[Effect of potassium iodide and streptomycin on experimental tuberculosis in mice].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This concerns a case of an infant born with goiter and hypothyroidism whose mother had taken potassium iodide during pregnancy in the form of a respiratory eupneic syrup. Laboratory tests revealed the etiology of the goiter by demonstrating that it concerned a transitory, acquired hormone production disturbance. The tests gave an indication of the course of the condition, leading to substitute hormone therapy being stopped after six weeks. The euthyroidism was then checked on two occastions.
Serum thyroxine (T4), triiodothyronine (T3) and thyrotropin (TSH) concentrations were measured in 13 patients with chronic obstructive pulmonary disease receiving saturated solution of potassium iodide (SSKI). All had a low serum T4 and a high serum TSH concentration. However, serum T3 levels were normal in eight. Recovery of normal thyroid function was observed in each of the seven patients in whom the iodide was discontinued. The same hormones were measured in four normal subjects who received 30 drops of SSKI daily for 11 weeks. An increase in serum TSH levels was preceded by a fall in serum concentrations of T4 and to some extent, T3. Upon SSKI withdrawal subsequent increases in the serum concentrations of both thyroid hormones, but particularly T3, resulted in the return of serum TSH to baseline levels. None of the subjects developed clinical hypothyroidism. It is not apparent why the normal subjects did not exhibit clinical or laboratory evidence of hypothyroidism while the patients with chronic pulmonary disease did. A younger age and the shorter duration of iodide administration in the normal subjects may have played a role.
In iodine deficiency areas, an increased T3/T4 ratio in serum was reported earlier. In this study the influence of potassium iodide on the T3/T4 ratio was investigated. Treatment with 200 mug KI per day for only 4 weeks normalized the initially elevated T3/T4 ratio in 16 nontoxic goiter patients (24.6 plus or minus 9.9 times 10-3, mean plus or minus S.D., before, respectively 18.9 plus or minus 5.5 times 10-3 after KI treatment, p smaller than 0.0025). The mean basal TSH levels (1.42 plus or minus 0.68 before, respectively 1.29 plus or minus 0.52 mugU/ml after KI), and the TSH increase 30 min after 200 mug TRH i.v. (5.54 plus or minus 4.22 and 6.50 plus or minus 5.09 mugU/ml, respectively) did not change significantly. Since the normalization of the T3/T4 ratio in nontoxic goiter patients was independent from changes in the TSH levels, this effect of KI obviously represents an example of thyroidal autoregulation.
This study was undertaken to examine the effects of immunization with Sporothrix schenckii and oral potassium iodide (KJ) administration on the chemiluminescence (CL) response of mouse polymorphonuclear leukocytes (PMNs) in experimental murine sporotrichosis. When N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) particles were used as foreign bodies to be phagocytosed, the time to the peak CL response of the PMNs in an immunized group was shortened in comparison with a non-immunized control group, and the CL intensity was found to be prolonged. Whereas administration of KJ resulted in a reduction of the CL intensity in non-immunized mice, in immunized mice it caused a rise in CL intensity. When the foreign bodies used as targets for phagocytosis were Sp. schenckii, changes similar to the above occurred, but CL production was reduced.
Blocking the thyroid gland when administering radioiodinated materials is a common practice. Since pharmacologic quantities of potassium iodide (KI) in the range of 100-300 mg daily are usually administered for this purpose, the potential exists for iodide toxicity. Concomitant with the tracer administration is the risk produced from ionizing radiation. Reports in the literature demonstrated thyroid function abnormalities in patients administered iodides. Based on the latter observations the object of the present investigation is to determine the effectiveness of thyroid blocking with a lesser daily quantity of KI. Fifteen adult hip replacement patients (7 men, 8 women; 58.2 +/- 11.5 years) received 2.5 mg Ki orally every 12th hour twice daily 2 days prior to surgery and 125I-fibrinogen [(3,700 kBq)(100 microCi)], and each day up to 10 days thereafter. Thyroid and precordial counts were obtained daily and the latter two were used for calculating the 125I thyroid uptake. These data were used for estimating the thyroid blood disappearance and cancer risk. An attempt was made to compare the radiation risk to that from KI ingestion. The 125I% thyroid uptake for the study population (n = 15) was 1.83 +/- 1.25%. This compares to a thyroid uptake of 0.064 +/- 0.037% in a published report using 300 mg KI daily in the course of an 125I-fibrinogen test. The mean thyroid radiation dose for the study population was 6.09 cGy after receiving 5 mg KI daily. The specific risk estimate (SRE) for contracting thyroid cancer was calculated to be 4.5B-04. The NCRP calculated thyroid function risk after ingesting KI is 1-10E-07.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: Iodide administration to animals, living in iodine-deficient areas, can induce oxidative processes in the thyroid gland and increase concentration of lipid peroxidation (LPO). Propylthiouracil (PTU)--a well-known antithyroid drug--may also act as an antioxidant. There are some reports, which consider the protective ability of this drug against LPO. The goal of the study was to evaluate oxidative processes and the protective role of PTU in three rat organs during treatment with pharmacological doses of iodide. MATERIAL AND METHODS: Schiff's bases (SB) concentrations (a parameter of oxidative stress) were measured in liver, lung and kidney homogenates of male Wistar rats. For 2 weeks the animals received iodides in their diet in the following concentrations: Group 1--Controls (standard diet, approx. 0.7 mg of potassium iodide per kg; KI/kg); Group 2--diet containing 0.25 mg KI/kg; Group 3--diet with 4.0 mg KI/kg; Group 4--diet with 8.0 mg KI/kg. Group 5--standard diet with 0.1% of PTU in drinking water for two weeks. Subsequent tree groups (6-8) received KI in their diet in doses as above, respectively, together with PTU. RESULTS: We noted increased SB levels in the lungs and in the liver, compared to those observed in the control group. We also found decreased SB concentrations in liver and lung homogenates after the administration of PTU but, unexpectedly, the level of SB increased in kidney homogenates of all the groups. CONCLUSIONS: The results of this study indicate that iodine is involved in oxidative processes in different organs and PTU protects against iodine-induced oxidative stress.
During metabolism studies of radiolabeled proteins in 126 participants four patients were suspected of being sensitive to potassium iodide (Kl) because they repeatedly developed urticaria and other symptoms after Kl administration. Two of the four patients suspected of Kl sensitivity and 10 control patients were orally challenged with Kl to document and characterize Kl sensitivity and to evaluate the possible association(s) of Kl sensitivity with urticaria, hypocomplementemia, and vasculitis. The Kl challenges in the two sensitive patients precipitated urticaria, angioedema, polymyalgias, conjunctivitis, and coryza. One of these two patients also developed a severe systemic illness characterized by fever, headache, peritonitis, episcleritis, and pneumonitis. The four sensitive patients were strikingly similar in that they exhibited hypocomplementemia and dermal vasculitis associated with chronic urticaria or systemic lupus erythematosus, suggesting that other patients with similar clinical features may be sensitive to Kl and that Kl may precipitate severe systemic illness in them.
The effect of 1000 ppm potassium perchlorate (KClO4), 1000 ppm potassium iodide (KI) or 1000 ppm propylthiouracil (PTU) in the diet on the development of thyroid tumors was studied histologically and biochemically in Wistar rats given a single ip injection of 280 mg of N-bis(2-hydroxypropyl)nitrosamine (DHPN) per 100 g body weight. Basal diet containing 100 ppm KClO4, 1000 ppm KI or 1000 ppm PTU was given for 19 weeks from week 2 to week 20. The incidence of thyroid adenomas at the end of week 20 of the experiment was 100% (20/20) in rats treated with DHPN followed by KClO4, 85% (17/20) in rats given DHPN followed by KI, 95% (19/20) in rats given DHPN followed by PTU, and 5% (1/20) in rats given DHPN alone. The incidence of thyroid cancers was 100% (20/20) in rats treated with DHPN followed by KClO4, 65% (13/20) in rats treated with DHPN followed by KI and 0% (0/20) in rats treated with DHPN followed by or not followed by PTU. Rats given KClO4, KI or PTU alone and untreated rats had no thyroid tumors. The mean values of TSH in serum were 2.94 +/- 0.79 ng/ml in rats treated with DHPN followed by KClO4, 9.40 +/- 16.0 ng/ml in rats treated with DHPN followed by KI and 60.94 +/- 20.60 ng/ml in rats treated with DHPN followed by PTU. It was confirmed that (1) KClO4, PTU and KI promote the development of thyroid tumor in rats treated with DHPN, (2) the promoting effect of KClO4 or KI is stronger than that of PTU and (3) the value of TSH in serum is not parallel to the promoting effect on the development of thyroid tumor.
One hundred and nineteen patients with Graves' hyperthyroidism who were treated with 131I alone or 131I followed by potassium iodide (131I + KI) were studied retrospectively. Patients in both groups who required only a single dose of 131I for successful treatment of hyperthyroidism had similar age, gland size, 24-h radioactive iodine uptake, pretreatment serum T4 concentrations, and radioactive iodine treatment dose. Seven weeks after 131I, mean serum T4 concentrations were 12.3 +/- 6.1 micrograms/dl (mean +/- SD) in patients who received 131I alone and 8.0 +/- 3.9 micrograms/dl in patients who received 131I + KI (p less than 0.001). Sixty percent of the patients who received 131I + KI and remained euthyroid 1 yr after 131I treatment developed documented transient hypothyroidism while receiving KI (serum T4, 1.4 +/- 0.9 micrograms/dl). Patients with transient hypothyroidism receiving KI had larger estimated thyroid gland weights when hypothyroid than patients whose hypothyroidism was permanent (32 +/- 6 vs. 16 +/- 11 g; P less than 0.001). The overall incidence of hypothyroidism 1 yr after treatment with 131I was 58% in each of the two groups. Sixteen percent of each group were not successfully treated by a single dose of 131I and required further therapy. Adjunctive KI effectively treated thyrotoxicosis more rapidly than 131I alone without adversely affecting outcome at 1 yr; however, patients taking KI more often develop transient hypothyroidism.
Phalloidin, a bicyclic peptide from the poisonous Amanita phalloides mushroom, stimulates the viscosimetrically determined polymerization of G-actin to F-actin in 0.6 m potassium iodide, a medium in which spontaneous polymerization does not occur. The cytochalasins B, D, E, and G (CB, CD, etc.) and the chaetoglobosins A, B, C, E, F, and J (Ch-A, Ch-B, etc.) have been found to influence the rat of polymerization in different ways, depending on their chemical structure and concentrations applied. Class I cytotoxins, e.g., CB, CG, Ch-C, Ch-E, and Ch-F, which exert on F-actin a weak degradative power (DP, "Spudich effect"), increase the polymerization rate when present in a ratio of 4 mol to 1 mol of actin. Polymerization is slightly enhanced or retarded at molar ratios ranging from 0.04:1 to 0.4:1. Class III cytotoxins of strong degradative power, i.e., high affinity for actin, such as CE, Ch-B, and Ch-J, decrease the polymerization rate at a molar ratio of 4:1 during the first 30-40 min; however, they increase it at a molar ratio of 0.4:1. Members of class II (CD, Ch-A) exert an effect that can be interpreted as a combination of the effects of class I and class III cytotoxins. An explanation of this difference in behavior is offered on the basis of experiments on F-actin degradation by Ch-J and its reconstitution by phalloidin in the presence of Ch-J.