Antacid-induced osteomalacia: a case report with a histomorphometric analysis

The case of a 75-year-old woman with severe osteomalacia secondary to ingestion of large amounts of an aluminum-containing antacid is reported. Biochemical analysis revealed signs of phosphate malabsorption and increased levels of bone markers (S-alkaline phosphatase and U-hydroxyproline). A 99mTc-bone scan revealed multiple areas of increased uptake. The patient was normocalcaemic, with normal serum levels of intact parathyroid hormone and 25-hydroxyvitamin D. Serum 1,25-dihydroxyvitamin D was high normal. A transiliac bone biopsy from the patient showed severe osteomalacia. Symptoms, biochemical parameters, bone scan and bone morphology were all normalized 1 year after stoppage of antacid ingestion and treatment with vitamin D2. calcium phosphate and sodium fluoride because of severe osteopeni. The characteristics of this condition and the role of phosphate depletion and aluminum in the pathogenesis of bone lesions are discussed.     

In Vivo performance of ophthalmic preparations of betamethasone and phenylephrine hydrochloride in the rabbit eye: Effect of polyvinyl alcohol

The effect of different concentrations of polyvinyl alcohol 14000 and 72000 (PVA 14 and 72) on the activity of betamethasone and phenylephrine hydrochloride in the rabbit eye was investigated. The polymer of higher molecular weight exerts a more pronounced effect at relatively lower viscosities. Effects on the intraocular pressure are more responsive to changes in viscosity than those on pupillary response.     

Diurnal rhythm in serum osteocalcin: Relation with sleep,growth hormone,and PTH(1–84)

Summary We examined the role of sleep, growth hormone (GH), and parathyroid hormone [PTH(1–84)] as regulators of the diurnal rhythm of the osteoblastic bone marker, serum osteocalcin (OC). Nine normal subjects were followed with hourly blood sampling during one 24-hour period with norsleep deprivation. We found that the rhythm in serum OC did not exhibit significant changes (P>0.50). Serum OC (mean±SE) was 30.9±2.5 μg/liter during sleep (2330-0730 hours) versus 29.9±4.9 μg/liter during sleep deprivation (not significantly different). The serum GH rhythm was significantly different on the two occasions (P<0.01). A maximum GH peak (mean±SE) of 10.3±2.4 μg/liter occurred at 0136 hours±6 minutes during sleep compared with a maximal peak of 7.6±1.2 μg/liter (P<0.01) at 0245 hours ±20 minutes (P<0.01) during sleep deprivation. During sleep (2330-0730 hours), mean serum GH was 3.61±0.60 μg/liter compared with 2.39±0.40 μg/liter during sleep deprivation (P<0.005). Small insignificant changes occurred in serum PTH(1–84) and serum ionized calcium during the two occasions. We conclude that sleep and GH are not acute controlling factors of the diurnal rhythm in serum OC and the role of serum PTH(1–84) remains unsettled.     

Endoscopic ultrasonographic study of the azygos vein before and after endoscopic obliteration of esophagogastric varices by injection sclerotherapy

BACKGROUND AND STUDY AIMS: The azygos vein plays an important role as a drainage system for the superior portosystemic collateral circulation in portal hypertensive patients. Endoscopic ultrasonography (EUS) and Doppler EUS allow the performance of hemodynamic studies of the azygos vein. In this study, we observed the changes in the azygos vein which occur with variceal obliteration by endoscopic injection sclerotherapy (EIS). PATIENTS AND METHODS: We recruited patients with portal hypertension and bleeding varices who were not on portal pressure-lowering agents and who were scheduled for the EIS program. EUS was performed in these patients to study the azygos vein at the start of EIS. The azygos vein diameter, maximal velocity (Vmax), and blood flow volume index (BFVI) were measured. After variceal obliteration and within 1 week, another EUS study of the azygos vein was carried out. RESULTS: Out of 40 patients recruited into the study variceal obliteration and EUS assessment of the azygos vein, within 1 week of obliteration, was achieved in 33. We noticed a significant increase in azygos vein diameter (P<0.001) and BFVI (P=0.001) following variceal obliteration. No significant change was observed in Vmax (P>0.05). In one patient, marked caliber irregularities were observed in the azygos vein after variceal obliteration. CONCLUSIONS: Using EUS and Doppler EUS, hemodynamic studies of the azygos vein blood flow can be performed, allowing the monitoring of the effects of EIS and variceal obliteration on the superior portosystemic collateral circulation. The clinical significance of the observed changes in azygos blood flow that occur with variceal obliteration should be investigated in further studies and correlated with short-term and long-term outcome.     

Inflammation and Metabolic Complications in HIV

Purpose of Review

We aim to provide an in-depth review of recent literature highlighting the role of inflammation involving the adipose tissue, liver, skeletal muscles, and gastrointestinal tract in the development of metabolic complications among persons living with HIV (PLWH).

Recent Findings

Recent studies in PLWH have demonstrated a significant association between circulating inflammatory markers and development of insulin resistance and metabolic complications. In adipose tissue, pro-inflammatory cytokine expression inhibits adipocyte insulin signaling, which alters lipid and glucose homeostasis. Increased lipolysis and lipogenesis elevate levels of circulating free fatty acids and promote ectopic fat deposition in liver and skeletal muscles. This leads to lipotoxicity characterized by a pro-inflammatory response with worsening insulin resistance. Finally, HIV is associated with gastrointestinal tract inflammation and changes in the gut microbiome resulting in reduced diversity, which is an additional risk factor for diabetes.

Summary

Metabolic complications in PLWH are in part due to chronic, multisite tissue inflammation resulting in dysregulation of glucose and lipid trafficking, utilization, and storage.

     

Vitamin D,autoimmunity and recurrent pregnancy loss: More than an association

Recurrent pregnancy loss (RPL) affects close to 1% of couples; however, the etiology is known in only about 50% of the cases. Recent studies show that autoimmune dysregulation is a probable cause of RPL, which in some cases may be overlooked. In order for a pregnancy to proceed to term, early modulation of immunologic response is required to induce tolerance to the semi‐allogenic fetus. Certain subsets of both the innate and adaptive immune responses play a role in the induction of fetomaternal tolerance. A relatively predominant T‐cell helper (Th) 2 and T regulatory (Treg) cell population seem to favor a better pregnancy outcome, whereas Th1 and Th17 cell populations appear to have an opposite effect. Lately, the role of vitamin D in the modulation of immune response was established. Vitamin D has been shown to promote a more favorable environment for pregnancy through various mechanisms, such as enhancement of the shift toward Th2 cells and regulation of immune cell differentiation and cytokine secretion. Therefore, it seems that vitamin D deficiency sways the balance toward a worse outcome and may play a part in recurrent pregnancy loss. This review sheds light on the immunologic changes, which occur in early pregnancy and the regulatory role vitamin D has in the maintenance of this delicate balance.     

Breastfeeding and autoimmunity: Programing health from the beginning

Breast milk is not only a completely adapted nutrition source for the newborn but also an impressive array of immune‐active molecules that afford protection against infections and shape mucosal immune responses. Decisive imprinting events might be modulated during the first months of life with potential health long‐term effects, enhancing the importance of breastfeeding as a major influence on the immune system correct development and modifying disease susceptibility. The aim of this review was to clarify the link between breastfeeding and autoimmune diseases, inquiring the related mechanisms, based on data available in the literature. Being breastfed was associated with a lower incidence of diabetes, celiac disease, multiple sclerosis and asthma, explained by the protection against early infections, anti‐inflammatory properties, antigen‐specific tolerance induction, and regulation of infant's microbiome. The protective role of human milk in idiopathic juvenile arthritis, rheumatoid arthritis, and inflammatory bowel diseases remains controversial. On the other hand, the breastfeeding mother faces a health‐challenging period in life. High levels of prolactin may lead either to the development of autoimmune diseases in susceptible mothers or exacerbations of current immune‐mediated disorders. These features raise the question if mothers with autoimmune diseases, mainly systemic lupus erythematosus, should avoid breastfeeding.