Marc Bonnyns

PRECLINICAL HYPOTHYROIDISM: A RISK FACTOR FOR CORONARY HEART-DISEASE

Abstract In a systematic study, 406 female and 400 male patients admitted to clinical wards for miscellaneous non-thyroid diseases were screened for thyroid antibodies and serum-cholesterol levels. The clinical and laboratory data were analysed by computer. In the female population asymptomatic thyroiditis (i.e., preclinical hypothyroidism) represents an important risk-factor for coronary heart-disease (C.H.D.). It abolishes the well-established sex-ratio for C.H.D. Increased levels of serum-cholesterol may play a part in this pathogenic mechanism. However, an alternative explanation is that a genetic factor may be responsible both for the tendency to develop atherosclerosis and for the lymphocytic thyroiditis.

CLINICAL AND PATHOLOGICAL SIGNIFICANCE OF ASYMPTOMATIC ATROPHIC THYROIDITIS: A Condition of Latent Hypothyroidism

Abstract By the Boyden tanned-red-cell test, thyroglobulin antibodies (T.G.A.) have been detected in a large percentage of over 2000 patients admitted to hospital for various diseases. Post-mortem controls in nearly 250 cases with and without circulating T.G.A. have indicated a very high correspondence of these antibodies with the presence of a process of atrophic asymptomatic thyroiditis. This condition, which is to be distinguished from Hashimotos thyroiditis, is prevalent in women and its incidence increases with age. Its development is associated with other autoimmune diseases, with diabetes, and with obesity. Although clinical signs of hypothyroidism are absent, biological signs are indicative of latent thyroid failure.

Coma due to water intoxication in beer drinkers

Abstract Twelve cases of neurological syndrome due to severe hyponatraemia were investigated. Serum-sodium levels ranged between 120 and 98 meq. per litre. Neurological signs included disorders of consciousness (stage I and II coma) sometimes associated with pyramidal signs or epileptic attacks. In all cases where the electroencephalogram was recorded, it showed diffuse theta and delta waves. Hypokalaemia was frequent. In no case were there signs of intracranial hypertension. Necropsy in three cases, after correction of hyponatraemia, showed no lesions of cerebral œdema, but there were lesions characteristic of alcoholic encephalopathy in two cases. In all twelve cases, a sodium-depletion factor lay at the origin of the hyponatraemia, often associated with a dilution factor. In the seven most severe cases of hyponatraemia there was beer potomania. The importance of this factor in the pathogenesis of hyponatraemia may be explained by sodium deficiency in the diet, the absorption of large quantities of water, and the possible role of inappropriate secretion of antidiuretic hormone in these alcoholic patients. Under adequate treatment the neurological symptoms disappeared in all cases.

Natural history of primary myxedema

It is generally admitted that primary myxedema in adults is the outcome of autoimmune atrophic thyroiditis. The present review traces the natural history of this process from its incipient biologic and genetic anomalies up to its protracted asymptomatic course, clinical development, and eventual lethal complications. The apprehension of preclinical hypothyroidism may change a clinicians outlook on early diagnosis and therapy.

Asymptomatic Atrophic Thyroiditis

Asymptomatic atrophic thyroiditis (AAT), one of the three variants of autoimmune thyroiditis, is characterized by the presence of serum antithyroid antibodies in good correlation with thyroid lymphoplasmocytic infiltrations. AAT affects 5-15% of the general population and is especially prevalent in elderly women. Patients with AAT have no goitre and are clinically euthyroid. While circulating thyroid hormones are always in the normal range, peak TSH and TRH and basal TSH values are increased in two thirds of the cases. There is a familial aggregation of AAT and a frequent association with other autoimmune diseases. Development of overt hypothyroidism in AAT patients is not rare. Preventive thyroid replacement therapy is indicated in patients with elevated basal TSH levels.

LONG‐ACTING THYROID STIMULATOR AND THYROID FUNCTION IN RELATIVES OF PATIENTS WITH GRAVES’DISEASE

In ten families, fifty relatives and seven husbands of ten patients with untreated Graves’disease were submitted to clinical examination, biological and immunological investigations. They were compared with fifty control subjects. In the relatives, thyroid diseases were found in 26%, positive LATS‐IgG responses in 30%, thyroid antibodies in 23% and abnormal NBEI in 30%. The mean LATS response was significantly greater than in controls. With one exception no overt hyperthyroidism was found in the relatives on the basis of serum PBI, T3 resin uptake test, total T4 and TSH level. From the analysis of the pedigrees, no definite mode of inheritance can be found for LATS and NBEI. These data suggest the existence of a thyroid metabolic anomaly in the families of patients with thyrotoxicosis and argue against LATS as the cause of the hyperthyroidism of Graves’disease.

Screening for thyroid diseases.

Sirs, Once again, the cost-benefit ratio of screening for thyroid diseases was questioned in a recent issue of this journal (Small et al., 1990). The authors suggested that screening is unjustified except in a selective group of medical patients. Recently, in a one-year study, we reported the prevalence of thyroid biochemical abnormalities (TBA) in 4302 patients at admission in the department of medicine (Bonnyns & Bourdoux, 1990). Roughly, we observed a similar prevalence of thyroid disease (2%) and a slightly higher prevalence of low serum T3 or T4 (18.6%). However, our results deserve some comments. In our patients with low-T4 syndrome, a low serum TBG accounted for 82% of these results while 7.5% were hypothyroid. Unexpectedly, elevated T4 and/or T3 were observed in 6.7% of our patients of whom 36% had also elevated serum TBG while 13% were hyperthyroid. All other patients with high T4 or T3 were euthyroid and most of them had acute non-thyroid illness. In our study, in euthyroid sick patients with normal TBG, hyperthyroxinaemia was by far more frequent than the classical picture of low-T4 syndrome. Thyroid disease accounted for 16.6% of patients with TBA and one out of 100 ill patients presented with hyper or hypo-thyroidism diagnosed solely on the basis of biochemical thyroid screening. As treatment of thyroid disease was usually followed by a marked improvement in the non-thyroid illness, we strongly advocate a biochemical thyroid screening in hospitalized patients, particularly in those over 50-60 years. Such biochemical screening is efficient when it includes a concomitant determination of TBG and provided results are correctly interpreted. M . Bonnyns and P . Bourdoux Saint Pierre University Hospital, Free University of Brussels, Belgium

Thyroidal release after oral administration of TRH in normal subjects

The oral administration of 40 mg TRH to 17 normal volunteers induced a greater TSH response in females than in males, contrasting with an identical pattern of total T3 and T4 (TT3, TT4) and of free T3 and T4 (FT3, FT4). TSH peaked at 180 min while thyroid hormones (total and free) reached their maximum at 360 min. The drop in the T4 to T3 ratio (total and free hormones) observed at 360 minis consistent with an initial preferential T3 secretion. At 360 min the thyroglobulin (Tg) levels were still in the basal range while at 24 h a significant increase was observed, essentially in female subjects. Thus T3, T4 and Tg seem to be sequentially secreted by the thyroid in response to a prolonged TSH stimulus.

The diagnosis of pheochromocytoma. Review of the literature apropos of a case

SummaryA case of pheochromocytoma is described and confirmed by histological and biochemical study of the adrenal medulla. The authors review in detail the current methods of establishing the diagnosis of this disease and they briefly comment on the possible treatments.