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S. VANNAS, M.D.; C. A. HERNBERG, M.D.; G. af BJÖRKESTEN, M.D.

AMA Arch Ophthalmol. 1959;62(3):370-380.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Proliferative diabetic retinopathy occurs as a dreaded complication of labile juvenile diabetes difficult to control with insulin. Prophylactically and therapeutically the blood sugar, fluid and electrolyte balance, and corticotropin (ACTH) and corticosteroid activity must be controlled.¹⁹ Among the drugs employed are cyanocobalamin (vitamin B₁₂) and antifragility and lipotropic substances.^6,11,15,19 It is sometimes possible to delay the disease, especially in the incipient phase, for years even.

When the proliferative process has burst out, however, the cure or at least the prevention of its progress often fails, unfortunately. Recurrent hemorrhages lead sooner or later to incurable blindness—and to painful secondary glaucoma—if the patient lives long enough.

Numerous experimental observations and clinical investigations show that the development of diabetic retinopathy is associated with adrenal cortical hyperfunction which may even be the cause of the retinopathy.^5-7,9 Hypophysectomy reduces the adrenal function. On the other hand, it is possible that both diabetes and diabetic retinopathy . . . [Full Text PDF of this Article]

Author Affiliations
Helsinki, Finland

From the Ophthalmic Hospital of the Helsinki University, the Finnish Red Cross Hospital, and the Maria Hospital.

Footnotes
Submitted for publication Dec. 31, 1958.

Presented at the meeting of the Finnish Ophthalmological Society, Helsinki, Nov. 29, 1958.

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