Neuro-osteoarthropathy (Charcot's joint) in diabetes mellitus following revascularization surgery. Three case reports and a review of the literature.

The initial primary defect in the development of neuro-osteoarthropathy is neuropathy. Our case reports and a review of the literature strongly implicate a neurally initiated vascular reflex leading to increased blood flow. This may play a pivotal role in the development of Charcot's joint in the neuropathic limb. Mechanical trauma in an insensitive foot is contributory, but it is probably a secondary mechanism.

Hyperthyroidism and diabetes mellitus. An analysis of 70 patients.

Hyperthyroidism developed in 70 patients with diabetes mellitus. Nine patients had masked hyperthyroidism with weight loss as the main sign. Diabetic control deteriorated in 28 of 48 insulin-dependent patients and in four of 22 taking hypoglycemic agents orally. Recurrent ketoacidosis occurred in two. Insulin requirements increased in 11 of 48 by 25% to 100% (mean, 50%). Following treatment of the hyperthyroidism, insulin requirements decreased in 13 of 48 by 20% to 100% (mean, 35%). Four of 22 patients were changed from orally ingested hypoglycemic drugs to insulin. Because of similar symptoms, underlying hyperthyroidism must be considered in any patient whose diabetes is poorly controlled.

Neuropathic arthropathy in the diabetic foot.

Neuropathic arthropathy (Charcot's joint) is a relatively painless, progressive and degenerative condition due to underlying neurologic deficits. Although a variety of neurologic disorders may produce this arthropathy, diabetes mellitus has become the most common cause. In diabetes, the foot and ankle are the sites most often involved, particularly the tarsometatarsal and tarsal joints. In addition to neuropathy, trauma is an essential factor in producing the arthropathy.

Primary adrenocortical insufficiency (Addison's disease).

In the United States the etiology of most cases of adrenal gland atrophy or destruction is unknown. Autoimmune processes may be responsible. With rare exceptions, all three zones of the adrenal cortex are destroyed and there is reduced glucocorticoid, mineralocorticoid and androgen secretion. Although the deficiency of glucocorticoid is probably the most severe threat to life, treatment is available to correct all the deficiencies. Patient education and preparedness can prevent serious complications.

Plasma and cerebrosponal fluid amino acid levels in diabetic ketoacidosis before and after corrective therapy.

To evaluate the effect of insulin-saline-bicarbonate therapy on amino acid metabolism in diabetic ketoacidosis, arterial and venous blood samples as well as cerebrospinal fluid (CSF) were obtained from six patients before and after initiation of corrective therapy. Levels of CSF glutamine were decreased while alanine alpha-amino-n-butyrate, valine, isoleucine and leucine were increased significantly compared to a control group composed of six normal, postabsorptive adults free of any neurologic disease. Following therapy, CSF levels of alanine, alpha-amino-n-butyrate, valine, isoleucine, and leucine declined while glutamine levels did not change. Admission arterial plasma levels of the glycogenic amino acids were lower than normal while the branched-chain amino acids were elevated. Plasma alanine and glutamine arterio-venous (A-V) differences across forearm tissue were larger. After four hours of corrective therapy, arterial plasma levels of most of the amino acids had declined sharply and A-V differences for glutamine and alanine were markedly reduced (p smaller than.025 and p smaller than.01, paired t, respectively). Coincident with the decrease in A-V amino acid differences, plasma glucagon and free fatty acid levels declined significantly. These data suggest that the effect exerted by insulin-saline-bicarbonate therapy on amino acid metabolism is manifested by diminished A-V plasma alanine and glutamine differences across forearm tissue. Thus, the role played by the splanchnic bed both before and following corrective measures may be secondary to substrate availability.

Plasma renin activity and blood volume in uncontrolled diabetes. Ketoacidosis, a state of secondary aldosteronism.

The renin-angiotensin-aldosterone system was evaluated in two types of uncontrolled diabetes: a) diabetic ketoacidosis, and b) nonketotic hyperglycemia. In thirteen patients with ketoacidosis, mean plasma renin activity (PRA) was 58 plus or minus 12 (S.E.M.) ng. per milliliter per hour and in four patients, plasma aldosterone was 82 plus or minus 17 ng. per 100 ml. Corresponding values for upright salt-depleted subjects were 13 plus or minus 2 and 62 plus or minus 8. In eleven diabetics with nonketotic hyperglycemia (mean glucose 318 plus or minus 19 mg. per cent), mean blood volume was 4,660 ml. and PRA 2.1 plus or minus .7. After control of the diabetes (mean glucose 129 plus or minus 13) blood volume was 4,553 ml. and PRA 3.3 plus or minus 1 (NS). The results suggest that: 1) diabetic ketoacidosis is a state of severe secondary aldosteronism, 2) no significant change in blood volume or PRA occurs during short periods of hyperglycemia, and 3) insulin is not necessary for renin release.