Diabetes and its Long-term Complications in General Practice: a Survey in a Well-defined Population

The aim of this study was to assess the prevalence of long-termcomplications in all patients with non-insulin-dependent diabetesmellitus, who were known to their general practitioners (GPs).During one year 19 GPs in the area of Hoogeveen in the Netherlandsexamined their non-insulin-dependent (NIDDM) patients, includingthose under specialist's care. A detailed protocol was used;the GPs were trained in the diagnostic procedures. Complicationswere either already known from the records or newly discoveredduring screening. In a population of 41940 14.5/1000 patientswith diabetes were identified: 12/1000 NIDDM and 2.5/1000 insulin-dependent-diabetesmellitus (IDDM). Of the 509 NIDDM patients, 387 (76%) couldbe screened for late complications. Signs and symptoms of latecomplications were found in many patients: retinopathy (14%),nephropathy (57%), neuropathy (68%) and macroangiopathy (53%).The prevalence of serious complications was: proliferative retino-and maculopathy (3.3%); diabetic foot (2.6%); renal failure(2.5%). The systemic screening revealed a high number of previouslyunknown cases. It is concluded that many patients with NIDDMdevelop signs and symptoms of late complications. Most casesare identified by systemic screening only. More long-term studiesof the prognosis of late com plications in NIDDM are needed.     

CHANGES IN RESISTANCE TO MOUTH OPENING INDUCED BY DEPOLARIZING AND NON-DEPOLARIZING NEUROMUSCULAR RELAXANTS

Mouth opening was measured in 43 children anaesthetized withisoflurane and paralysed with vecuronium or suxamethonium. Measurementsof mouth opening were made for up to 10 min after loss of theadductor pollicis twitch and cessation of muscle fasciculations.In 22 patients receiving suxamethonium, a significant (P <0.001) reduction in mean mouth opening occurred in the 60 safter loss of twitch and cessation of fasciculations. Mouthopening reductions could last for up to 10 min after the lossof twitch, beyond the return of the twitch. One patient experienced"masseter spasm"; he did not develop malignant hyperpyrexiaduring 2.5 h of isoflurane anaesthesia. Patients receiving vecuroniumshowed a significant (P < 0.0006) increase in mouth opening.In 20 subjects, mouth opening was generated with a small (1.67N) and a larger (4.32 N) force. Proportionally equal reductionsin mouth opening were obtained with either force after suxamethoniumadministration. Relatively equal increases with either forcefollowed vecuronium administration. Isolated masseter spasmis not pathognomonic for malignant hyperpyrexia. If the diagnosisof malignant hyperpyrexia is contemplated, signs of hypermetabolism,such as increases in end-tidal carbon dioxide concentrationduring constant minute ventilation, should be sought.     

医疗体操对脑卒中肢体运动功能的影响

目的 :观察以神经肌肉促通技术为理论基础的医疗体操对脑卒中患者运动功能的影响。方法 :脑卒中偏瘫患者 94例 ,分成早期体操组、后期体操组、对照组。分别于发病一个月内、一个月后按医疗体操编排的动作进行训练 ,采用Fugl Meger评价法评定肢体运动功能、上肢关节疼痛、关节活动度。结果 :1.体操组肢体运动功能治疗后较治疗前改善 ,早期体操组较对照组改善明显 (P <0 .0 0 1)。 2 .早期体操组关节疼痛发生程度较对照组减轻 (P <0 .0 1)。 3、关节活动度受限的发生较对照组明显减少 (P <0 .0 0 1) ,对关节活动度已受限的患者有明显的扩大作用 (P<0 .0 0 1)。结论 :医疗体操能有效地维持和扩大关节活动度 ,提高肢体运动功能 ,对关节疼痛有一定的防治作用。适用于脑卒中肢体功能障碍患者普及康复治疗     

雪旺细胞在局灶性脑损伤大鼠脑内的存活和迁移

目的 :了解雪旺细胞移植入局灶性脑损伤大鼠脑内后的存活、迁移情况。方法 :SD大鼠采用 Feeney's自由落体撞击法制成局灶性脑损伤模型。雪旺细胞以 Hoechst33342荧光素进行荧光标记 ,在大鼠损伤后即刻移植入脑损伤区。移植后 3天、7天、14天、2 8天、6 0天、90天处死大鼠 ,观察细胞标记荧光情况。结果 :3天、7天时移植的雪旺细胞大量存活于损伤区、海马、侧脑室的脉络丛组织中。 14天后可观察到细胞沿软脑膜、室管膜、血管周间隙迁移 ,并在胼胝体部位排列成索条状。 6 0天时雪旺细胞的标记荧光减弱 ,细胞密度减少。 90天时已观察不到荧光。并在雪旺细胞存活区有巨噬细胞浸润。结论 :雪旺细胞移植入大鼠脑损伤区后可存活并沿特定部位迁移 ,可能由于血脑屏障破坏等因素 ,机体对其有免疫排斥反应     

Value of ambulatory electrocardiographic monitoring to identify increased risk of sudden death in patients with left ventricular dysfunction and heart failure

To examine the predictive value of ventricular arrhythmias onambulatory electrocardiographic (ECG) monitoring, 211 patientswith left ventricular dysfunction and congestive heart failure(76% men, age 63±4 years, left ventricular ejection fraction0.26 ± 0.10) were studied. During a follow-up of 21 ±11 months, there were 45 cardiac deaths: 22 were due to progressivepump failure and 23 were sudden. Patients with a low left ventricularejection fraction ( 0.27) and ventricular tachycardia on 24h ECG were at higher risk of dying suddenly and from progressivepump failure (both P<0.0001). Patients who died suddenlywere found to have significantly longer (P=0.003) and faster(P=0.029) ventricular tachycardias on their baseline ambulatoryECG, than survivors. This association was not observed in patientswho died of progressive pump failure. Therefore, low left ventricularejection fraction and ventricular tachycardia on 24 h ECG recordingpredict an increased risk of cardiac mortality. Our resultsalso suggest that longer and faster ventricular tachycardiarecorded by 24 h ECG may identify patients at risk of suddendeath, a finding which has not been described before.     

EARLY AGALACTOSYLATION OF IgG IS ASSOCIATED WITH A MORE PROGRESSIVE DISEASE COURSE IN PATIENTS WITH RHEUMATOID ARTHRITIS: RESULTS OF A FOLLOW-UP STUDY

The clinical significance of the percentage agalactosyl IgGoligosaccharides [%G(O)] was investigated in serum of a well-characterizedcohort of 127 female RA patients who were followed for a meanduration of 6 yr. The %G(O) was determined in the first availableserum sample which was obtained at a mean of 3.4 yr after symptomonset. It could be shown that patients with a %G(O) more than2 S.D. above the mean level of controls (n = 34), had significantlymore erosions, disease activity, and were treated with moresecond-line drugs, than patients without an increased %G(O)(n = 93), both at the time the serum sample was obtained, andduring follow-up. These findings suggest that G(O) may serveas an indicator for the disease course in patients with RA. KEY WORDS: Agalactosyl IgG, Prognosis, Outcome     

FATAL CHOLESTATIC HEPATITIS CAUSED BY D-PENICILLAMINE

A 37-yr-old woman with RF-positive RA developed cholestatichepatitis after 10 days of D-penicillamine therapy. This wasdiscontinued immediately. The cholestasis persisted for theremaining 14 months of her life. Severe hypercholesterolemiadeveloped with xanthelasmata and eventually pancytopenia, whichwas caused by a massive infiltration of the bone marrow by lipidcontaining foam cells. The patient died of sepsis. Review ofthe literature shows intrahepatic cholestasis to be a rare andidiosyncratic complication of D-penicillamine therapy. To ourknowledge, ours is the first documented case of persistent cholestaticicterus. KEY WORDS: Cholestatic hepatitis, Jaundice, Adverse reactions, Drug-allergy, D-Penicillamine     

Determination of left ventricular volume by two-dimensional echocardiography: comparison with magnetic resonance imaging

Left ventricular volume was determined in 12 healthy volunteersusing a newly developed two-dimensional echocardio-graphic delineationmethod. The results were compared with those of magnetic resonanceimaging, which served as the method of reference. Left ventricularend-diastolic volume was 123 ± 12 ml, echocardiographicallydefined, and 121 ± 12 ml calculated with magnetic resonanceimaging. End-systolic volume was 41 ± 7 ml on echocardiographyand 37±6 ml on magnetic resonance imaging. Left ventricularejection fraction was 67 ± 4%, echocardiographicallydefined, and 70 ± 5%, calculated with magnetic resonanceimaging. There was no statistical difference for any of themeasured parameters. Interstudy and inter-observer variabilitywas minimal. In conclusion, in healthy volunteers left ventricularvolume was accurately defined, using this newly developed two-dimensionalechocardiographic delineation method. During endocardial delineationa dynamic display is continuously available on a second window,allowing precise visual edge-detection. Moreover, correctionscan be made easily and quickly. These two advantages enhancethe accuracy of the method, even in cases of poor echogenicity.     

Deuterium Isotope Effect on the Metabolism of the Flame Retardant Tris(2,3-dibromopropyl) Phosphate in the Isolated Perfused Rat Liver

The metabolism of tris(2,3-dibromopropyl) phosphate (Tris-BP)was compared with that of completely deuterated Tris-BP (D15-Tris-BP)in an isolated, recirculating rat liver perfusion system inorder to determine the relative quantitative importance of twodifferent biotransformation pathways of Tris-BP: (i) cytochromeP450-mediated metabolism and (ii) GSH S-transferase-mediatedmetabolism. To accomplish this we quantitated the biliary excretionof S-(3-hydroxypropyl)glutathione (GSOH) as a marker metabolitefor cytochrome P450-mediated metabolism and that of S-(2,3-dihydroxypropyl)glutathione (GSOHOH) as a marker metabolite for GSH S-transferase-mediatedmetabolism. Completedeuterium substitution of Tris-BP significantlydecreased the formation of GSOH, whereas there was no effecton the formation of GSOHOH. Because our previous studies showeda large decrease in genotoxicity of D15-Tris-BP compared toTris-BP, the present results support our hypothesis that cytochromeP450-mediated metabolism is responsible for the genotoxic effectsof Tris BP in the rat liver.     

Induction of Cytochrome P450 Isoenzymes after Toxicokinetic Interactions between 2,3,7,8-Tetrachlorodibenzo-p-dioxin and 2,2',4,4',5,5'-Hexachlorobiphenyl in the Liver of the Mouse

One group of male C57BL/6J mice received a single oral doseof 1 nmol 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg. Sixother groups received single oral doses of 100, 300, or 1000µmol2,2',4,4',5,5'-hexachlorobiphenyl (HxCB)/kg, alone or in combinationwith 1 nmol/kg TCDD. Liver deposition of both compounds wasstudied at Day 3 after dosage. Hepatic CYP1A1 and CYP1A2 proteinlevels and related 7-ethoxyres-orufin-O-deethylation (EROD)and acetanilide 4-hydroxylation (ACOH) activities were alsostudied. A significant increase in the hepatic deposition ofTCDD was observed in all three mixed dose groups but TCDD didnot influence hepatic HxCB deposition. TCDD did increase bothCYP1A1 and CYP1A2 protein levels. In the HxCB-treated groups,CYP1A2 levels were also increased in a dose-dependent way butCYP1A1 levels were not increased. CYP1A2 activities (ACOH),but not protein levels, in the TCDD groups cotreated with HxCBwere higher than those in the group treated with TCDD alone.CYP1A1-dependent EROD activity and CYPlA2-dependent ACOH activitywere induced in all treated dose groups. It is concluded thatthe present results do not confirm a direct role of CYP1A2 inductionin the increase of hepatic TCDD levels by HxCB cotreatment inthe mixed HxCB/TCDD dose groups. However, in this aspect, thediscrepancy between CYP1A2 activities and protein levels remainsto be explained.