Effects of psychological intervention on panic attack patients in the emergency department.

For patients initially seen in the emergency department (ED) for panic attack, this study evaluated the effect of two brief psychological interventions in the ED on later utilization of emergency, psychiatric, and nonpsychiatric medical department services. Each of the two intervention groups received usual ED care, a brochure on panic disorder, and a referral to treatment at the psychiatry department; one of the two groups also received 20-30 minutes of contact with a representative from the psychiatry department. Both intervention groups were compared with a historical control group. The contact condition reduced ED use after the initial visit to the ED, although all three groups had more visits to the psychiatry department and to all nonpsychiatric departments. This decrease was statistically significant (P = 0.0017) when compared with the brochure condition but not when compared with the historical control group (P = 0.0672). The decrease seen in ED use is an important therapeutic and economic finding.

Paradox as epistemological jump.

Recent articles on paradoxical interventions tend to view them as something given by a therapist to a patient, thus unintentionally adopting a unidirectional view of causality and an outmoded epistemology. It is postulated that change takes place in the context of a patient-therapist relationship and that when that relationship becomes paradoxical it becomes more difficult for the patient to view himself as a reified "thing." Paradox effects change, then, by altering the meaning of experience and modifying epistemological assumptions.

Levothyroxine replacement dose for primary hypothyroidism decreases with age.

We studied 23 elderly (other than 65) and 44 younger ambulatory adult patients with primary hypothyroidism to ascertain the dose of levothyroxine needed for complete replacement in relation to age. The elderly patients (average age, 75.7 years) needed an average 118 microgram/d whereas the younger patients (average age, 48.1 years) needed 158 microgram/d. The data indicate that thyroxine requirement may decrease continuously with age. This decrease probably reflects the progressive decrease in thyroxine degradation rate that occurs with age.

Clinical hypothyroidism in the elderly--a preventable disorder?

Among 27 ambulatory aged patients receiving thyroxine therapy for hypothyroidism, 4 had the "failing thyroid syndrome" (FTS) and 23 had frank clinical hypothyroidism. Patients with FTS are asymptomatic and the subnormal thyroid function is recognized only by a high level of serum thyrotropin (TSH) with a normal level of thyroid hormone (thyroxine or triiodothyronine). They require a smaller dosage of thyroid hormone for replacement initially. Identification of these cases through routine blood analyses for TSH in patients at risk (those with a history of Graves' disease or Hashimoto's thyroiditis) may permit early treatment of incipient hypothyroidism and the prevention of clinical hypothyroidism. Since there is a reduction in the thyroxine dosage required for complete replacement with age, the expected final replacement dosage when the thyroid fails completely is less than that reported for younger adults. This is true for patients with FTS, for patients with newly diagnosed clinical hypothyroidism, and for patients with long-established hypothyroidism receiving replacement therapy. The thyroid replacement dosage should be adjusted both for age and for body weight to avoid overdosage and thyroid toxicity, to which the elderly are particularly sensitive.

Variable thyrotropin response to thyrotropin-releasing hormone after small decreases in plasma free thyroid hormone concentrations in patients with nonthyroidal diseases.

Although a normal serum thyrotropin (TSH) concentration is generally considered to be the most important finding to support the clinical impression of euthyroidism in patients with nonthyroidal diseases and decreased serum triiodothyronine (T(3)), the regulation of TSH secretion in sick patients has not been studied previously. Accordingly, we studied the regulation of TSH secretion in 23 patients with nonthyroidal diseases; 15 of the patients had decreased serum T(3). TSH regulation was studied by measuring the TSH response to injected thyrotropin-releasing hormone (TRH) before and after effecting a small decrease in serum thyroxine (T(4)) and/or T(3) concentrations by iodide treatment, 262 mg daily for 10 d. Iodide treatment significantly decreased (> 10%) the free T(4) index (FT(4)-I) and/or free T(3) index (FT(3)-I) in all patients. FT(4)-I values were correlated (0.611, P < 0.001), with free T(4) concentration determined by equilibrium dialysis. Despite decreased FT(4)-I and/or FT(3)-I after iodide treatment in all patients, the TSH response to TRH after iodide treatment was augmented in only 8 of 15 patients who had decreased serum T(3) (group 1) and in only 5 of 8 patients who had a normal serum T(3). Mean base-line TSH concentration was increased significantly (P < 0.05) from 0.9+/-0.1 to 1.5+/-0.3 muU/ml in group 1 only. Comparison of the mean TSH response to TRH showed that there was no significant difference between groups 1 and 2. Moreover, no significant difference in thyroidal parameters was observed between patients who had augmented TSH response to TRH after iodides and those who had either similar or decreased TSH response irrespective of the initial serum T(3). These studies show that an augmented TSH response to TRH in response to a small reduction in serum T(4) and T(3) concentration occurred in only 57% of the entire group of patients with nonthyroidal diseases and that the presence or absence of a normal TSH response to this stimulus did not seem to be related to the base-line serum T(3) concentration. Because an increase in serum TSH in response to decreased serum T(4) and T(3) did not occur in about one-half of patients with nonthyroidal diseases, normal serum TSH may not be a reliable index of the euthyroid state in these patients.