by a slow saline infusion. 30 min later they received a bolus dose of clonidine (150 micrograms p.o.), followed 30 min later by a bolus dose of naloxone (10 mg i.v.) or a corresponding volume of isotonic sodium cloride (I.S.) for control. No significant changes occurred in blood GH concentration after clonidine administration and naloxone did not induce GH response at clonidine. These results suggest that in obese subjects the impairment of GH release after clonidine is not mediated via receptors sensitivity to naloxone.

Adolescent↗