The autoimmune attack in type 1 diabetes is not only targeted to β cells. We assessed the prevalence of thyroid peroxidase (aTPO), parietal cell (PCA), antiadrenal (AAA) and endomysial antibodies (EmA‐IgA), and of overt autoimmune disease in type 1 diabetes, in relation to gender, age, duration of disease, age at onset, β‐cell antibody status (ICA, GADA, IA2A) and HLA‐DQ type. Sera from 399 type 1 diabetic patients (M/F: 188/211; mean age: 26 ± 16 years; duration: 9 ± 8 years) were tested for ICA, PCA, AAA and EmA‐IgA by indirect immunofluorescence, and for IA2A (tyrosine phosphatase antibodies), GADA (glutamic acid decarboxylase‐65 antibodies) and aTPO by radiobinding assays. The prevalence rates were: GADA 70%; IA2A, 44%; ICA, 39%; aTPO, 22%; PCA, 18%; EmA‐IgA, 2%; and AAA, 1%. aTPO status was determined by female gender (β = − 1·15, P = 0·002), age (β = 0·02, P = 0·01) and GADA + (β = 1·06, P = 0·02), but not by HLA‐DQ type or IA2A status. Dysthyroidism (P < 0·0001) was more frequent in aTPO + subjects. PCA status was determined by age (β = 0·03, P = 0·002). We also observed an association between PCA + and GADA + (OR = 1·9, P = 0·049), aTPO + (OR = 1·9, P = 0·04) and HLA DQA1*0501‐DQB1*0301 status (OR = 2·4, P = 0·045). Iron deficiency anaemia (OR = 3·0, P = 0·003) and pernicious anaemia (OR = 40, P < 0·0001) were more frequent in PCA + subjects. EmA‐IgA + was linked to HLA DQA1*0501‐DQB1*0201 + (OR = 7·5, P = 0·039), and coeliac disease was found in three patients. No patient had Addison's disease. In conclusion, GADA but not IA2A indicate the presence of thyrogastric autoimmunity in type 1 diabetes. aTPO have a female preponderance, PCA are weakly associated with HLA DQA1*0501‐DQB1*0301 and EmA‐IgA + with HLA DQA1*0501‐DQB1*0201.

Free iron is capable of stimulating the production of free radicals which cause oxidative damage such as lipid peroxidation. One of the most important mechanisms of antioxidant defense is thus the sequestration of iron in a redox-inactive form by transferrin. In diabetes mellitus, increased oxidative stress and lipid peroxidation contribute to chronic complications but it is not known if this is related to abnormalities in transferrin function. In this study we investigated the role of transferrin concentration and glycation. The antioxidant capacity of apotransferrin to inhibit lipid peroxidation by iron-binding decreased in a concentration-dependent manner from 89% at > or = 2 mg/ml to 42% at 0.5 mg/ml. Pre-incubation of apotransferrin with glucose for 14 days resulted in a concentration-dependent increase of glycation: 1, 5 and 13 micromol fructosamine/g transferrin at 0, 5.6 and 33.3 mmol/l glucose respectively, p < 0.001. This was accompanied by a decrease in the iron-binding antioxidant capacity of apotransferrin. In contrast, transferrin glycation by up to 33.3 mmol/l glucose did not affect chemiluminescence-quenching antioxidant capacity, which is iron-independent. Colorimetric evaluation of total iron binding capacity in the presence of an excess of iron (iron/transferrin molar ratio = 2.4) also decreased from 0.726 to 0.696 and 0.585mg/g transferrin after 0, 5.6 and 33.3 mmol/l glucose, respectively, p < 0.01. In conclusion, these results suggest that lower transferrin concentration and its glycation can, by enhancing the pro-oxidant effects of iron, contribute to the increased lipid peroxidation observed in diabetes.

Abbreviations: ANOVA, analysis of variance; AUC ROC , area under the curve for receiver operating characteristics; CV, coefficient of variation; Nl, normal range; PCA, parietal cell antibody; sTfR, soluble transferrin receptor.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Soluble Transferrin Receptor LevelA new marker of iron deficiency anemia, a common manifestation of gastric autoimmunity in type 1 diabetesOBJECTIVE -A total of 15-20% of type 1 diabetic patients have parietal cell antibodies (PCAs). PCA ϩ subjects are at increased risk for iron deficiency anemia and atrophic gastritis. Recently, soluble transferrin receptor (sTfR) levels have proven to be a sensitive indicator for iron deficiency. They are, in contrast with ferritin levels, independent of inflammation, liver and hormonal status, and sex. We are the first to evaluate sTfR levels in type 1 diabetes and tested the hypothesis of higher sTfR levels in patients with PCAs and/or autoimmune gastritis.RESEARCH DESIGN AND METHODS -We examined 148 type 1 diabetic patients (85 men and 63 women; 50 were PCA ϩ ) and 59 sex-and age-matched control subjects (30 men and 29 women). The main outcome measures were sTfR levels, iron deficiency anemia, and atrophic gastritis. Logistical regression analysis tested risk factors for iron deficiency.RESULTS -Iron deficiency was present in 38 subjects. Iron (P Ͻ 0.0001) and ferritin (P Ͻ 0.0001) levels but not sTfR levels were lower in women. sTfR levels were similar in diabetic and control subjects but were higher in PCA ϩ subjects (P = 0.015). In diabetic subjects, iron deficiency anemia was more prevalent in PCA ϩ than in PCA -patients (odds ratio 3.07, P = 0.013) and was associated with sex (P = 0.0001), age (P = 0.046), and sTfR (P = 0.0008) levels. Atrophic gastritis was present in 15 of 28 PCA ϩ and in 1 of 11 PCA -diabetic subjects (P = 0.014). sTfR levels tended to be higher in patients with atrophic gastritis (P = 0.062).CONCLUSIONS -In type 1 diabetes, sTfR levels can be used to diagnose iron deficiency anemia, which is more prevalent in PCA ϩ subjects. sTfR levels are higher in PCA ϩ individuals who are at risk for developing atrophic gastritis.

Propylene glycol, an alcohol frequently used as a solvent in medical preparations, is considered non-toxic. We found that this solvent, used in a commercially available IV nitroglycerin solution, may cause hyperosmolality, hemolysis and lactic acidosis. The influence of kidney function as the main determinant in causing accumulation of this solvent and consequently hyperosmolality is emphasized. A review of the literature dealing with propylene glycol is given. The possible mechanisms of neurological disturbances occurring during IV nitroglycerin therapy are discussed.