The serum prolactin (PRL), luteinizing hormone (LH), testosterone (T) and estradiol (E) levels were investigated in a group of male paranoid schizophrenics with delusional ideas of homosexual content, in a group of male paranoid schizophrenics without delusional ideas of homosexual content, and in a group of healthy, male heterosexual subjects. Only male paranoid schizophrenics with delusional ideas of homosexual content had significantly lower serum PRL values and significantly higher serum E levels than those of the age-matched group of normal, male heterosexual controls; also, these patients tended to have higher (though not to a statistically significant degree) serum LH and T levels than those of normal controls. Findings of this study are discussed within the framework of the possible involvement of endocrine factors in the occurrence of delusional ideas of homosexual content in male patients with paranoid schizophrenia.

Fifteen male paranoid schizophrenics underwent an initial 4-week therapy with haloperidol 7.5 mg/day, and a subsequent 4-week treatment with haloperidol 15 mg/day, p.o. (group I). Another 15 male paranoid schizophrenics received an initial 4-week treatment with haloperidol 30 mg/day, and a subsequent 4-week therapy with haloperidol 60 mg/day, p.o. (group II). In each group of patients, serum prolactin (PRL), luteinizing hormone (LH) and testosterone (T) levels were measured before treatment and at the end of the two consecutive periods of treatment. A dose-related increase in serum PRL levels was found in both groups of medicated patients. Serum LH levels were not significantly affected by haloperidol treatment. A significant decrease in serum T levels was detected only in group II medicated patients, i.e., in the patients who were treated with relatively high daily doses (30 or 60 mg/day) of haloperidol.

The mean values of serum thyroxine (T₄), in vitro radioactive triiodothyronine uptake and free-thyroxine index (FTI) in 41 drug-free schizophrenic patients did not differ significantly from those of euthyroid controls. Following 6 weeks’ treatment of 24 schizophrenics with chlorpromazine, trifluoperazine or clozapine, a significant decrease in serum T₄ and FTI was noted after chlorpromazine and clozapine, whereas after trifluoperazine only serum T₄ decreased, but not FTI. The questions arising from these fíndings are discussed and the need for a future investigation of serum triiodothyronine and serum TSH in schizophrenic patients before and after neuroleptic treatment is stressed.

Determinations of ABO blood types was carried out in 38 patients with obsessive-compulsive neurosis, 48 schizophrenics with anancastic symptomatology, 31 depressives with anancastic symptomatology, 260 schizophrenics free of anancastic symptomatology and 65 depressives free of anancastic symptomatology. Results were compared with a representative sample of the general population. The findings of the present study provide evidence of an association between obsessive-compulsive neurosis and phenotype A, whilst a similar association between ABO blood types and anancastic symptomatology occurring in the course of psychotic disorders was not found. The significance of these findings is discussed with regard to current diagnostic and aetiological issues in obsessive-compulsive neurosis.

Results of the present study provide evidence of: 1) a positive association between bipolar affective disorder and blood type O and a corresponding negative association between the former and blood type A, 2) a positive association between unipolar affective disorder and blood type O, and 3) a positive association between involutional depression and blood type A and a corresponding negative association between the former and blood types B and O. Sex does not appear to modify the ABO blood types' distribution in patients with bipolar, unipolar affective disorder, or involutional depression, and the same holds for early- or late-onset of the illness in patients with bipolar or unipolar affective disorders. Findings in the present study do not support the validity of the bipolar-unipolar distinction of affective disorders, and provide evidence in favour of the view that involutional depression is a genetically distinct nosological entity.