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Potassium iodide was given to 17 cases of Basedow's disease in comparison to 12 normal controls for 5 weeks. In the thyrotoxic patients, the maximum decrease in serum T3 and T4 levels was observed 2 and 3 weeks, respectively, but in some cases remained normal even at 5 weeks. The euthyroid persons showed a small decrease in T4 and T3 and an increase in serum TSH.
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Potassium iodide therapy has a history of more than 150 years. It has been tried in many diseases in the past. However, with the development of modern medications indications for potassium iodide therapy are very limited. It is well known that potassium iodide is the drug of choice for sporotrichosis. Subacute nodular migratory panniculitis and erythema nodosum have also been treated successfully with this drug.
We studied the effect of potassium iodide on the chemotaxis of neutrophil in 15 healthy subjects with a modified Boyden chamber method. Orally administered potassium iodide (15 mg/kg/day for 3 days) significantly inhibited the neutrophil chemotaxis in peripheral blood. It is postulated that the therapeutic effect of potassium iodide on erythema nodosum, nodular vasculitis, and Sweet's syndrome might be mediated through the inhibition of neutrophil chemotaxis by this agent.
Potassium iodide is the preferred thyroid blocker for personnel handling radioiodine and is recommended as a prophylaxis for the population in the near-field of a nuclear reactor which would be likely to be exposed to radioiodine in an accidental breach of containment. However, in hot and humid climates, this hygroscopic chemical has a poor shelf life due to hydrolytic loss of iodine vapors. On the other hand, another iodine-rich salt, potassium iodate (KIO3), is quite stable and has a much longer shelf life. The present study compares potassium iodide and KIO3 as thyroid blockers and examines the appropriate time at which they should be administered in case of radioiodine exposure. Either of the two were given in recommended dosage (100 mg stable iodine per 70 kg body weight) at -2, 0, +2, +4, +6, and +8 h after administration of tracer quantities of radioiodine (131I) to age-, weight-, and sex-matched rats. 131I uptake in thyroid was measured 24 h after its administration in the experimental animals and compared with placebo administered controls. Results suggest that KIO3 is as effective a thyroid blocking agent as potassium iodide. In comparison to controls, 24-h thyroid uptake of 131I can be substantially reduced if potassium iodide or KIO3 is given to the animals within 2-4 h after exposure to 131I. Another noteworthy observation is that KIO3 is effective even at 8 h when administered at twice the usual dosage in comparison to the single dose, which does not show appreciable thyroid blocking properties after 8 h.
Potassium iodide (KI) has been shown to have an antigoitrogenic action and to inhibit in vivo thyroid protein biosynthesis. Beef thyroid slices were used to clarify further the mechanism of action of KI. Incubations were performed in Krebs-Ringer-bicarbonate (KRB) buffer under 95%O2 and 5% CO2. KI caused a slight decrease in the uptake of [3H]eucine by the tissue. When labelled leucine incorporation into protein was measured it was found that 10(-6) M KI caused a marked inhibition. Increasing concentrations of KI up to 10(-3) M did not further increase this inhibition. This effect of KI was reduced by simultaneous addition of 0.5 mM KClO4 or 1 mM methylmercaptoimidazole (MMI). In several experiments it was found that equimolar amounts of thyroxine (T4) or triiodothyronine (T3) were more potent than KI in inhibiting thyroid protein biosynthesis. In double plabelled studies KI decreased [3H]leucine incorporation into thyroid soluble proteins and into immunoprecipitable thyroglobulin (T4) while it did not modify that of [14C]galactosamine. When tissue specificity was examined, KI failed to alter [3H]leucine incorporation into proteins either in the liver or in the submaxillary gland. The present results indicate that intracellular KI is necessary to exert its effect on protein synthesis, and that this effect is mediated through a organic form of iodine, probably iodothyronines. This action of KI is specific for the thyroid gland.
The stability of potassium iodide in iodized salt has been studied with respect to the purity of the salt used as raw material. It has been found that the iodized salt prepared from high purity salt and preserved under proper conditions (protection from light, humidity and high temperatures) keeps, for several months, the most of the initially added potassium iodide, without any addition of stabilizers, except for a small bicarbonate.
OBJECTIVE: To determine the effectiveness of levothyroxine and potassium iodide in treating patients with benign solitary cold thyroid nodules. DESIGN: Randomized controlled study. SETTING: Outpatient clinic at a university hospital. PATIENTS: 80 patients with solitary solid cold thyroid nodules found to be benign at cytologic examination were randomly assigned to no treatment, suppressive levothyroxine (thyroid-stimulating hormone level, < 0.3 mU/L), or low-dose potassium iodide (2 mg every 2 weeks). Seventy patients completed the 1-year study. After 1 year, patients receiving treatment discontinued drug therapy and were re-evaluated 4 months later; patients receiving no treatment were given levothyroxine and were followed for a second year. MEASUREMENTS: Nodule volume was measured by ultrasonography at 4-month intervals by an observer masked to treatment assignment. RESULTS: Mean nodule volume decreased by 40% of the basal volume in the 23 patients receiving levothyroxine (P < 0.001) and by 23% of the basal volume in the 25 patients receiving potassium iodide (P = 0.053). Volume slightly increased in the 22 untreated patients (P = 0.085). A clinically relevant reduction in nodule volume (> or = 50%) was observed in 9 of 23 patients treated with levothyroxine, in 5 of 25 patients treated with potassium iodide, and in none of 22 untreated patients (P = 0.004). Only nodules with a volume of 10 mL or less were reduced; nodules with volumes of 5 mL or less shrank most frequently. Nodule volume did not relevantly increase in treated patients but did increase in 3 of the 22 untreated patients. Drug withdrawal resulted in an increased mean nodule volume (P = 0.004) after 4 months. CONCLUSIONS: Levothyroxine and, to a lesser extent, potassium iodide are effective in arresting the growth or in reducing the volume of benign solitary solid cold thyroid nodules, especially small ones; discontinuation of therapy may result in resumed nodule growth.
The ultrastructural changes produced by iodine-potassium iodide solution on yeast cells of Sporothrix schenckii were investigated by transmission electron microscopy in order to clarify the mechanism of oral potassium iodide therapy for sporotrichosis. Yeast cells were dipped with solutions containing various concentrations of iodine. The rate of germination decreased markedly between the range of iodine concentrations from 0.63 microgram/ml to 5.0 micrograms/ml. No significant ultrastructural changes were seen at the concentration of the iodine of 1.25 microgram/ml (80% germination) or less. In the concentration of 2.5 micrograms/ml (50% germination), normal cells and degenerated cells coexisted. When the cells were treated with 5.0 micrograms of iodine per ml (0% germination) or more, their interior structures were completely destroyed. It is assumed that iodine treatment of the organism causes rapid destruction in the whole cell.
The consequences of iodine deficiency occurring still in Poland include serious health disorders in the population, such as psycho- somatic retardation, hypothyroidism, endemic goitre, even cretinism. Administration of iodized edible salt with daily diet is an effective method for prevention of iodine deficiency. The condition of success is the proper level of potassium iodide in this salt and adequate distribution of iodized salt in various regions of the country. Successful iodine prophylaxis should be based on iodination of edible salt in amounts of 30 +/- 10 mg of KJ/kg. The permission given in the period from February to May 1994 by the General Sanitary Inspector for the production and marketing of edible salt iodized in proportions of 30 +/- 10 mg KJ/kg opened the possibility of starting its production in salt mines. The purpose of the presently reported work was to assess, in cooperation with the Province Sanitary Epidemiological Stations, the adequacy of iodination of the Polish edible salt produced in the years 1994-1995. The study was carried out according to the Polish Standard "Salt (Sodium Chloride) /PN-80/C-84081.35. Potassium iodide determination by photo colorimetric method." In 1995 the number of edible salt samples analyzed was 2484, and this number included 2129 samples of iodized salt. Potassium iodide content agreeing with the above permission was found in 122 samples, that is in 57.4% of iodized salt samples. In 603 samples (28.3%) of iodized salt this content was below that given in the permissions. In 1994 this study was carried out taking 2172 samples of edible salt, including 1586 samples of iodized salt. The content of potassium iodide agreeing with the permissions (30 +/- 10 mg/kg) was found in 342 samples (28, 1%), but 272 (22.4%) samples of iodized salt produced by salt mines contained lower amounts of potassium iodide than the amount indicated in the permissions, but still within the limits set down in the Polish Standard (20 +/- 5 mg/kg). The obtained results (57.4%) indicate an improvement of the process of salt iodination as compared with the results obtained in 1992 and 1993 (38.3%) and 1994 (28.1%). However, varying amounts of potassium iodide differing from the accepted values were found in salt declared as iodized.
A 73-year-old man was initially seen with a 15-year history of intermittent fevers and had been treated for culture-negative subacute bacterial endocarditis. He had been taking potassium iodide as a bronchorrheic agent for approximately the same 15-year period, and, when potassium iodide therapy was discontinued, the fever resolved and has not recurred during 2 1/2 years of observation. The possible mechanisms of fever caused by potassium iodide and current clinical indications for potassium iodide use are described.
The development of iododerma in a 75-year-old male following administration of potassium iodide is described. Recovery from the allergic manifestation of iododerma occurred after discontinuation of potassium iodide. The adverse effects of potassium iodide and the general signs of acute and chronic iodine toxicity are reviewed.
A clinical picture and dynamics of metabolic indicators were examined in 40 goats suffering from iodopenia; the examinations took place in the course of potassium iodide application. Crystalline kalium iodatum was administered to all animals in barley groats at a dose of 0.5 g per animal/day within three weeks; then a three-week withdrawal followed and the treatment was repeated within the same time period. The thyroid gland consistency started to change at the end of the 3rd week of treatment when the tough elastic to tough thyroid became the soft one. The goiter started to disappear gradually from the 8th week of experiment and the physiological state of this organ was normal in most animals in the 11th week. Among the biochemical indicators, the most sensitive response to treatment was recorded in iodine and thyroxine concentrations in blood serum since their significant increase in comparison with the values before potassium iodide application was obvious on day 14 of treatment (P < 0.01). Return of total lipids and cholesterol content to the physiological limits occurred within two weeks while in glucose it was in the 7th week of treatment. A significant increase in serum immunoglobulins was recorded from day 14 to the end of experiment (P < 0.01). Among the minerals analyzed, positive responses in blood serum to potassium iodide intake were determined in the concentrations of calcium, phosphorus, copper and zinc. Application of potassium iodide to affected goats had positive effects on the dynamics of leukocytes from the end of the 2nd week (P < 0.01), of erythrocytes from the 7th week (P < 0.01), of hemoglobin and hematocrit value at the end of experiment (P < 0.05 and P < 0.01, resp.).
Hyperthyroidism developed in three patients during the administration of potassium iodide given for the purpose of blocking the thyroid uptake of radioactive iodine liberated in the course of the 125I-fibrinogen test. In a consecutive series of 31 geriatric patients, who received potassium iodide for the same reason, biochemical hyperthyroidism developed in three instances and significant depression of thyroid function was observed in 10. The performance and the interpretation of the 125I-fibrinogen test are unaffected if iodide is not administered to the patient. The possible hazards to some patients of either induced hyperthyroidism or faulty assessment of thyroid function may be greater than the risk of thyroid irradiation. It is suggested that for the performance of the 125I-fibrinogen test potassium iodide need not be given to the elderly and should be given in a dose of 30 mg daily for two weeks to younger patients. Under certain circumstances potassium perchlorate may be a preferable drug for preventing the accumulation of radioactive iodine by the thyroid.
We assessed the efficacy of the combination of propranolol and potassium iodide in the preparation of patients with Graves' disease for thyroid surgery. Potassium iodide was given orally in a dose of 60 mg three times a day for 10 days before operation in 10 patients who were already receiving propranolol. In contrast to previous experience with either drug used singly, the combined regimen caused a significant fall in mean serum total thyroxine and triiodothyronine to levels in the euthyroid range before operation (P less than 0.001). There was also a significant fall (P less than 0.05) before operation and transient rise after operation in serum reverse triiodothyronine. These preliminary results suggest that the combination of potassium iodide and propranolol may prove to be the optimum preoperative preparation for patients with Graves' disease.
300 microgram of potassium iodide daily were administered over a period of two weeks to 12 children with goitre. Basal TSH concentrations, maximal TSH increase after TRH and integrated TSH secretion after TRH were significantly decreased in this group whereas the increase of total thyroxine (T4-RIA) did not reach significance. It appears that in the development of iodine deficiency goitre in children a sensitive feed-back system is predominant. Early administration of iodine or even better general iodinated salt prophylaxis seem to be the pathogenetically correct approach in solving the common goitre problem.