Retinopathy and Plasma Growth Hormone Levels in Idiopathic Hemochromatosis with Diabetes

Abstract

In patients with idiopathic hemochromatosis, retinopathy was investigated by ophthalmoscopy and fluorescein angiography and was present in eight out of 23; this prevalence is similar to that reported in patients with diabetes aged between 30 and 60 years at onset of diabetes and with the same duration of the disease; in these eight patients retinopathy was of mild degree, with no impairment of visual acuity, fewer than 10 microaneurysms in each fundus, and no other retinal abnormatic islets directly. These studies confirm that anticholinergic drugs may be useful adjuvants in treating these patients.

Roles of prolactin and related members of the prolactin/growth hormone/placental lactogen family in angiogenesis

“…Likewise, in two patients given GH following hypophysectomy, retinal neovascularization continued to develop (Ray et al 1968). Finally, GH deficiency in diabetic subjects is associated with reduced retinopathy when compared with diabetic controls (Merimee et al 1970, Passa et al 1977, Merimee 1978.…”

“…The initial implication stems from the observation that retinal neovascularization in diabetic patients diminished after the ablation of the pituitary gland (Poulsen 1953, Flyvberg 1990, Merimee 1990. Although the reduction in retinal vasculature could be attributed to the elimination of other pituitary hormones, the role of GH was supported by the correlation between diabetic retinopathy and elevated GH levels in the circulation (Johansen & Hansen 1969, Hansen & Johansen 1970, Passa et al 1977, Sundkvist et al 1984. Likewise, in two patients given GH following hypophysectomy, retinal neovascularization continued to develop (Ray et al 1968).…”

Growth hormone, prolactin and thyrotrophin responses to thyrotrophin-releasing hormone in diabetic patients

“…Pituitary ablation has been used to treat severe retinopathy with some success (Luft, Olwercroner and Sjogren, 1955;Joplin et al, 1965;Cullen et al, 1971;Kohner et al, 1976), and Lundbaek et al (1970and Lundbaek et al ( , 1971) have suggested a causal relationship between GH and the development of retinopathy in diabetics. This is also suggested by the report that retinopathy is worsened when GH is administered to pituitary-ablated patients (Ray et al, 1968). Secretion of GH is abnormal in some diabetics, plasma levels being elevated with more frequent and higher peaks compared to normal subjects (Corral et al, 1974).…”

“…Secretion of GH is abnormal in some diabetics, plasma levels being elevated with more frequent and higher peaks compared to normal subjects (Corral et al, 1974). In addition, the patterns of GH response to different stimuli such as exercise (Hansen, 1970;1971), glucose loading (Knopf et al, 1973), arginine (Passa et al, 1977), glucagon (Waldhausl et al, 1976) and the suppressive effect of TRH on L-dopa-promoted GH release (Dolva, Torjesen and Hanssen, 1976) are normal in diabetics. It is also possible that in diabetes there is an altered sensitivity in the mechanism for GH release which allows various stimuli either to produce an exaggerated pattern of GH release or, as with TRH, to promote release of GH, an effect which does not occur normally.…”

“…Plasma GH levels are also raised more easily in diabetics by stimuli such as exercise (Hansen, 1970(Hansen, , 1971, arginine (Passa, Rousselie and Ganville, 1977) and glucagon (Waldhausl et al, 1976). These quantitative differences in GH responses may partly explain the raised plasma GH levels in diabetics, but, in addition there may be qualitative differences in GH release as occurs in anorexia nervosa (Maeda et al, 1976;Harrower et al, 1977b) and chronic renal failure (Gonzalez-Barcena et al, 1973;Czernikow et al, 1976) where plasma GH levels are also often raised.…”