Iron Deficiency Anemia Associated With Acid-Modifying Medications: Two Cases and Literature Review

Iron deficiency anemia is often listed among potential adverse effects of gastric acid-suppressive medications, given that gastric acidity promotes intestinal absorption of nonheme iron. Additionally, the antacid calcium carbonate can inhibit iron absorption. However, there is little direct clinical evidence that proton-pump inhibitors, histamine-2 receptor antagonists, or calcium carbonate cause iron deficiency anemia. Most case reports have had substantial limitations (e.g., minimal follow-up and presence of other causes of iron deficiency), and retrospective cohort studies have lacked sufficient patient-specific detail to make strong causal inferences. We present 2 cases—both with detailed, prospective 10-year follow-up—in which combinations of proton-pump inhibitors, histamine-2 receptor antagonists and calcium carbonate were clearly associated with development of iron deficiency anemia. Overt iron-deficiency anemia is probably uncommon in patients who use acid-modifying medications and who have no other conditions that predispose to iron deficiency. Nevertheless, clinicians should be aware of this potential complication, given widespread use of these agents.     

Factors influencing development of residual stresses during crystallization firing in a novel lithium silicate glass-ceramic

ObjectiveDevelopment of residual stresses is a potential source of premature fractures in glassy materials, being of special interest in novel lithium silicate glass-ceramics that require a crystallization firing to achieve their final mechanical properties. The aim of this work was to assess the influence of various firing tray systems and the application of different cooling protocols on the development of residual stresses in Suprinity PC crowns. Their effect on the in vitro lifetime of the restorations was also studied.MethodsThirty crowns were milled out of Suprinity PC blocks and crystallized using one of five different commercial firing tray systems (n = 6). Samples in each group were cooled following a fast (FC = 5.5 °C/s), a slow (SC = 0.4 °C/s) or the manufacturer’s reference cooling (REF ). Obtained crowns were sagittally or transversally sectioned and the magnitude and distribution of residual stresses was determined using the light birefringence method. Extra crowns of three of the subgroups (n = 8) were produced and submitted to chewing simulation for 10⁶ cycles or until fracture ensued.ResultsAverage residual stresses ranged between 0 and 1.5 MPa (peaks of 5 MPa). Highest stress magnitudes were observed at the support areas of groups using firing pins, leading to thermal cracks in FC samples and premature failures in the REF subgroup. The use of fibrous pads and firing pastes limited the development of residual stresses, whereas application of SC regimes extended the lifetime of the restorations.SignificanceDevelopment of residual stresses during crystallization firing in lithium silicate glass-ceramics results critical for their mechanical performance and should be therefore avoided by ensuring a homogenous cooling of the structures.     

大鼠脑缺血损伤后锂盐治疗对海马CA1区的影响

目的探讨大鼠局灶脑缺血损伤后锂盐治疗对海马CA1神经元形态学变化的影响。方法将SD大鼠随机分为假手术组(SH组)、缺血-再灌注组(IR组)和缺血损伤后氯化锂治疗组(LI组),按处死时间不同,将各组再分为三个亚组:SH1d、SH2d、SH3d组;IR1dI、R2dI、R3d组;LI1d、LI2d、LI3d组。线栓法制作大鼠大脑中动脉闭塞(MCAO)局灶脑缺血模型,1.5 h后再灌注。LI组于脑缺血后1 h,氯化锂(3 mmol/kg)腹腔注射,每天一次至处死。SH组和IR组以生理盐水替代。HE染色比较各组缺血损伤后1、2、3 d海马CA1区神经元损伤程度。结果虽然LI组与IR组的CA1区存活锥体细胞数存在类似下降趋势,但LI2d组、LI3d组分别较IR2d组I、R3d组存活锥体细胞数明显增多(P<0.01)。结论大鼠局灶脑缺血后氯化锂的治疗能减轻海马神经元的损伤程度。     

Carbonate apatite crystals in primary normophosphatemic tumoral calcinosis

A 66‐year‐old woman developed firm, painless, slowly growing nodular masses over her elbows, fingers, toes, and left hip over four years. Aspiration of the elbow mass revealed a white chalky material that was shown to be carbonate apatite on infrared spectroscopy and energy dispersive X‐ray spectroscopy. We discuss the classification of tumoral calcinosis and the nature of the calcium deposits. Tumoral calcinosis should be differentiated from tophaceous gout and calcium pyrophosphate dihydrate crystal deposition disease. Polarizing light microscopy and crystal analysis by X‐ray and infrared spectroscopy, electron or X‐ray diffraction will confirm the diagnosis. Secondary causes of tumoral calcinosis should also be excluded.     

Electrocrystallization of calcium carbonate on carbon-based electrodes

Calcium carbonate was deposited by electrochemical reduction of oxygen to hydroxyl ions at various carbon-based electrodes. Although some vaterite was observed during earlier stages of the electrodeposition, the predominant polymorph during later stages was calcite. The average crystal size reached a value of 15 μm after 10 h at a glassy carbon electrode but the crystal growth rate was substantially accelerated when oxygen was catalytically reduced. The same average size of the calcite crystals in this case (Pt/C electrode) was reached within a period of 1.5 h. Efficient removal of CaCO₃ from water was demonstrated when using a porous aerogel carbon electrode and a potential sufficiently negative to promote reduction of water molecules within the pores.     

几种造血刺激剂拮抗干扰素对粒-单系祖细胞的抑制效应

本实验用C_(57)BL/6j小鼠CFU-GM集落形成的方法观察了三种CSF和氢化可的松、锂盐及硒盐对CFU-GM的影响及其对IFN的CFU-GM抑制作用的阻断作用。结果表明,三种CSF能部分拮抗IFN的CFU-GM抑制效应;微量的硒酸钠,碳酸锂均可刺激CFU-GM增殖,并使IFN200IU抑制的CFU-GM产率提高200％以上;微量的氢化可的松也能部分阻断IFN的CFU-GM抑制。     

Alteration of cytochrome P-450 by prolonged administration of imipramine and/or lithium to rats

Summary The aim of this study was to investigate imipramine-induced alterations of cytochrome P-450 and to determine whether prolonged concomitant administration of imipramine and lithium results in a pharmacokinetic interaction.Male Wistar rats received imipramine (10 mg/kg i. p.) at 12 h intervals or lithium chloride (100 mg/kg in drinking water) or they were treated with the combination of these drugs for 2 weeks. The long term treatment with imipramine produced a very complex alteration of cytochrome P-450: imipramine increased the level of the cytochrome, but it decreased the rate of its own aromatic hydroxylation in position 2. The rate of N-demethylation in the side chain was not changed. Consequently, in the case of both hydroxylation and demethylation, calculated molecular activities were decreased to 48% and 70% respectively. This differential change in activities corresponded well to the observed decrease of absorption in difference spectra (type I) produced in microsomes by imipramine. Carbamazepine-induced type I difference spectra were also decreased by imipramine pretreatment, but to a lesser extent. In contrast, hexobarbital type I binding was increased by imipramine treatment while type II difference spectra produced by metyrapone were not affected. The preliminary SDS-PAGE analysis of cytochrome P-450 isoenzymes of control and imipramine treated rats showed that the investigated antidepressant markedly intensified a protein band at 50.11 kD while bands at 51.28 kD, 56.20 kD and 56.88 kD were less intensive. These results indicate that the alteration of cytochrome P-450 by imipramine treatment is not only of quantitative but also of qualitative character. Lithium alone given to rats affected neither the concentration of cytochrome P-450 in microsomal protein nor the rate of imipramine metabolism in vitro. Lithium given jointly with imipramine reduced imipramine-induced elevation of cytochrome P-450. This, however, did not cause any change in the rate of imipramine metabolism in vitro and accordingly in imipramine pharmacokinetics in vivo. The concentration of lithium in the blood plasma tended to increase by concurrent administration of imipramine.Send offprint requests to K. J. Netter at the above address     

改良锂清除试验──一种在人体测量肾小管钠转运功能的方法

在常用的七小时锂清除试验方法基础上，我们观察了实验开始后第四小时血清理浓度与血清理代表浓度的关系，二者密切相关，ｙ＝０．９０９ｘ＋０．１７，ｒ＝０．９５２，Ｐ＜０．００５。应用此方程式，可将原方案中两次取血减为一次。另外，我们还总结出正常人锂清除率和锂排泄分数的参照值分别为８．４～３１．６ｍｌ／ｍｉｎ和９．６％～２６．３％。     

Lithium increases slow wave sleep: possible mediation by brain 5-HT2 receptors?

The effect of lithium on slow wave sleep (SWS) was studied in ten normal male volunteers using home based cassette sleep recording and automatic sleep stage analysis. Lithium increased SWS, an effect consisten with a reduction in brain 5-HT₂ receptor function.