Malnutrition and subsequent ischemic heart disease in former prisoners of war of world war II and the Korean conflict

The harsh treatment of former prisoners of war (POWs) of World War II and the Korean conflict resulted in severe malnutrition. Although rarely linked to specific long-term medical problems, a specific marker of malnutrition, self-reported lower limb edema (presumably due to a vitamin B deficiency) was associated with a three-fold increase in subsequent death attributed to ischemic heart disease (IHD) during the follow-up period from 1967 through 1975. Although there is at present no medical basis for linking edema, which is perhaps a marker for some unmeasured risk factor, to subsequent IHD, this finding may nonetheless have medical implications for the group of former POWs and other populations with severe dietary deficiency. It also suggests there may be a need to reexamine currently held theories on malnutrition and subsequent chronic disease.     

Chronic anemia as a complication of parvovirus B19 infection in a pediatric kidney transplant patient

. This is a report of unexplained anemia that persisted for 4 months in an adolescent renal transplant patient receiving immunosuppression that included prednisone, tacrolimus, and mycophenolate mofetil. This patient required monthly blood transfusions for fatigue, palpitations, and hematocrit levels between 15% and 17%. In addition, his posttransplant course was notable for the development of insulin-dependent diabetes mellitus. While receiving low-dose prednisone, he was switched from tacrolimus to cyclosporin and tapered off insulin injections over the next 2 months. At 4.5 months post-transplantation, further diagnostic evaluation was suggestive of parvovirus B19 infection as the cause for our patient’s chronic anemia. After testing negative for serum-specific parvovirus B19 IgM and IgG antibodies, parvovirus B19 infection was detected in blood by the polymerase chain reaction. Treatment with intravenous immunoglobulin (1 g/kg per day × 2 days) resulted in normalization of both his reticulocyte count and hematocrit within 6 weeks. At 4 months after receiving the immunoglobulin infusion, he has maintained a normal hematocrit level and stable renal function without requiring further blood transfusions. Received August 23, 1996; received in revised form and accepted November 20, 1996     

Proteinuria and other renal functions in Wilson’s disease

Renal lesions have repeatedly been described in Wilson’s disease (WD). We investigated the excretion of total protein, albumin, low (LMW) and high molecular weight (HMW) proteins, N-acetyl-β-D-glucosaminidase (NAG), and calcium, as well as creatinine clearance, in 24-h urine samples of 41 patients with WD aged 6 – 37 (mean 17) years who had been treated for a period of 0 – 15 (mean 4.5) years with D-penicillamine (900 mg/day). The amount of all protein excreted was significantly increased compared with controls, 39% of patients presenting with total proteinuria more than two standard deviations from the mean of controls. The changes in protein excretion depended on the duration of treatment. LMW proteinuria was elevated almost exclusively in the first 2 years after the start of treatment, indicating early tubular damage. This is supported by an initially high excretion of β₂-microglobulin, NAG, and calcium. Increased excretion of HMW proteins, including albumin, persisted over longer periods, which suggests glomerular injury in some patients, possibly related to the use of D-penicillamine. Creatinine clearance remained roughly within normal limits. We propose that renal function should regularly be checked in patients with WD. Received October 26, 1995; received in revised form August 27, 1996; accepted September 20, 1996     

Iatrogenic Creutzfeldt–Jakob disease subsequent to dural graft: persisting risk after 1987

The first case of Creutzfeldt-Jakob disease (CJD) related to the use of a dura mater graft of cadaveric origin was identified in 1987 and this procedure is now considered as one of the main causes of iatrogenic CJD. Although the decontamination procedure for the preparation of graft material was modified, the product was withdrawn from the market in many countries a few years later and replaced by synthetic material. In this context, two patients treated in our institution developed CJD following a cadaveric dural graft performed after cerebral and lumbar trauma. Their clinical presentation, showing predominant cerebellar symptoms, late deterioration and myoclonic jerks, and a rapid disease course until death, was similar to that of previously reported cases involving the iatrogenic form. As the graft for one of the patients was performed in 1991 (several years after modification of the decontamination procedure), this fourth reported case suggests that the risk of iatrogenic CJD may have persisted in some patients treated after 1987, when grafts of cadaveric origin were totally abandoned.     

Pulmonary Sequestration In A Child With Acute Myelold Leukemia

The article describes a relatively rare congenital anomaly that was difficult to diagnose in a 10-year-old child with acute nonlymphoblastic leukemia. Just at diagnosis of leukemia, the patient showed a pathologic chest radiograph because of a parenchymal thickening at the right lung apex. The presence of bronchopneumonia was suspected, and broad-spectrum antibiotic therapy was started with subsequent antifungal treatment for persistent fever and concurrent chemotherapy-induced marrow aplasia, which did not favor pulmonary infiltrate recovery. Continuous culture tests, including bronchial swab, proved negative for Koch-Weeks bacillus, fungal organisms, and other pathogens. Computed tomography, however, was suggestive of Aspergillus lung involvement, and apical sepmentectomy was performed. The anatomic pathologist suggested the diagnosis of intralobar sequestration. In summary, when pulmonary pathology with an excavation is found in a leukemic child, one must consider the possibility of pulmonary sequestration complicated by an infectious disease.     

脑型肌酸激酶同功酶在脑血管病中的意义 Ⅱ.急性脑血管病患者血清和脑脊液中CKBB变化及与CT片上病损大小的关系

用改良的ELISA检测25例正常对照组和32例急性脑血管病患者的血清和脑脊液(CSF)中的脑型肌酸激酶同功酶BB(creatine kinase isoenzyme BB)浓度。32例急性脑血管病患者CSF CKBB平均水平为16.62±8.3ng/ml,明显高于对照组(7.5—4.8ng/ml)。发病24h内CSFCKBB轻微增高,24～48h达高峰,以后下降,7天左右尚未恢复正常。病初CSF CKBB水平明显高于恢复期。9例高血压性脑出血的血肿出血量(按CT片上血肿大小计算)与患者CSF CKBB有密切关系(r=0.8127,P<0.01)。血肿体积(X)与CSF CKBB浓度(y)的回归方程y—7.945±0.872X。     

Effects of epidermal growth factor in the mammalian central nervous system: Its possible implications in brain pathologies and therapeutic applications

The development and maintenance of the normal functional integrity of the mammalian central nervous system is under the influence of a number of growth and trophic factors. One such growth factor, epidermal growth factor, has been detected in the mammalian brain and found to be associated with various brain regions and cell types. This small ubiquitous polypeptide can influence the proliferation, Metabolism, and differentiation of both glia and neurons in the central nervous system. We discuss the effects of epidermal growth factor on glial and neuronal cell function in an attempt to understand its role in development and maintenance of normal brain integrity. In addition, we review its possible implications in several pathological states in the central nervous system and speculate on therapeutic applications for this growth factor. © 1992 Wiley-Liss, Inc.     

Comparison of acid reduction in antiulcer operations

Background: Three acid-reducing operations have recently been described for the laparoscopic treatment of peptic ulcer disease. These consist of a posterior truncal vagotomy combined with either (1) an anterior seromyotomy (SERO), (2) an anterior highly selective vagotomy (AHSV), or (3) a linear stapled lesser curvature excision (STAP). The purpose of this study was to investigate the physiologic effects of these procedures in terms of basal and maximal acid outputs. Methods: Fifty New Zealand rabbits were prospectively randomized into five open laparotomy groups (n= 10): a control group without vagal manipulation (CON), a bilateral truncal vagotomy with pyloromyotomy group (VP), a SERO group, an AHSV group, and a STAP group. All animals underwent placement of a gastrostomy tube for subsequent gastric secretory analysis. On postoperative day 6, basal acid outputs (BAO) and maximal acid outputs (MAO) following IV pentagastrin stimulation (30 μg/kg/h) were measured. Results were compared statistically using the ANOVA method. Results: Pentagastrin stimulation was associated with a significant increase in MAO in the CON group (p < 0.05 vs BAO); however, this response was effectively blunted in all the experimental groups. There were no differences in BAO or MAO between any of the vagotomized groups (SERO, HSV, STAP, VP). Conclusions: We conclude that the three acid-reducing procedures modified for laparoscopy are equally efficacious in reducing gastric acid secretion and that they compare favorably with VP. To our knowledge, this is the first report comparing basal and stimulated gastric acid secretion between these new acid-reducing techniques. Received: 27 March 1996/Accepted: 17 July 1996     

Chorea as a presenting feature of variant Creutzfeldt-Jakob disease.

We report on a patient with pathologically proven variant Creutzfeld-Jakob disease in whom chorea was a presenting feature of the disease, and was unaccompanied by the typical prodrome of psychiatric disturbance or sensory symptoms.     

Suggestive linkage to chromosome 19 in a large Cuban family with late‐onset Parkinson's disease

The identification of disease genes using family‐based approaches has provided important insights into the pathogenesis of Parkinson's disease (PD) demonstrating the importance of genetic studies on monogenic forms of the disease. We studied a large Cuban family with typical, late‐onset PD and probable autosomal dominant inheritance. Mean age at onset was 61.2 years (±12.53, 45–76). Other phenotypes such as essential tremor and atypical parkinsonism were observed in this family. We carried out a genome‐wide scan and linkage analyses. The genetic data were analyzed using a conservative model in which only patients with clinically definite or likely PD were considered affected, other phenotypes were regarded as “unknown.” Multipoint analyses yielded a maximum LOD of 2.26 between markers D19S221 and D19S840. Haplotype analysis showed a region on chromosome 19 shared by six of seven PD patients. The essential tremor phenotype and the atypical parkinsonism do not segregate with this haplotype, suggesting a different etiology. Our findings suggest the presence of a novel locus for PD on chromosome 19p13.3–q12. We propose that an oligogenic model with moderate contribution of two or three genes rather than a “pure” monogenic model might explain better the wide range in age at onset, the reduced penetrance and the phenotypical variability observed in PD families. © 2003 Movement Disorder Society