What is the Role of Hyperbaric Oxygen in the Management of Diabetic Foot Disease?

Systemic hyperbaric oxygen (HBO) is accomplished when a patient is breathing 100% oxygen in an environment with increased barometric pressure. A typical HBO treatment protocol of diabetic foot ulcer involves 20 to 40 sessions. Treatment is usually given as daily 90- to 120-minute HBO sessions at pressures between 2.0 and 2.5 absolute atmospheres. The wide use of HBO as treatment of diabetic foot ulcers over the past decades has been founded on weak scientific ground (ie, few and small prospective studies with methodologic limitations on top of case series). However, the consistency in positive outcome in these trials evaluating HBO on ulcer healing is noteworthy because these findings are in concert with data from in vitro and physiologic studies supporting the theoretic framework of HBO reversing hypoxia-induced pathology. Two well-designed randomized double-blinded placebo-controlled studies have in recent years put HBO on firmer ground as treatment of a selection of diabetic patients with chronic foot. Some evidence indicates that microvascular parameters such as transcutaneous (partial) oxygen pressure (TcPO(2)) could be useful in predicting which patients will benefit from therapy. Health economic studies suggest potential cost-effectiveness of HBO. But because these analyses are limited by their deficient primary clinical data, they should be interpreted with caution. Thus, HBO is only indicated in a selected group of patients with chronic diabetic foot ulcers. Several key issues remain to be addressed such as developing robust criteria to determine which patients are likely to benefit and when to start and stop treatment

Hyperbaric oxygen therapy reduces the risk of QTc interval prolongation in patients with diabetes and hard-to-heal foot ulcers.

Heart rate corrected QT (QTc) interval prolongation is a risk factor associated with increased mortality. Hyperbaric oxygen therapy (HBO) has previously been shown to have acute beneficial effects on QTc dispersion. The aim of this study was to evaluate long-term effects of HBO on QTc time in diabetic patients with hard-to-heal foot ulcers

Biochemical diagnosis of primary hyperparathyroidism: Analysis of the sensitivity of total and ionized calcium in combination with PTH.

OBJECTIVES: To investigate the accuracy of the biochemical diagnosis of primary hyperparathyroidism (pHPT) in a consecutive series of patients with operatively verified disease. DESIGN AND SUBJECTS: Four hundred thirty-six patients with pHPT, 340 women and 96 men, were reviewed. Biochemical variables, including total calcium (Ca), ionized calcium (Cai) and PTH were analyzed and registered in a prospective database. RESULTS: In the subgroup of patients with more mild hypercalcemia (Ca below 2.70mmol/L) the correlation between Ca and Cai was poor. 19 respectively 18 patients had preoperatively a Ca respectively Cai level within the reference range. Further 35 patients had preoperatively a normal level of PTH. The diagnostic sensitivities for Ca, Cai and the combination of Ca and Cai were 96%, 96% and 99%. CONCLUSION: If calcium and ionized calcium are not used in the diagnostic workup of pHPT some 4% of the patients will be overlooked. We recommend analyzing both Ca and Cai in the diagnostic workup of pHPT

HNF1B variant without hyperglycaemia as a cause of isolated profound hypomagnesaemia

A young man presented unconscious with severe hyponatraemia, hypokalaemia, hypomagnesaemia and metabolic alkalosis. After 4 months of treatment in hospital, the hypomagnesaemia persisted. The patient had no signs of diabetes mellitus, and radiology showed no abnormalities of the kidneys, pancreas or genitourinary tract. A parenteral magnesium load demonstrated renal wasting with increased fractional urinary excretion of magnesium. Genetic tests for Gitelman as well as Bartter syndromes were negative. However, a wider genetic panel revealed that the patient was heterozygous for a deletion on chromosome band 17q12, encompassing the whole HNF1B gene.This case highlights the importance of considering pathogenic HNF1B variants in isolated profound hypomagnesaemia caused by renal wasting. Pathogenic HNF1B variants may partly mimic hypomagnesaemia found in Gitelman and Bartter syndromes and may be present without other features linked to HNF1B variants, including diabetes mellitus