the same type of practice. A few physicians on leaving a psychiatric hospital are faced with a limited licence. The need is for more individual physicians, clinics, hospitals and medical schools to provide supportive supervision for physicians at this stage of rehabilitation, which is often the most difficult phase of treatment because so few such opportunities are currently available. The advice "Physician, heal thyself" has not worked. We need an expanded
outlook and network for physicians with psychiatric illnesses. MERVILLE 0. VINCENT, BA, MD, CM, MRC PSYCH, FRCP[C] Executive director M. RUTH TATHAM, MD Staff physician Homewood Sanitarium of Guciph Guciph, ON
References 1. VAILLANT GE, SOBOWALE NC, MCARTHUR C:
Some psychologic vulnerabilities of physicians.
N Engi I Med 287: 372, 1972 Physicians' use of mood-altering drugs. A 20-year follow-up report. N Engi I Med 282: 365, 1970 3. VINCENT MO: Physicians and alcoholism. Rep Alcohol 27: 5, 1969 4. Pa.itso. M: Drug and alcohol problems in physicians. Psychiatr Opinion 12: 14, 1975 5. JONES RE: Do psychiatrists cover up addiction of physicians? Ibid, p 36
2. VAILLANT GE, BRIGHTON JR, MCARTHUR C:
6. SHAPIRO
ET,
PINSKER
H,
SHALE
JH
III:
Mentally ill physician as practitioner. JAMA 232: 725, 1975 7. American Medical Association, council on mental health: The sick physician: impairment by psychiatric disorders, including alcoholism and drug dependence. JAMA 223: 684, 1973
Clinical application of triiodothyronine measurement Recent availability of the radioimmunoassay method for the measurement of serum triiodothyronine (T3) has increased our knowledge of the role of T3 in normal and abnormal thyroid function. Some established facts are: approximately 50 ,.g of T3 is secreted daily, compared with 80 .g of thyroxine (T4); blood concentrations of T3 approximate 100 ng/dl and of T4, 4 to 8 p.g/dl; in metabolic activity T3 is three times more potent than T4; and the biologic half-life of T3 is 2 days v. 7 days for T4. Thus T3 may be extremely important in metabolism. It has been suggested1 that T4 be viewed as a prohormone for T3, while T3 has two sources - direct secretion from the thyroid gland and peripheral monodeiodination of T4. The prohormone view has been challenged, however, by Chopra, Solomon and Chua Teco,2 who found normal values of T3 in clinically hypothyroid patients with an elevated value of serum thyroid stimLilating hormone (TSH) and subnormal values of free T4. They concluded that a normal concentration of free serum T3 in the absence of a normal concentration of free serum T4 is not sufficient to sustain euthyroidism. The measurement of T3 concentration in the blood presents problems: the cost will probably be higher than for T4 and T3 resin uptake determinations, and will not eliminate the need for these two standard tests. Assay for Ti must be sensitive enough to allow quantitative distinction between T3 and T4. Another methodologic variable is the degree of in vivo binding of T3 to thyroxine-binding globulin (TBG). Fortunately T3 is bound weakly to serum albumin and not at all to thyroxine-binding prealbumin. The most disturbing aspect of these considerations is the conclusion reached by Gharib, Ryan and Mayberry3 that certain local factors, perhaps dietary io-
dide, influence serum T3 values. Since the technical aspects of the assay method restrict its use to large centres, the problem of deriving information on normal values is of paramount importance and limits its usefulness. Even within a geographically localized population the intake of dietary iodide and exposure to iodine-containing compounds may not be uniform. Increased concentrations of serum T3 have been found in thyrotoxicosis (with or without concomitant increase in T4), in multinodular goitre, in autonomously functioning thyroid adenomas, in the early stages of development of Graves disease, after operation or iodine-13 1 (1311) therapy for thyrotoxicosis and as a compensatory mechanism in a failing thyroid gland. Determination of T3 is of greatest clinical assistance in patients who appear to be hyperthyroid but have normal concentrations of serum T4 and TBG and a normal 1311 uptake value, and in patients who appear euthyroid despite low concentrations of L and normal values of TBG, 1311 uptake and TSH. In the former, obtaining a T3 concentration that is abnormally high may obviate the need for a T3 suppression test. In the latter, the normal serum TSH value may indicate a euthyroid state or secondary hypothyroidism, so that the finding of a normal T3 concentration is crucial in establishing the true status of the thyroid gland. Patients with goitres from iodine deficiency or with enzymatic defects may have a normal concentration of T3 but a low concentration of T4 as a result of the selective stimulation of T3 production by elevated serum TSH levels. A recent study,4 although reporting on a limited number of subjects, indicated that serial estimations of T3 may provide the most reliable method of monitoring relapse in hyperthyroidism after discontinuation of antithyroid drug therapy. Elsewhere in this issue (page
Z96 CMA JOURNAL/AUGUST 21, 1976/VOL. 115
338) Walfish reviews these and other aspects of T3 and T4 interrelations. The practising physician need not yet order serum T3 measurement routinely; much information may be derived from the T4 value and T3 resin uptake or the free thyroxine index, coupled with 131J uptake (for hyperthyroidism) and with serum TSH value (for hypothyroidism). The basal metabolic rate, used to distinguish apparent hypo- or hyperthyroidism from true dysfunction, is no longer available in most centres. The recent interest in T3 metabolism does not mean that administration of T3 preparations will provide better therapy in situations where T4 preparations are now useful. Pure synthetic T4 is the preparation of choice because it is converted to T3 even in athyrotic patients, and because the serum concentration is conveniently measured in most laboratories. The use of pure T3 would impose the serious limitation that the T3 assay is not widely available as a check on appropriateness of dosage. Suppression of serum TSH applies only in the treatment of hypothyroidism, and the serum TSH assay is not universally available. C. REYNOLDS, MD, CM, MS, FRcP[C] Department of medicine St. Paul's Hospital Faculty of medicine University of British Columbia Vancouver, BC
References 1. OPPENHEIMER JH, SCHWARtZ HL, SURKs MI:
Propylthiouracil inhibits conversion of Lthyroxine to L-triiodothyronine. An explanation of the antithyroxine effect of propylthiouracil and evidence supporting the concept that triiodothyronine is the active, thyroid hormone. J Clin Invest 51: 2493, 1972 2. CHOPRA II, SOLOMON DH, CHUA Taco ON: Thyroxine. Just a prohormone or a hormone too? J Clin Endocrinol Metab 36: 1050, 1973 3. GHARIB H, RYAN RS. MAYBERRY WE: Tniodothyronine (T3) radioimmunoassay: a critical evaluation. Mayo Clin Proc 47: 934, 1972 4. MARSOEN
P.
HOWORTH
PJN,
CHALKLEY
5,
et al: Hormonal pattern of relapse in hyperthyroidism. Lancet 1: 944, 1975
outlook and network for physicians with psychiatric illnesses. MERVILLE 0. VINCENT, BA, MD, CM, MRC PSYCH, FRCP[C] Executive director M. RUTH TATHAM, MD Staff physician Homewood Sanitarium of Guciph Guciph, ON
References 1. VAILLANT GE, SOBOWALE NC, MCARTHUR C:
Some psychologic vulnerabilities of physicians.
N Engi I Med 287: 372, 1972 Physicians' use of mood-altering drugs. A 20-year follow-up report. N Engi I Med 282: 365, 1970 3. VINCENT MO: Physicians and alcoholism. Rep Alcohol 27: 5, 1969 4. Pa.itso. M: Drug and alcohol problems in physicians. Psychiatr Opinion 12: 14, 1975 5. JONES RE: Do psychiatrists cover up addiction of physicians? Ibid, p 36
2. VAILLANT GE, BRIGHTON JR, MCARTHUR C:
6. SHAPIRO
ET,
PINSKER
H,
SHALE
JH
III:
Mentally ill physician as practitioner. JAMA 232: 725, 1975 7. American Medical Association, council on mental health: The sick physician: impairment by psychiatric disorders, including alcoholism and drug dependence. JAMA 223: 684, 1973
Clinical application of triiodothyronine measurement Recent availability of the radioimmunoassay method for the measurement of serum triiodothyronine (T3) has increased our knowledge of the role of T3 in normal and abnormal thyroid function. Some established facts are: approximately 50 ,.g of T3 is secreted daily, compared with 80 .g of thyroxine (T4); blood concentrations of T3 approximate 100 ng/dl and of T4, 4 to 8 p.g/dl; in metabolic activity T3 is three times more potent than T4; and the biologic half-life of T3 is 2 days v. 7 days for T4. Thus T3 may be extremely important in metabolism. It has been suggested1 that T4 be viewed as a prohormone for T3, while T3 has two sources - direct secretion from the thyroid gland and peripheral monodeiodination of T4. The prohormone view has been challenged, however, by Chopra, Solomon and Chua Teco,2 who found normal values of T3 in clinically hypothyroid patients with an elevated value of serum thyroid stimLilating hormone (TSH) and subnormal values of free T4. They concluded that a normal concentration of free serum T3 in the absence of a normal concentration of free serum T4 is not sufficient to sustain euthyroidism. The measurement of T3 concentration in the blood presents problems: the cost will probably be higher than for T4 and T3 resin uptake determinations, and will not eliminate the need for these two standard tests. Assay for Ti must be sensitive enough to allow quantitative distinction between T3 and T4. Another methodologic variable is the degree of in vivo binding of T3 to thyroxine-binding globulin (TBG). Fortunately T3 is bound weakly to serum albumin and not at all to thyroxine-binding prealbumin. The most disturbing aspect of these considerations is the conclusion reached by Gharib, Ryan and Mayberry3 that certain local factors, perhaps dietary io-
dide, influence serum T3 values. Since the technical aspects of the assay method restrict its use to large centres, the problem of deriving information on normal values is of paramount importance and limits its usefulness. Even within a geographically localized population the intake of dietary iodide and exposure to iodine-containing compounds may not be uniform. Increased concentrations of serum T3 have been found in thyrotoxicosis (with or without concomitant increase in T4), in multinodular goitre, in autonomously functioning thyroid adenomas, in the early stages of development of Graves disease, after operation or iodine-13 1 (1311) therapy for thyrotoxicosis and as a compensatory mechanism in a failing thyroid gland. Determination of T3 is of greatest clinical assistance in patients who appear to be hyperthyroid but have normal concentrations of serum T4 and TBG and a normal 1311 uptake value, and in patients who appear euthyroid despite low concentrations of L and normal values of TBG, 1311 uptake and TSH. In the former, obtaining a T3 concentration that is abnormally high may obviate the need for a T3 suppression test. In the latter, the normal serum TSH value may indicate a euthyroid state or secondary hypothyroidism, so that the finding of a normal T3 concentration is crucial in establishing the true status of the thyroid gland. Patients with goitres from iodine deficiency or with enzymatic defects may have a normal concentration of T3 but a low concentration of T4 as a result of the selective stimulation of T3 production by elevated serum TSH levels. A recent study,4 although reporting on a limited number of subjects, indicated that serial estimations of T3 may provide the most reliable method of monitoring relapse in hyperthyroidism after discontinuation of antithyroid drug therapy. Elsewhere in this issue (page
Z96 CMA JOURNAL/AUGUST 21, 1976/VOL. 115
338) Walfish reviews these and other aspects of T3 and T4 interrelations. The practising physician need not yet order serum T3 measurement routinely; much information may be derived from the T4 value and T3 resin uptake or the free thyroxine index, coupled with 131J uptake (for hyperthyroidism) and with serum TSH value (for hypothyroidism). The basal metabolic rate, used to distinguish apparent hypo- or hyperthyroidism from true dysfunction, is no longer available in most centres. The recent interest in T3 metabolism does not mean that administration of T3 preparations will provide better therapy in situations where T4 preparations are now useful. Pure synthetic T4 is the preparation of choice because it is converted to T3 even in athyrotic patients, and because the serum concentration is conveniently measured in most laboratories. The use of pure T3 would impose the serious limitation that the T3 assay is not widely available as a check on appropriateness of dosage. Suppression of serum TSH applies only in the treatment of hypothyroidism, and the serum TSH assay is not universally available. C. REYNOLDS, MD, CM, MS, FRcP[C] Department of medicine St. Paul's Hospital Faculty of medicine University of British Columbia Vancouver, BC
References 1. OPPENHEIMER JH, SCHWARtZ HL, SURKs MI:
Propylthiouracil inhibits conversion of Lthyroxine to L-triiodothyronine. An explanation of the antithyroxine effect of propylthiouracil and evidence supporting the concept that triiodothyronine is the active, thyroid hormone. J Clin Invest 51: 2493, 1972 2. CHOPRA II, SOLOMON DH, CHUA Taco ON: Thyroxine. Just a prohormone or a hormone too? J Clin Endocrinol Metab 36: 1050, 1973 3. GHARIB H, RYAN RS. MAYBERRY WE: Tniodothyronine (T3) radioimmunoassay: a critical evaluation. Mayo Clin Proc 47: 934, 1972 4. MARSOEN
P.
HOWORTH
PJN,
CHALKLEY
5,
et al: Hormonal pattern of relapse in hyperthyroidism. Lancet 1: 944, 1975
