Anorexia, weakness, restlessness and parkinsonism associated with hypokalemia following radioactive iodine therapy

Media

Part of Acta Medica Philippina

Title
Anorexia, weakness, restlessness and parkinsonism associated with hypokalemia following radioactive iodine therapy
Creator
Campos, Paulo C.
Lamas, Irineo
Manipol, Visitation
Clemente, Alicia O.
Language
English
Source
Volume XV (2) October-December 1958
Year
1958
Subject
Iodine -- Isotopes -- Therapeutic use
Thyroid gland -- Cancer -- Treatment
Hypokalemia -- Diagnosis
Medicine -- Periodicals
Rights
In Copyright - Educational Use Permitted
Fulltext
ANOREXIA, WEAKNESS, RESTLESSNESS AND PARKINSONISM ASSOCIATED WITH HYPOKALE· MIA FOLLOWING RADIOACTIVE IODINE THERAPY PAULO C. CAMPOS, M.D., IRINEO LAWAS, B.S.Chem. VISITACION MANIPOL, B.S.Chem. and ALICIA 0. CLEMENTE U. P. - P. G. H. Medical Cente,. 111 a series of 52 hyperthyroid patients treated with varying doses of radioactive iodine, we have observed in 10 of the patients symptoms very suggestive of a thyrotoxic aggravation - a worsening of the exophthalmos, tremors, irritability, increased weight loss and hyperhydrosis. This aggravation usually appeared within the first two weeks following therapy and generally associated with elevation of the protein bound iodine values. Exacerbation of the hyperthyroid state following radioactive iodine therapy has been described in the literature and has occasionally been rel'errl'<I to as the "thyroxine release syndrome." This paper, however, deals with a set of symptoms observed in four of the 52 patients - symptoms which we feel are apart from those in the thyroxine release syndrome. The uniformity of the signs and symptoms Jlresented by the four patients, the consistency in the time of appearance and the correspondence of the biochemical observations in all the patients excited our curiosity. It is possible that the four cases are those of a delayed, severe or at~rpical thyroxine release syndrome. They seem more likely to be what many would call cases of thyroid storm or thyroirl crisis - a vague anrl ill rlefined syndrome which has defied undel'stanrling. CASES CASE No. 1 : L..L\l., -17 years old, female, Filipino, marrierl, developed t:>xophthalmos, itritabilitr. loss of weight and bluning· of vision of six weeks' dunit1on. She also had all the signs and symptoms of hyperthyroidism. She was given 6.8 millicuries of RAI. There was marked improvement after the treatment. 12:l 124 ACT A MEDI CA PBILJPPINA Three weeks after the treatment, she developed anorexia, marked weakness, restlessness, insomnia, dizziness, intention tremors, mask-1ike facies and Parkinson-like movements. Laboratory results: Blood sugar (2-10-58) - 112 mg. per cent Cholesterol (2-10-58) -180 mg. per cent Protein bound iodine (12-10-57) - 4.0 gamma per cent ( 2- 8-58) - 2.9 gamma per cent ( 9-26-58) - 3.3 gamma per cent Sodium (2-7-68) -141 meg/L Potassium (2-7-68) -3.1 meg/L Blood pressure - normal. CASE No. 2.: P.B., 47 years old, male, Filipino, married, businessman, had an the typical signs of toxicity (palpitation, hyper-irritabi1ity and fine tremors). He was seen by an outside physician and was given 9 millicuries. There was immediate improvement after the treatment with marked diminution of the signs an<l symptoms. Four weeks later, he developed anorexia, marked weakness, coarse tremors, sweating and insomnia. This weakness was first noticed in the lower extremities, so much that the patient could not stand up. It later progressed to complete paralysis of the upper and lower extremities. Auricular fibrillation which disappeared two weeks after RAI therapy recurred and the patient showed Grade V failure on admission. Laboratory results (10-7-58) : Sugar ---------------- 104 mg. per cent NPN ----------------- 34 mg. per cent Uric Acid ------------- 3.5 mg. per cent Cholesterol ____________ 226 mg. per cent Protein-bound iodine ____ 5.1 ganuna per cent Sodium ---------------144 meq/L Potassium ------------- 2.2 meq/L Chlorides -------------- 99 meq/L Blood pressure ---------normal CASE No. 3.: B.B., 44 years old, male, Filipino, married, lawyer, had an enlarged thyroid, exophthalmos and all the typ. ieal signs of toxic goiter for the past 6 years. A month ago, he HYPOKALEMIA AFl'ER RADIOIODINE THERAPY 125 was given RAI therapy - 6.8 millicuries. There was marked improvement immediateJy after the treatment, both symptomaticaUy and objectively. There was regression of the exophthalmos; paJpitation, restlessness and irritability were markedly diminished. Three weeks after the treatment he cleveloped auricular fibrillation, marked weakness, anorexia, restlessness ancl insomnia. In addition, he showed Parkinson-like movements of the upper and lower extremities. He was admitted with a temperature of 37.5°C.; Blood pressure - 166/90; Pulse rate - 120; Respiration rate - 24. Laboratory results : 1or, m,,. per "'nt 47 •• 2.2" Pro!cin·hnuruli<>dine. l!hJOd p..,....,.,._normal 9 m11. l"'r cent 9 mir. Pf!• cenl 127 ..-i/L .... 127 me<r/L ... CASE No. -:1.: E.P .. 53 years old, female, Filipino, nurse, marrierl, has been having toxic symptoms for the past 6 months. Exophthahnos was nokd 2 months ago. She received 7.62 milJicuries of RAJ. Four weeks later, she developed anorexia, marked weakness, restlessness and intention tremors, particularly of the lower extremities. She was anoretic and unable to sleep. Tremors progressed to classical Parkinsonism with typical masklike facies. This set of symptoms subsided after 10 clays. The patient is now obviously well. Laboratory results: (10-22-5~) 13S meq/I. 148 """l/L .... 163 meq/L (11·'·58) rH hlood 7.4! Pot.. .. ium • Chloride~ •.. Su.irnr Cho!erterol . Ph01phoro111 P.R.!. '·' •• 3.2" Pf!•<'<!•I 111-11-681 Uriner~ l7·kelo9terlod1 . BIPf"I n ....... ure-nnrrnal ••• Ill m(I" •• ..,,. <'<1111 . ... 263 •••• l!.2"' 3.2 .... 12 J'tftmmn. 1>er«nt f!J.13·6~) 7.6 mfl",/U hr•. .1.2~ mg,/24 hr• 126 ACfA MEDICA PHILIPPINA DISCUSSION These four cases have been investigated with particular emphasis on various biochemical parameters among which were: protein-bound iodine, cholesterol, blood suPr. calciumphosphorous, pH (blood), uric acid, serum electrolytes, urinary 17-KS and 17-0H steroid excretion, anrl electrocardiog.raphic examinations. Calcium-phosphorus values seem to be perfectly normal and no physical signs (Chvostek's, Trousseau's, Erb's) suggestive of hypoparathyroidism were demonstrable in any of the patients. Blood sugar values in all the patients were completely normal. Cholesterol values were perfectly within the normal range in all the cases. Protein-bound iodine was elevated within the first two weeks in two cases with progressive diminution within the 3rd week. The values at the time the symptoms were observed, however, ranged from elevated to low values. The serum electrolyte results were interesting. Sodium was normal in all the cases, but potassium values were persistently low, ranging from 2.2 to 3.5 meq/L at the period when the symptoms were most evident. Curiously, the lo\\'est potassium value observed (2.2 meq/L) was in the patient with quadriplegia. Chlorides were perfectly normal. The blood pressure was normal in all the cases. COMMENTS Aside from the obvious background of a severe thyrotoxic disease and equall:i.• obvious measures to suppress it, we have no definite idea what produces this set of symptoms and how it is produced. We can only suggest that whatever it is, it seems to be intimately or remotely related with potassium metabolism. One instinctively wondt>rs if the adrenal cortex might bt: the culprit. There are, however, no clinical signs that may suggest an increased or decreased arlrenocortical activity; 17-KS and 17-0H steroid excretion was normal. Moreover, we wonder why all these symptoms have not been more frequently obHerved after surgical removal of the gland. There is also the possibility that the development of the symptoms depend on the retention in the body of substances resulting from the destructiori of the HYPOKALEMIA AFI'ER RADIOIODINE THERAPY 127 gland rather than from the sudden removal of such substances from the body. Another possibility is that some of the radioactive iodine introduced may produce radioactive metabolic by.products which act on liver cells and result in the production of the symptoms. The level of radioactivity alone, however, does not seems to be a very important factor, for two reasons; ( 1) we have given much bigger doses for patients with cardiov111.scular complaints without observing this phenomenon and (2) the syndrome appears when radioactivity detectable in the liver is almost negligible. The marked anorexia observed with these patients suggest that the liver is somehow involved. It is also possible that these patients may have from the very onset some form of sub-clinical Parkinsonism. Even in such a situation, however, one can not ignore the fact that some biochemical event occurring in these patients has contributed to making this Parkinsonism clinically manifest. We feel justified in describing the set of symptoms as a syndrome for a number of reasons: 1. If it is a thyroid storm, then we may have here some biochemical data relative to a heretofore very vague syndrome. 2. In view of the almost classifical Parkinsonism that is observed, a stud:t• of the syndrome, may help considerably in elucidating the heretofore obscure problem of Parkinsonism. 3. In view of the consistent hypokalemia, one wonders at the wide possibilities for investigation. SUMMARY This paper covers our observation on four cases which we feel might represent some lmusual observations in connection with thyrotoxicosis and radioactive iodine therapy. They present principally in the form of anorexia, marked weakness occasionally progressing to complete quadriplegia, restlessness, tremors later on progressing •Parkinson-like movement, and auricular fibrillation. These symptoms come on ·or about the 3rd or 4th week after therapy and are especially observed in the severely thyrotoxic cases, regardless of whether or not they have received previous antithyroid therapy. The salient features of these cases can be summarized as follows: 128 ACTA MBDICA PBILIPPINA 1. All the cases uniformly presente<l marked weakness. Two cases showed classical Parkinson-like movement and masklike facies. 2. The syndrome appeared uniformly on the 3rd or ·Ith week after therapy. 3. All the patients presented significant hypokalernia corresponding to the severity of the manifestations. 4. AU the cases were severely thyrotoxic. Two were rendered euthyroid with Tapazole whi1e the others did not have any antithyroid preparation. 5. Calcium-phosphorus values were normal in all. 6. Cholesterol values were normal in all. 7. Protein-bound iodine values showed no rdation to the symptoms. Some presented elevated, others normal, while still others depressed PBI values. 8. Blood pH in a few was normal; this makes the possibility of alkalosis and acidosis coming into the picture quite unlikely. 9. Blood sugar was normal in all. 10. Serum sodium and chlorides were normal. 11. 24 hour 17-KS and 17-0H steroid excretion \nts within the normal range. 12. All the symptoms lasted from one to four weeks with spontaneous improvement in an cases. ACKNOWLEDGMENTS Acknowledgment is hereby made to Dr. Mario Gutierrez of the Department of Medicine, P.G.H., who helped take care of the cases; to Dr. Angel Florentin, also of the Department of Medicine, who did the urine 17-KS and 17-0H studies; to Mrs. Serapia Roque-Rubio, who did the serum electrolyte studies; and to the numerous patients of the Thyroid Clinic who wholeheartedly cooperated in the investigations. HYPOKAl,EMIA AFTER RADIOIODINE THERAPY 129 .. . .. l t LU EEKS Fiv. l A Casi' of Thyrnxi1w Rt'le-ast' S.\"IHlrnnw. WEE.KS Fig. 2 Case No. 1. 13-0 ACTA MEDICA PHILIPPINA WEEKS Fig. 3 Case No. :!. wt t Ks Fig. 4 Case No. 3. IL4' ... _ BYPOKALEMIA APfER RADIOIODINE THERAPY 131 ... l i WEEKS Fig. !i Case No. '1. -.. , ~. ~ ~--l :rt: .. :1 ! - . ~ :i ! t ~ •' I, .. ~· Fig. 6 Changes in Laboratory Findings.
pages
123-131