Hypophosphatemia and refeeding: a corrective or a preventive attitude?

Hypophosphatemia is a rare but potentially lethal complication of the refeeding of cachectic patients. Up until now a careful monitoring of the serum phosphor level was recommended and the deficit was corrected as needed. Illustrated by two case reports we propose the use of a preventive schedule in patients with a normal renal function. We show that preventively treated patients do not develop hypophosphatemia and thereby avoid serious complications such as sudden death. In the presence of normal kidney function we propose to administer phosphor at 2 x 10 mmol/day orally or between 10 and 30 mmol IV depending on the initial phosphor levels. Further treatment is then adapted to measured levels. In the presence of kidney malfunction we propose to keep the corrective schedule.     

Periodontitis and diabetes—a complex relationship

Periodontitis is a common problem in patients with diabetes. The interrelation between diabetes mellitus and inflammatory periodontal disease has been intensively studied for more than 50 years. The relationship between these 2 maladies appears bidirectional—insofar that the presence of one condition tends to promote the other, and that the meticulous management of either may assist treatment of the other. Inflammation plays an important role in this interrelation, orchestrating both the periodontal disease and diabetes mellitus pathogeny and complications. Conversely, periodontal infection can seriously impair metabolic control of some diabetic patients. Moreover, treatment of periodontal disease and reduction of oral signs of inflammation may have a beneficial effect on diabetes. This review examines the relationships that exist between periodontal diseases and diabetes mellitus, with a focus on potential common pathophysiologic pathways including those associated with inflammation, altered host responses and insulin resistance     

Iron and pregnancy—a delicate balance

The review focuses on iron balance during pregnancy and postpartum in the Western affluent societies. Iron status and body iron can be monitored using serum ferritin, haemoglobin, serum soluble transferrin receptors (sTfR) and the sTfR/ferritin ratio. Requirements for absorbed iron increase during pregnancy from 0.8 mg/day in the first trimester to 7.5 mg/day in the third trimester. Average requirement during the entire gestation is ~4.4 mg/day. Intestinal iron absorption increases during pregnancy, but women with ample body iron reserves have lower absorption than those with depleted reserves, so increased absorption is, in part, due to progressive iron depletion. Apparently, women do not change dietary habits when they become pregnant. Non-pregnant Scandinavian women have a median dietary iron intake of ~9 mg/day, i.e. more than 90% of the women have an intake below the recommended ~18 mg/day. Non-pregnant women have a low iron status, 42% have serum ferritin levels ≤30 μg/l, i.e. small or depleted iron reserves and 2–4% have iron deficiency anaemia; only 14–20% have ferritin levels >70 μg/l corresponding to body iron of ≥500 mg. The association between high haemoglobin during gestation and a low birth weight of the newborns is caused by inappropriate haemodilution. In placebo-controlled studies on healthy pregnant women, there is no relationship between the women’s haemoglobin and birth weight of the newborns and no increased frequency of preeclampsia in women taking iron supplements.     

Is there a difference between a chief of cardiology and a chief of medicine?

The job of Chief of Medicine demands considerably more administrative effort than the Chief of Cardiology. However, one can still maintain a significant presence in cardiology as a Chief of Medicine. Each job has its own merits, joys, and irritations.     

Appendicopathy—a clinical and diagnostic dilemma

Purpose

The term “neurogenic appendicopathy” has been used for patients operated on for acute appendicitis with their appendices lacking signs of acute inflammation. The aim of this retrospective study was to clarify the presence of potential neurogenic appendicopathies, analyzing patients’ clinical symptoms and their corresponding appendiceal specimens.

Methods

One hundred twenty-one patients were identified showing a histological diagnosis of chronic appendicitis. Eventually, 40 patients qualified for the potential diagnosis “neurogenic appendicopathy.” Appendix specimens were immunohistochemically examined for the expression of S-100, vasoactive intestinal polypeptide (VIP), and substance P. Controls consisted of 110 patients with acute appendicitis and 120 patients following appendectomies operated on for other reasons.

Results

Eventually, 40 of 120 patients qualified for the potential diagnosis “neurogenic appendicopathy.” Compared to patients with acute appendicitis, there was only little difference in clinical symptoms. Histologically, neuromas, thought of being characteristic of neurogenic appendicopathy, were demonstrated significantly more often in the control group (p?=?0.01). S-100 was significantly more expressed in the appendicopathy group (p?=?0.0024), but nearly 50 % of control specimens showed an intense staining, too. S-100⁺ neurofibers were significantly (p?=?0.00122) more often found in the mucosa of appendicopathy specimens, but this was true for only 25 % of specimens. VIP was more strongly expressed in control specimens (p?=?0.0211). Substance P was of no diagnostic value.

Conclusions

Our study could not confirm the neurogenic origin of appendicopathies. Yet, clinical data strongly suggest the existence of the entity “appendicopathy.” Therefore, we suggest removing a macroscopically unaffected appendix in patients with appendicitis-like symptoms if, on laparoscopy, no other cause can be found.     

Glycoxidation and Diabetic Complications: Modern Lessons and a Warning?

Reviews in Endocrine and Metabolic Disorders -     

Shiga toxin 2a and Enteroaggregative Escherichia coli – a deadly combination

In 2011, a Shiga toxin (Stx) type 2a-producing enteroaggregative E. coli (EAEC) strain of serotype O104:H4 caused a large lethal outbreak in Northern Europe. Until recently, the pathogenic mechanisms explaining the high virulence of the strain have remained unclear. Our laboratories have shown that EAEC genes encoded on the pAA virulence plasmid, particularly the AggR-regulated AAF/I fimbriae, enhance inflammation and enable the outbreak strain to both adhere to epithelial cells and translocate Stx2a across the intestinal epithelium, possibly explaining the high incidence of the life threatening post-diarrheal sequelae of hemolytic uremic syndrome. Epidemiologic evidence supports a model of EAEC pathogenesis comprising the concerted action of multiple virulence factors along with induction of inflammation. Here, we suggest a model for the pathogenesis of the O104:H4 outbreak strain that includes contributions from EAEC alone, but incorporating additional injury induced by Stx2a.     

Acute Respiratory Failure in a Patient with Sarcoidosis and Immunodeficiency—An Unusual Presentation and a Complicated Course

Pulmonary sarcoidosis is usually a chronic, insidious disease resulting from granuloma formation in the lung parenchyma. The epithelioid non-caseating granulomata of sarcoidosis are the result of a T-helper1-mediated immune reaction to an unknown self or foreign antigen. We describe the case of a patient with sarcoidosis and a coexistent common variable immunodeficiency who presented with rapidly progressive respiratory failure. This unusual presentation was followed by a complicated course with recurrent pneumoccocal infections, which could be explained by the coexistence of common variable immunodeficiency. Physicians should be alert to the possibility of sarcoidosis even when the clinical presentation is of acute respiratory distress syndrome (ARDS) since early treatment with steroids can be lifesaving. The detection of accompanying hypogammaglobulinemia is also crucial, as treatment with intravenous immunoglobulins (IVIG) together with steroids can improve the patients outcome.     

Dental deafferentation and brain damage: A review and a hypothesis

In the last few decades, neurobiological and human brain imaging research have greatly advanced our understanding of brain mechanisms that support perception and memory, as well as their function in daily activities. Knowledge of the neurobiological mechanisms behind the deafferentation of stomatognathic systems has also expanded greatly in recent decades. In particular, current studies reveal that the peripheral deafferentations of stomatognathic systems may be projected globally into the central nervous system (CNS) and become an associated critical factor in triggering and aggravating neurodegenerative diseases.This review explores basic neurobiological mechanisms associated with the deafferentation of stomatognathic systems. Further included is a discussion on tooth loss and other dental deafferentation (DD) mechanisms, with a focus on dental and masticatory apparatuses associated with brain functions and which may underlie the changes observed in the aging brain. A new hypothesis is presented where DD and changes in the functionality of teeth and the masticatory apparatus may cause brain damage as a result of altered cerebral circulation and dysfunctional homeostasis. Furthermore, multiple recurrent reorganizations of the brain may be a triggering or contributing risk factor in the onset and progression of neurodegenerative conditions such as Alzheimer's disease (AD). A growing understanding of the association between DD and brain aging may lead to solutions in treating and preventing cognitive decline and neurodegenerative diseases.