M D Hein | PubMed Health

PubMed1993

Increased in vitro thyrotropic activity of partially sialated human chorionic gonadotropin extracted from hydatidiform moles of patients with hyperthyroidism.

The intrinsic thyrotropic activity of hCG purified from normal pregnancy urine has been demonstrated in several laboratories. hCG has a specific thyrotropic potency of about 0.04-0.5 microU bovine (b) TSH/IU hCG, depending on the bioassay system. The corresponding potency for hCG derived from pathological sources, such as hydatidiform moles and choriocarcinoma tissue, or from the serum of these patients has not been studied as extensively. Since the biological activity of glycoproteins can be strongly influenced by variations in the oligosaccharide side-chain composition, we have investigated the effect of anion exchange chromatography on the thyrotropic potency of hCG derived from the hydatidiform mole and serum of three hyperthyroid patients with molar pregnancy. The activity for the fraction of total molar hCG immunoreactivity that was not retained by an anion exchange column (0.18-0.90 microM bTSH/IU hCG) was about twice that of the corresponding serum and molar hCG fraction eluting during the NaCl gradient elution (0.08-0.40 microU bTSH/IU hCG). The unretained hCG fraction corresponds to a previously described hCG precursor that is partially desialated in the C-terminal region of the beta-subunit.

Adult↗

PubMed1990

Review: thyroid function in psychiatric illness.

The development of highly sensitive immunometric assays for thyroid-stimulating hormone (TSH) has provided increased understanding of thyroid hormone regulation but, paradoxically, has contributed to a kaleidoscopic complexity of thyroid function test variability in hospitalized patients with nonthyroidal illness (NTI). In primary hypothyroidism, an elevated TSH is the most sensitive chemical index available, although early cases may show a hyperresponse of TSH to thyrotropin-releasing hormone (TRH) stimulation when the TSH is still within the normal range. The ability of the new TSH assays to discriminate between normal and low levels now allows the diagnosis of thyrotoxicosis to be confirmed by a suppressed TSH in the presence of elevated serum thyroxine (T4) and/or triiodothyronine (T3). The TRH stimulation test is virtually obsolete for the diagnosis of thyrotoxicosis but remains of much interest in the investigation of psychiatric syndromes. Approximately 25% of patients with depression have a blunted TSH response (a rise of less than 5 microU/mL) that differs from thyrotoxicosis, wherein the TSH response is suppressed under 1 microU/mL. The cause of the blunted TSH is uncertain but is not due to hyperthyroidism. In contrast, close to 15% may have a TSH hyperresponse to TRH and/or elevated antithyroid antibodies. Thyroid hormone treatment may benefit the depression in some of these cases. In the sick thyroid state of nonthyroidal illness, a low T3 level is the initial manifestation. In more severe cases, the T4 also falls, the free T4 level in this situation is variable, both normal and low levels being reported from different laboratories. A diagnosis of hypothyroidism requiring treatment with thyroid hormone therapy is unlikely unless there is a concomitant lowfree T4 and elevated TSH in a patient who is not in the process of recovery. In acute psychiatric admissions, there is a high frequency of hyperthyroxinemia. The TSH in these cases is generally either normal or high, suggesting central activation of the hypothalamic-pituitary-thyroid axis. In most instances, the thyroid function tests normalize within 2 weeks, and treatment directed toward the thyroid gland is not indicated. Suppressed TSH levels, usually associated with a normal free T4, has also been described in such patients. Finally, various medications utilized in psychiatric practice have diverse effects on thyroid function and can cause diagnostic difficulty. These include lithium, phenytoin sodium, and carbamazepine, and their effects are reviewed.

Diagnosis, Differential↗

PubMed1989

Pentagastrin stimulation of calcitonin in pheochromocytoma does not always indicate multiple endocrine neoplasia type II.

The diagnosis of pheochromocytoma in a 48-year-old man was confirmed by elevated catecholamine secretion and a left adrenal mass on computerized tomography. Because of a plausible family history for Multiple Endocrine Neoplasia Type II, a calcitonin level was determined which was elevated, and pentagastrin stimulation caused a 235% increase. These findings normalized following surgical removal of the single adrenal tumor. It is concluded that pentagastrin stimulation of calcitonin is not necessarily diagnostic of medullary thyroid carcinoma, and such a response in a patient presenting with pheochromocytoma may not indicate underlying Multiple Endocrine Neoplasia Type II.

Adrenal Gland Neoplasms↗