Rarity of Diabetic Retinopathy in Patients With Acromegaly

Ballintine, Elmer J.

doi:10.1001/archinte.1981.00340130069016

Cited by 18 publications

(7 citation statements)

References 13 publications

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“…In addition, there was no evidence of BRB breakdown. These observations agreed with the absence of increased retinopathy incidence in acromegalic patients (39) or in patients receiving GH replacement therapy (40). Altogether, these results demonstrated the lack of effect of high circulating IGF-I on the BRB and retinal tissues.…”

Section: Discussionsupporting

confidence: 85%

Increased Intraocular Insulin-like Growth Factor-I Triggers Blood-Retinal Barrier Breakdown

Haurigot

Villacampa

Ribera

et al. 2009

Journal of Biological Chemistry

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Blood-retinal barrier (BRB) breakdown is a key event in diabetic retinopathy and other ocular disorders that leads to increased retinal vascular permeability. This causes edema and tissue damage resulting in visual impairment. Insulin-like growth factor-I (IGF-I) is involved in these processes, although the relative contribution of increased systemic versus intraocular IGF-I remains controversial. Here, to elucidate the role of this factor in BRB breakdown, transgenic mice with either local or systemic elevations of IGF-I have been examined. High intraocular IGF-I, resulting from overexpression of IGF-I in the retina, increased IGF-I receptor content and signaling and led to accumulation of vascular endothelial growth factor. This was parallel to up-regulation of vascular Intercellular adhesion molecule I and retinal infiltration by bone marrow-derived microglial cells. These alterations resulted in increased vessel paracellular permeability to both low and high molecular weight compounds in IGF-I-overexpressing retinas and agreed with the loss of vascular tight junction integrity observed by electron microscopy and the altered junctional protein content. In contrast, mice with chronically elevated serum IGF-I did not show alterations in the retinal vasculature structure and permeability, indicating that circulating IGF-I cannot initiate BRB breakdown. Consistent with a key role of IGF-I signaling in retinal diseases, a strong up-regulation of the IGF-I receptor in human retinas with marked gliosis was also observed. Thus, this study demonstrates that intraocular IGF-I, but not systemic IGF-I, is sufficient to trigger processes leading to BRB breakdown and increased retinal vascular permeability. Therefore, therapeutic interventions designed to counteract local IGF-I effects may prove successful to prevent BRB disruption.

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Section: Discussionsupporting

confidence: 85%

Increased Intraocular Insulin-like Growth Factor-I Triggers Blood-Retinal Barrier Breakdown

Haurigot

Villacampa

Ribera

et al. 2009

Journal of Biological Chemistry

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“…Late diabetic complications were present in seven of the 31 clinical diabetics. Late complications of diabetes are believed to be rare in patients with acromegaly (Hamwi et al, 1960;Gordon et al, 1962;Ballintine et al, 1981) and the details of these patients are therefore given in Table 9. Now that it is possible to reduce the GH level to normal in some patients with acromegaly, it is important to study the effect this has on the diabetes.…”

Section: )mentioning

confidence: 99%

Acromegaly

Nabarro

1987

Clinical Endocrinology

500

303

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SUMMARY A personal series of 256 cases of acromegaly/gigantism seen over a 20‐year period from 1963 is described. The insidious nature of the condition resulted in delay in diagnosis which was often made by a doctor when seeing the patient for an unrelated problem. Other features which commonly led to the diagnosis being made were headache, change in appearance, carpal tunnel syndrome, amenorrhoea and diabetes. The Hardy system for grading the radiological appearance of the pituitary tumour was used. Widely invasive tumours were not common but tended to occur in patients with younger age of onset and high GH levels. The occurrence of various symptoms and clinical features was noted and the changes resulting from reducing the GH level to normal. The incidence of hypertension, but not of coronary artery disease, is increased and the blood pressure may be reduced following successful treatment. The effects on the upper and lower respiratory tract are reported as well as sleep apnoea and problems associated with anaesthesia. Skin manifestations included sweating, pigmented skin tags, acanthosis nigricans and cutis verticis gyrata. In the skeletal system the incidence of kyphoscoliosis and osteoarthritis especially of the hip is reported: the question of hip replacement is discussed. Diabetes mellitus disappeared in most cases if the acromegaly was cured. In men but not in women the incidence of colloid nodular goitre was increased as was hyperthyroidism in middle‐aged women. In two patients a parathyroid adenoma was present: hypercalcaemia was present in five additional patients, but the cause was not determined. The common occurrence of amenorrhoea in the younger women was noted, it was not always associated with hyperprolactinaemia, and often responded to successful treatment of the acromegaly. The association of acromegaly with hirsutism and galactorrhoea is confirmed. The incidence of impotence and loss of libido in the men is discussed: in a proportion of those in whom the acromegaly was cured, potency returned, but in a number depression occurred and what was believed to be psychogenic impotence persisted. Hyperprolactinaemia was found in 49 out of 151 patients with active acromegaly in whom the prolactin level was measured. Previous reports have indicated a doubling of death rates in acromegalics. In this series there were 47 deaths observed compared to 37.2 expected. The increased death rate was in women of all ages and in men under the age of 55. The increased deaths in the women were from cardiovascular and cerebrovascular causes and from breast cancer. To demonstrate cure it is emphasized that not only must the GH level be reduced to normal, but that suppression following a glucose load must be demonstrated and disappearance of abnormal responses for example to TRH, that would mark the persistence of adenoma cells, confirmed. Even so, late relapse may occur and GH levels should be checked regularly. Long‐term follow up (mean 9.4 years) of 102 patients after transsphenoidal surgery is reported. Eighteen pat...

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“…Indeed, the improvement in diabetic retinopathy after hypophysectomy can occur independently of GH‐suppression (18), clinical trials with the GH antagonist pegvisomant yield negative results (19), and circulating IGF‐I levels do not predict the incidence and progression of diabetic retinopathy (20). Moreover, severe cases of diabetic retinopathy are rare in patients with acromegaly (21), and diabetic retinopathy occurs in patients with congenital IGF‐I deficiency (Laron syndrome; Ref. 22).…”

Section: Diabetic Retinopathy and The Pituitary Glandmentioning

confidence: 99%

Prolactin and vasoinhibins: Endogenous players in diabetic retinopathy

et al. 2011

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SummaryDiabetic retinopathy is a disease of the retinal microvasculature that develops as a complication of diabetes mellitus and constitutes a major cause of blindness in adults of all ages. Diabetic retinopathy is characterized by the loss of capillary cells leading to increased vasopermeability, ischemia, and hypoxia that trigger the excessive formation of new blood vessels in the retina. The influence of the pituitary gland in the pathophysiology of diabetic retinopathy was recognized nearly six decades ago, but the contribution of pituitary hormones to this disease remains unclear. Recent studies have shown that the pituitary hormone prolactin is proteolytically cleaved to vasoinhibins, a family of peptides with potent antivasopermeability, vasoconstrictive, and antiangiogenic actions that can protect the eye against the deleterious effects of the diabetic state. In this review, we summarize what is known about the changes in the circulating levels of prolactin and vasoinhibins during diabetes and diabetic retinopathy as well as the implications of these changes for the development and progression of the disease with particular attention to hyperprolactinemia in pregnancy and postpartum. We discuss the effects of prolactin and vasoinhibins that may impact diabetic retinopathy and suggest these hormones as important targets for therapeutic interventions.

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Rarity of Diabetic Retinopathy in Patients With Acromegaly

Cited by 18 publications

References 13 publications

Increased Intraocular Insulin-like Growth Factor-I Triggers Blood-Retinal Barrier Breakdown

Increased Intraocular Insulin-like Growth Factor-I Triggers Blood-Retinal Barrier Breakdown

Acromegaly

Prolactin and vasoinhibins: Endogenous players in diabetic retinopathy

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