ObjectiveIn vitro experiments and in vivo studies on rodents demonstrate that N-terminal 14, 15, 16, 17, and 18 kDa fragments prolactin-related vasoinhibin (PRL-V) of human PRL are natural inhibitors of neovascularization in the retina and elsewhere. These N-terminal PRL fragments belong to a family of peptides named vasoinhibins, which act as endogenous regulators of angiogenesis and vascular function. These observations led to the hypothesis that PRL-V could play a role in the pathophysiology of diabetic retinopathy in humans. The purpose of this study was to investigate whether patients with diabetes mellitus and diabetic retinopathy have aberrant concentrations of PRL-V in the circulating blood.Research designWe performed a case–control study and developed a new technique to semi-quantitatively determine PRL-V in serum samples from 48 male subjects. The case group consisted of 21 patients with diabetes mellitus and proliferative or non-proliferative diabetic retinopathy. The control group consisted of 27 healthy subjects with no history of diabetes mellitus.MethodsFor the detection of PRL-V, we developed a new analytical method, consisting of immunologic and laser-induced fluorescence techniques.ResultsThe case group had significantly lower PRL-V serum concentrations than the control group (P=0.041). There was no significant difference between patients with proliferative and those with non-proliferative diabetic retinopathy.ConclusionWe conclude that given the antiangiogenic and antivasopermeability actions of PRL-V, the decreased serum levels of PRL-V in patients with diabetes mellitus could contribute to the development and progression of diabetic retinopathy.

Serum triiodothyronine (T3) concentrations have been measured in 7 patients with euthyroid endocrine exophthalmos and in 8 patients with hyperthyroidism. These results have been assessed in relation to other tests of thyroid function. The non-suppressibility of euthyroid endocrine exophthalmos is due to elevated endogenous T3 levels and correlated to a negative response of the pituitary gland to TRH. In hyperthyroid patients who are euthyroid under antithyroid drug therapy, no general correlation of routine laboratory data with T3 levels, suppressibility and TRH response could be found. There is a gap between normal T3 and T4 levels and the restoration of the normal TRH response. A condition is described in which euthyroid patients show thyrotoxic behaviour of the pituitary receptors.

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