The incidence and mechanism of painless myocardial ischaemia on exercise testing in diabetic patients is not clear. Therefore, two studies were performed. Retrospectively, all exercise tests carried out in our hospital during the past 5 years were reviewed for silent ischaemia. Prospectively, diabetic patients with known or suspected coronary artery disease underwent autonomic function testing and a second exercise test. Of 1653 exercise tests reviewed, 247 were positive (ST depression greater than 0.1 mV). Of the 29 diabetic patients with positive tests 20 (69%) had painless ST depression, compared with 77 (35%) of the 218 non-diabetic patients (p less than 0.001). The diabetic patients with painful and painless ST depression were comparable for age, sex, therapy, but the 20 with no pain on exercise testing had a longer duration of diabetes and a higher incidence of microvascular complications than the 9 with pain (70 vs 22%, p less than 0.05). In the prospective study, 12 of 30 diabetic patients with positive exercise tests had pain in association with ST depression and 18 had no pain. Six patients had mild and 12 severe autonomic neuropathy on formal testing. Twelve had no autonomic dysfunction. Eleven (92%) of 12 patients with severe neuropathy had painless ST depression, compared with 7 (39%) of 18 without severe neuropathy (p less than 0.01). Thus, silent myocardial ischaemia on exercise testing is common among patients with diabetes mellitus and is associated with severe autonomic dysfunction.

Some surgeons avoid placing a jejunostomy in patients with complications, fearing either exacerbation of the disease during enteral feedings or complications from the jejunostomies. Eleven patients with hemorrhagic pancreatitis (four), pancreatic abscess (five), or infected pseudocyst (two) underwent placements of needle (five) or Red Robinson (six) jejunal catheters during laparotomy. Five patients had been given 30.8 +/- 16 liters of TPN over 25 +/- 12 days preoperatively. Only two patients received TPN postoperatively because of progressive sepsis with enteral intolerance to feedings. One of these patients developed a jejunal leak near the placement of the Red Robinson catheter. Both patients died of complications from their pancreatic disease. The remaining nine patients received 35.6 +/- 8.6 liters of enteral feedings over 31 +/- 6.8 days before resuming oral intake. Glucosuria and hyperglycemia were common, but easily managed. No catheters were lost, and diarrhea necessitating slowing and diluting the diet was unusual after the first week. Enteral feeding did not elevate amylase values. Therefore, jejunal feedings can be given safely in patients with severe acute pancreatic disease to provide prolonged nutrition without aggravating the disease.

We assessed the prevalence of previously unrecognized hemochromatosis among patients in whom diabetes mellitus was diagnosed after the age of 30 yr, and we evaluated the positive predictive value of biochemical screening tests for hemochromatosis in diabetic subjects. Thirty-eight of 572 patients screened (6.6%) had a serum ferritin level greater than 324 micrograms/L; 16 patients had normal levels on repeat testing. Four patients' serum ferritin levels fell to less than 400 micrograms/L. Seven of 18 patients with a persistently elevated serum ferritin level did not undergo a liver biopsy because of a recognized cause of hyperferritenemia (carcinoma, alcoholism, or systemic lupus erythematosus). The diagnosis of hemochromatosis seemed certain in 1 of 3 patients who were not biopsied for technical reasons. Of 8 patients biopsied, 2 had hemochromatosis, 4 had fatty liver, 1 had hemosiderosis, and 1 had a chronic inflammatory cell infiltrate with no iron deposition. Of 4 patients with a raised transferrin saturation level, 2 had raised serum ferritin levels and hemochromatosis, 1 had raised serum ferritin and hemosiderosis on liver biopsy, and 1 had a normal transferrin saturation level on repeat testing. Two of 3 cases of hemochromatosis had other clinical markers of the condition. Therefore, routine screening of diabetic patients for hemochromatosis is not necessary, because patients with hemochromatosis will often have other clinical features of the disease. When screening diabetic patients for hemochromatosis, it should be remembered that a persistently raised serum ferritin level has a low positive predictive value (16.6%) and that a normal transferrin saturation level does not exclude the diagnosis.

Serum ferritin was measured in 50 patients at diagnosis of diabetes mellitus (DM) and in 20 patients with established DM and poor metabolic control. Twenty-two patients had hyperferritinemia at diagnosis. Four patients had a recognised cause for their hyperferritinemia. In the remaining 18 patients ferritin levels decreased from a mean of 506 +/- 3.6 (SE) ug/l at diagnosis to 254 +/- 29.2 ug/l seven months later (p < 0.001). Metabolic control improved significantly over the same time. All 20 patients with established DM and poor metabolic control had normal ferritin levels. When compared with the newly diagnosed hyperferritinemic patients no difference was found in levels of glycosylated haemoglobin, but ferritin values differed significantly between the two groups (p < 0.001). These results indicate that transient hyperferritinemia is a feature of newly diagnosed DM but not of established DM with poor control. If used to screen diabetic patients for haemochromatosis, serum ferritin should be measured in established DM rather than at diagnosis.