Urethritis due to Chlamydia trachomatis.

Ninety-five men suffering from gonococcal urethritis were treated and observed. Forty-nine developed postgonococcal non-specific urethritis (PGU). Seventeen men were demonstrated to be free from PGU after careful observation; these formed a control group. Chlamydia trachomatis was isolated from urethral material from 26 (53%) of the PGU group but from none of the controls. This difference was highly significant (P less than 0-001). It confirms that C. tachomatis is a pathogen in the urethra. The presence of specific IgM antibody to C. trachomatis in serum from some men developing PGU, from whom that organism was isolated, suggests that the infection was recent in those cases. Ureaplasma urealyticum (T strain mycoplasma) was isolated from urethral material taken from 22 (45%) of the 49 men in the PGU group, and from 12 (71%) of the 17 in the control group. Mycoplasma hominis was isolated from 10 (20%) of the 49 men in the PGU group, and from four (24%) of the 17 men in the control group. Thus, no evidence was obtained that mycoplasmas (U. urealyticum, M. hominis) are patogenic in the urethra.

Inappropriate TSH secretion. Paradoxical rise in serum TSH in response to thyroxine therapy.

Serum thytropin (TSH) in a 45-year-old woman suffering from Hashimoto's thyroiditis and hypothyroidism rose over a period of 8 months from 23 to 98 muU/ml while on 0.15 mg of thyroxine daily. A significant pituitary tumor was excluded and the response of other anterior pituitary hormones to provocative stimuli were normal. The TSH response to thyrotropin releasing hormone (TRH) carried out after a year of therapy and while on 0.15 mg T4 was exaggerated and required 100 mug of triiodothyronine (T3) daily in addition to the thyroxine replacement to suppress it. After the completion of the T3 suppression test and while on 0.2 mg thyroxine, serum TSH rose from less than 0.5 to 27 muU/ml when seen last. It is postulated that in this patient there exists a partial selective resistance of the thyrotrophs to T4 and that the paradoxical increase in serum TSH associated with thyroxine therapy results from T4 dependent increase in the synthesis and secretion of endogenous TRH. Other possibilities include an as yet undetected pituitary microadenoma or a pituitary defect in the deiodination of T4.