Inflammatory diseases of the lung causing false-positive 131iodine whole body scans in the evaluation of papillary thyroid carcinoma. Two case reports.

The 131I whole body scan is commonly used to establish the presence of metastatic disease in papillary thyroid carcinoma. False-positive scans are rare, but have been reported. We present two cases of aberrant uptake of radioiodine after thyroidectomy and 131I ablation due to inflammatory conditions of the lung, aspergilloma, and respiratory bronchiolitis.

Impaired clearance, elimination, and metabolism of plasma cholesterol esters associated with hypercholesteremia in mice fed cyclopropenoid fatty acids.

Swiss-Webster mice were fed corn oil control diet or 0.7% cyclopropenoid fatty acid (CPFA) for 8 weeks and dosed iv with an equimolar suspension of [3H]cholesteryl palmitate and [14C]cholesteryl palmitoleate. Blood decline of labeled sterol was biphasic. There were no differences in vivo plasma cholesterol ester metabolism, elimination kinetics, or fecal elimination rate for labeled sterol from [3H]cholesteryl palmitate or [14C]cholesteryl palmitoleate within CPFA or control groups. However, compared to controls, CPFA animals diverted significantly more labeled sterol into saturated and diunsaturated cholesterol esters, less into mono- and tetraunsaturated esters, and showed decreased blood clearance and fecal elimination of labeled sterol. Biliary elimination was probably not impaired by depressed hepatic cholesterol esterase activity in CPFA-fed mice. The fundamental effect of CPFA on serum cholesterol concentration appears to reside in a severely imbalanced cholesterol ester profile. Results indicate that CPFA alter normal fatty acid profile of serum cholesterol esters by proportionally altering the C-2 fatty acyl composition of serum phospholipid, which is the substrate for lecithin:cholesterol acyltransferase, the major source of plasma cholesterol esters.

Altered lipid metabolism and impaired clearance of plasma cholesterol in mice fed cyclopropenoid fatty acids.

Swiss-Webster mice fed a diet containing 0.5% cyclopropenoid fatty acids (CPFA) for 6 weeks showed depressed growth rates and developed hypercholesteremia and increased concentrations of serum phospholipid and free cholesterol compared to control mice. No depression of cytochromes P-450 and b5 or microsomal mixed-function oxidase activities occurred to indicate impaired oxidative catabolism of serum cholesterol. Elimination of intragastrically administered [3H]cholesterol from blood was biphasic; there was no significant difference in first-order rate constants for absorption, distribution, and elimination processes between control and CPFA-fed animals. However, the area under the blood clearance curve for CPFA-fed animals was significantly increased (p less than or equal to 0.01) by 29% over controls, demonstrating a net increase in clearance time for exogenous cholesterol in CPFA-fed animals, thus contributing to their hypercholesteremia. In the CPFA-fed mice, the percentage of saturated fatty acid residues increased at the expense of monounsaturates in the cholesterol ester, triglyceride, and phosphatidyl choline fractions of serum lipids. Total polyene content of serum lipid was not altered; however, CPFA-fed animals demonstrated increased linoleic acid at the expense of arachidonic acid in all serum lipid fractions. Excessively saturated serum lipids may impede clearance of serum cholesterol in CPFA-fed animals by inhibited plasma lecithin-cholesterol acyltransferase (LCAT) and hepatic cholesterol esterase activities.

Humoral immunotoxicity of polychlorinated diphenyl ethers, phenoxyphenols, dioxins and furans present as contaminants of technical grade pentachlorophenol.

Previous studies have demonstrated that the humoral immune response in mice as measured by the splenic IgM response to sheep erythrocytes (SRBC) is highly sensitive to suppression by technical grade (86%) pentachlorophenol (T-PCP) whereas analytical grade (greater than 99%) PCP is not immunosuppressive. In the present studies, we have examined several contaminant fractions and purified isomers from T-PCP for their humoral immunosuppressive effect. C57BL/6 mice were treated with a single oral dose of the various contaminants 2 days prior to SRBC challenge and the peak splenic IgM antibody response was measured 5 days later. Under these exposure conditions, T-PCP produced a dose-related suppression of the antibody response whereas analytical grade PCP was without effect. The dose of T-PCP producing 50% immunosuppression relative to the vehicle-treated control (ID50) was 83 mg/kg. Results from studies using contaminant fractions extracted from T-PCP indicated that a chlorinated dioxin/furan fraction was significantly immunosuppressive, whereas a chlorinated phenoxyphenol fraction and a chlorinated diphenyl ether fraction were without effect when administered at dose levels expected to occur in the ID50 dose of T-PCP. Several purified phenoxyphenol isomers representing the major pre- and isopredioxins in T-PCP were also not immunosuppressive, nor was octachlorodibenzo-p-dioxin. The 1,2,3,4,6,7,8-hexachlorodioxin (HxCDD), 1,2,3,4,6,7,8-heptachlorodioxin (HpCDD), and 1,2,3,4,6,7,8-heptachlorofuran (HpCDF) isomers were all significantly immunosuppressive. The single, oral ID50s were 7.1, 85 and 208 micrograms/kg for HxCDD, HpCDD and HpCDF, respectively. Coadministration of HxCDD and HpCDD produced an additive immunosuppressive effect suggesting that the toxic dioxin and furan isomers present in T-PCP function in concert to produce the degree of immune suppression observed following T-PCP exposure. When analytical grade PCP was coadministered with HpCDD, the degree of immune suppression was equivalent to that produced by HpCDD alone, indicating no significant influence of PCP on dioxin-induced immunosuppression. The enhanced susceptibility of Ah-responsive C57BL/6 mice to T-PCP induced immune suppression as compared to Ah-nonresponsive DBA/2 mice and the correlation of immune suppression with P1-450 associated monoxygenase induction provided further evidence for the role of the toxic Ah-interactive dioxin and furan contaminants in T-PCP as the mediators of T-PCP immunotoxicity.