Macro-Vitamin B12 as Cause of Falsely Elevated Cobalamin Levels.

Introduction: High blood concentrations of vitamin B12 are often caused by over-supplementation. However, there are instances in which augmented vitamin B12 levels are seen in the absence of supplements. Macro-vitamin B12 is an underrated cause of supra-physiological cobalamin plasma levels. Case description: A 70-year-old man was referred to an ambulatory internal medicine centre because of high vitamin B12 levels yet he denied taking supplements. An X-ray showed a tumour in the right upper lobe of the lung, which triggered further examinations. An MRI scan of the brain came back normal as well as a CT scan of the abdomen, and colonoscopy. The pulmonologist requested a PET-CT scan, which showed an isolated 18-FDG uptake in the area of the lung mass that was detected earlier. The patient underwent surgery with adjuvant cis-platinum and gemcitabine and is still making good progress. The vitamin B12 levels persisted after successful treatment of lung adenocarcinoma; determination of vitamin B12 after PEG (polyethylene glycol) precipitation showed normal concentrations. Discussion: A high vitamin B12 plasma concentration in the absence of vitamin supplementation can be a daunting diagnostic problem for the internist, as there are several possible underlying causes. In this case the diagnosis of lung carcinoma was made, the patient was treated appropriately, yet this pathology had no correlation with the cobalamin levels. Conclusion: A high vitamin B12 concentration can be the impetus of thorough medical inquiries. Internists should be careful not to forget macro-vitamin B12 as a possible source of falsely elevated vitamin B12 values. LEARNING POINTS: When encountering an otherwise unexplainable B12 hypervitaminosis, the diagnosis of macro-vitamin B12 should be taken into account to avoid unnecessary extensive medical examinations.PEG precipitation can distinguish between a 'real' high vitamin B12 and macro-vitamin B12.A high vitamin B12 concentration is no guarantee for adequate cobalamin storage. In case of suspicion, a vitamin B12 measurement after PEG precipitation should be considered.

Effect of Exercise Intervention on Cardiac Function in Type 2 Diabetes Mellitus: A Systematic Review.

BACKGROUND: The effect of exercise on cardiac function/structure in type 2 diabetes mellitus (T2DM) with or without diabetic cardiomyopathy (DCM) is not yet completely understood. To date, results of studies have been controversial with variable outcomes due to the variety of exercise modalities. OBJECTIVES: The aim of the present review was to examine the impact of exercise intervention, and different types of exercise, on cardiac function and structure in T2DM through a systematic literature review, combining both pre-clinical and clinical studies. METHODS: A systematic literature search was performed on PubMed, Web of Science, and PEDro to identify studies up to 2 April 2018. Articles were included when well-defined exercise protocols were provided, and cardiac function in T2DM patients or validated animal models was examined. RESULTS: In diabetic animals, improvements in both diastolic and systolic function through exercise therapy were mainly attributed to reduced collagen deposition. In T2DM patients, improvements were observed in diastolic function, but not consistently in systolic function, after endurance (and combined resistance) exercise training. Different exercise intervention modalities and exercise types seemed equally effective in improving cardiac structure and function. CONCLUSION: Exercise training elicits significant improvements in diastolic function and beneficial remodeling in T2DM and DCM animal models, but not necessarily improvements in systolic function and left ventricular structure, regardless of exercise type. Therefore, exercise intervention should be a cornerstone in the treatment of T2DM patients not only to improve glycemic control but also to specifically enhance cardiac function.

Isolated Intestinal Angioedema in the Emergency Department.

BACKGROUND: Angioedema is a condition that can cause cutaneous and mucosal edema of practically any part of the body. Isolated edema of the intestines is a rather rare manifestation, but it can cause important morbidity. Hereditary angioedema as well as certain medications can give rise to intestinal angioedema. We have seen a rise in frequency of intestinal angioedema since the advent of angiotensin-converting enzyme inhibitors. Ultrasound of the abdomen is an inexpensive, safe, and easy tool that can help in the differential diagnosis. CASE REPORT: We describe the case of a 25-year-old woman who presented with acute abdominal pain. She was diagnosed with intestinal angioedema due to hereditary angioedema type I. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Misdiagnosis can lead to administering the wrong treatment or even unnecessary surgical interventions. Intestinal angioedema is best treated with purified C1-inhibitor, icatibant, or ecallantide. Fresh frozen plasma is to be avoided because it carries the risk of worsening the symptoms.

Osteomalacia with low alkaline phosphatase: a not so rare condition with important consequences.

Hypophosphatasia is a genetic disorder, characterised by a dysfunctional tissue-non-specific isoenzyme of alkaline phosphatase that impacts bone metabolism and predisposes to osteomalacia or rickets. The clinical presentation is very diverse, depending on the age of onset and the severity of the disease. Several forms of hypophosphatasia are recognised. We present a case of a 50-year-old woman with low impact fractures and loss of teeth at a young age. She also had a low alkaline phosphatase and was diagnosed with adult hypophosphatasia. Although the severe forms of hypophosphatasia are rather rare, the adult form is thought to occur quite frequently. As this condition is not well known by healthcare professionals, the time to diagnosis and initiation of adequate treatment is often postponed. When encountering a patient with low alkaline phosphatase, low bone density or a history of bone fractures, the possibility of hypophosphatasia should be considered.