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PubMed1994

Heart disease in the assessment and treatment of hypercholesterolemia: coronary artery disease and other atherosclerotic disease, family history, and left ventricular hypertrophy.

There appears to be little doubt that lowering serum cholesterol for reduction of risk for coronary artery disease (CAD) events in patients with established CAD is cost-effective and can decrease the rate of CAD events, stabilize atherosclerotic plaque progression, and reduce CAD mortality and all-cause mortality. Meta-analysis of clinical trials conducted in patients with CAD has shown a 26% reduction in CAD events and a 9% reduction in total mortality. It was generalized from the results of nine major, recent angiographically monitored clinical trials that an improvement in obstruction was seen in 8% of control patients and 25% of treated patients. In the recently released report of the second Adult Treatment Panel (ATP II) of the U.S. National Cholesterol Education Program, atherosclerotic disease status joins low-density lipoprotein cholesterol (LDL-C) level as central to the diagnosis and treatment algorithm. The ATP II evaluation process is divided into two categories according to whether atherosclerotic disease is present, and a lower LDL-C target level--100 mg/dL (2.6 mmol/L)--is set for secondary prevention. Initial therapy when LDL-C is > or = 100 mg/dL in a patient with atherosclerotic disease is the Step Two Diet, weight control, exercise, and control of other risk factors. Drug therapy may be considered after a relatively short trial of hygienic therapy if LDL-C remains > or = 130 mg/dL (3.4 mmol/L). Other, selected aspects of heart disease for general consideration in assessing CAD risk are family history and the presence of left ventricular hypertrophy (LVH). Family history of premature CAD is included in the ATP II algorithm, with different age considerations by gender added. Although LVH is not part of ATP II risk assessment, its presence as defined by echocardiography increases CAD risk six- to eightfold in both men and women.

Arteriosclerosis↗

PubMed1999

Evaluation of colonic diverticular disease in autosomal dominant polycystic kidney disease without end-stage renal disease.

A previous study had shown an increased prevalence (83%) of diverticula among patients with autosomal dominant polycystic kidney disease (ADPKD) with end-stage renal disease (ESRD) compared with other ESRD patients without ADPKD (32%). Others have also suggested an increased risk for diverticular complications in renal transplant recipients with ADPKD. To determine whether there was an increased occurrence of diverticula among non-ESRD patients with ADPKD, we studied 55 patients with ADPKD who were not receiving renal replacement therapy compared with 12 unaffected family members (non-ADPKD) and 59 random patients who had undergone barium enemas (control [C]). No study patient had a history of diverticular disease. All patients underwent a double-contrast barium enema after administration of glucagon. The occurrence, number, location, and size of diverticula were noted. There was no significant difference among the three groups in regard to sex (men: ADPKD, 42% versus non-ADPKD, 42% versus C, 37%) or age (ADPKD, 49.3 +/- 0.7 versus non-ADPKD, 51.2 +/- 2.1 versus C, 49 +/- 1 years). There was no significant difference in the percentage of patients with diverticula (ADPKD, 47% versus non-ADPKD, 58% versus C, 59%), the percentage with only right-colon diverticula (ADPKD, 5% versus non-ADPKD, 17% versus C, 5%), the mean number of diverticula in patients with diverticulosis (ADPKD, 13.8 versus non-ADPKD, 7.9 versus C, 9.9 diverticula), or the size of the largest diverticula (ADPKD, 9.5 versus non-ADPKD, 10.4 versus C, 10.5 mm). There was no significant difference in these variables between the patients with ADPKD with a creatinine clearance greater than 70 mL/min/1.73 m(2) (n = 25) or less than 70 mL/min/1.73 m(2). This study does not show the greater prevalence of diverticular disease in non-ESRD patients with ADPKD compared with the general population. Thus, patients with ADPKD need not be considered at greater risk for diverticular disease than the general population.

Diverticulum, Colon↗

PubMedDate not supplied

Infectious Diseases Society of America and Centers for Disease Control. Summary of a workshop on surveillance for congenital cytomegalovirus disease.

Each year in the United States, 30,000 to 40,000 infants are born congenitally infected with cytomegalovirus (CMV), and more than 9,000 of these children suffer permanent sequelae. The purpose of this workshop was to present and discuss current information on the epidemiology, diagnosis, treatment, and prevention of CMV disease in mothers and their infants. The participants concluded that congenital CMV disease is a significant public health problem that, to date, has been largely ignored. They also agreed that certain child-rearing practices, such as the common use of day-care centers and breast-feeding, have changed the epidemiology of CMV in the United States and that the next decade may bring an increase in congenital CMV disease in certain groups. Therefore, a national system for surveillance of congenital CMV disease was established; its goals are to characterize trends over time, to identify risk groups, and to lay the groundwork for evaluation of future intervention programs. In addition, the surveillance system will be used to educate the medical and lay communities about congenital CMV disease and to facilitate collaborative efforts in research.

Centers for Disease Control and Prevention, U.S.↗

PubMed1958

Hirshsprung's disease; the clinical differentiation and treatment of children with Hirschsprung's disease and pseudo-Hirschsprung's disease.

Hirschsprung's disease is marked by constipation from the time of birth, with the development, if uncorrected, of a protuberant abdomen and flared costal margins. The rectal ampulla is empty and the abdomen is filled with fecal masses. Pain is not prominent. Flatus is passed in large amounts. Encopresis does not occur. Barium enema shows the characteristic narrowed distal rectal segment and biopsy of the rectum shows absence of the ganglion cells of the myenteric plexus. Treatment is operative resection of the distal narrow segment and a primary anastomosis.Hirschsprung's disease may be mimicked in children with:1. Psychogenic constipation-pseudo-Hirschsprung's disease. Unlike Hirschsprung's disease, symptoms do not appear at birth, encopresis is common, and the barium enema shows no narrow distal segment.2. Mental retardation and cerebral defect.3. Corrected imperforate anus-on the basis of stenosis, imperfect innervation or poor habit training.4. Cretinism-with severe constipation and intestinal dilatation perhaps the presenting symptoms. Treatment of these four groups of children with severe constipation not due to Hirschsprung's disease is:For Group 1, open discussion with parent and child. Assumption by the physician of full control of the details of treatment, and relegation of parent to the role of the physician's agent in following the prescribed regimen. For Group 2, an enema regimen. Whereas fairly rapid restoration (and then persistence) of normal bowel habit can be expected in Group 1, the basic defects in Group 2 may require indefinite continuation of treatment. For Group 3, regular enema regimen, in the less severe cases-one identical with that used in Group 1, and dilatation of strictures or anoplasty. In Group 4, thyroid hormone therapy relieves the constipation of hypothyroidism and causes reversion of radiographic changes in the colon and rectum.

Abdominal Cavity↗

PubMedDate not supplied

Natural history of peptic ulcer disease in Poland. Part X. Peptic ulcer disease and urinary tract diseases and diabetes.

In this successive report on the coexistence of peptic ulcer disease with diseases of other systems the coincidence is described of peptic ulcer with urinary system diseases and diabetes. In a population of 5813 patients with peptic ulcer studied using the "Ulcer" informatic programme urinary tract diseases were found in 6.21%, and diabetes in 1.41%. Differences are discussed in the prevalence of peptic ulcer and urinary tract disease or diabetes between males and females, and the age of the patients and frequency of various locations of ulcer in these cases.

Adult↗

PubMed1995

Junctional proteins of keratinocytes in Grover's disease, Hailey-Hailey's disease and Darier's disease.

Alterations of junctional structures in non-immune mediated acantholytic diseases (Grover's, Hailey-Hailey's and Darier's diseases) were examined using monoclonal antibodies against desmosomal attachment constituents (desmoplakin I & II and plakoglobin), desmosomal intercellular cement glycoprotein (desmoglein), protein of adherens junction (vinculin), and protein of gap junction (43Kd connexin). Universal cell surface (transmembrane) glycoprotein CD44 was also studied. In acantholytic foci of these diseases, attachment plaque proteins had dissolved and diffused into the acantholytic cells. The normal dotted linear pattern of immunostaining on the cell membrane was totally lost. In contrast, CD44 was well preserved on the cell membranes of acantholytic cells. Adherens junction and gap junction proteins were mostly preserved. Acantholytic cells of pemphigus vulgaris were similarly studied. In these cells, desmosomal attachment plaque proteins were very well preserved, while intercellular cement substance (desmoglein), adherens junctional proteins (vinculin), and gap junction protein (connexin) were totally absent, either on the cell membrane or in the cytoplasm. Electron microscopy confirmed an early dissolution of attachment plaque. Internalized desmosomal structures were seldom found in acantholytic cells of non-immune diseases. It was concluded that the primary event in acantholysis in these three diseases is the dissolution of desmosomal attachment plaque.

Acantholysis↗

PubMed1997

[An imbalance between Th1 and Th2-like cytokines in patients with autoimmune diseases--differential diagnosis between Th1 dominant autoimmune diseases and Th2 dominant autoimmune diseases].

An imbalance between T helper cell (Th)1 and Th2-like cytokines has been described in several autoimmune diseases. Organ specific autoimmune diseases such as multiple sclerosis (MS) and inflammatory bowel diseases (IBD) are caused by Th1 dominant immune responses. On the contrary, systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome(SS) are characterized by Th2 dominant imbalance of cytokine production. It might be useful for differential diagnosis among patients with various autoimmune diseases such as SLE, SS, IBD, and MS to measure the serum levels of cytokines such as IL-10, IFN gamma, and TNF alpha using ultrasensitive enzyme-linked immunosorbent assay system.

Animals↗

PubMed1996

Comparison of proline endopeptidase activity in brain tissue from normal cases and cases with Alzheimer's disease, Lewy body dementia, Parkinson's disease and Huntington's disease.

Neuronal death associated with plaque and tangle formation characteristic of Alzheimer's disease (AD) may result from an underlying defect of intracellular protein catabolism. In an attempt to identify the proteolytic enzyme types responsible for aberrant protein processing, we have composed the levels of activity of proline endopeptidase in brain tissue samples (grey/white matter) from frontal, parietal, temporal and occipital lobes, from normal control cases, and cases with AD, Lewy body dementia (LBD), Parkinson's disease (PD) and Huntington's disease (HD). The activity of proline endopeptidase was significantly reduced in AD to approximately 65% of that of corresponding control tissue-this is of note since previous biochemical analyses have in general failed to detect altered activity of other protease types in AD tissues. However, this relatively selective reduction in proline endopeptidase activity in AD tissue (in terms of protease types investigated) is not specific for disease type, since activity was also reduced (65%-70% of control) in tissue samples from LBD, PD and HD cases. The data suggest that reduction in proline endopeptidase activity may be a characteristic of a generalized process of neurodegeneration. Although the precise cellular function of this enzyme in normal/ pathological tissues remains to be determined, the question arises as to whether pharmacological strategies designed to enhance proline endopeptidase activity in brain tissue may improve patient outcome in the above disorders.

Aged↗

PubMed1986

Alzheimer's disease, Parkinson's disease, and motoneurone disease: abiotrophic interaction between ageing and environment?

The hypothesis is that Alzheimer's disease, Parkinson's disease (PD), and motoneurone disease are due to environmental damage to specific regions of the central nervous system and that the damage remains subclinical for several decades but makes those affected especially prone to the consequences of age-related neuronal attrition. This proposal is based on the association between environmental factors and certain neurodegenerative diseases (eg, methylphenyltetra-hydropyridine and parkinsonism, poliovirus infection and post-poliomyelitis syndrome, chickling pea ingestion and lathyrism, an unidentified environmental factor and amyotrophic lateral sclerosis-PD complex of Guam, and trauma and pugilist's encephalopathy) and on the long latent period between exposure to environmental factor and the appearance of symptoms in some of these disorders. The practical implications of this hypothesis are that epidemiological attention should be focussed on the environment in early rather than late life, prevention may be a realistic goal if the cause of subclinical damage can be identified, a search should be undertaken for causal mechanisms linking subclinical neuronal damage due to an environmental factor and the normal ageing process, and (4) better understanding of the regional selective vulnerability of the nervous system to the ageing process might allow a rational approach to treatment.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1998

Linkage analysis of candidate genes in autoimmune thyroid disease. III. Detailed analysis of chromosome 14 localizes Graves' disease-1 (GD-1) close to multinodular goiter-1 (MNG-1). International Consortium for the Genetics of Autoimmune Thyroid Disease.

The autoimmune thyroid diseases [Graves' and Hashimoto's diseases (GD and HT)] develop in genetically susceptible individuals, but the genes responsible for this susceptibility remain unknown. To identify such genes, we have been testing candidate genes and chromosomal regions using highly polymorphic microsatellite markers. We recently reported evidence for the first locus linked to GD (GD-1) on chromosome 14q31 in a small group of families. We have now extended these studies and analyzed 53 multiplex families with GD and/or HT (323 individuals). Chromosome 14 was screened using 16 microsatellite markers spanning the entire chromosome. Three additional markers located inside candidate genes on chromosome 14 were also studied. Microsatellite markers were amplified using fluorescent-labeled primers and separated on an ABI-310 genetic analyzer. The data were analyzed using LIPED software for two-point logarithm of odds (LOD) score analysis and GeneHunter software for multipoint linkage analysis. No linkage of any marker was found to HT or autoimmune thyroid diseases (GD+HT). The previously identified GD-1 locus on 14q31 continued to show evidence of linkage to GD in this much larger set of families. The maximum LOD score was 2.1 obtained for marker D14S81 (theta=0.01), assuming a recessive mode of inheritance and a penetrance of 0.3. Multipoint analysis yielded a maximum LOD score of 2.5 between markers D14S81 and D14S1054. There was no evidence for heterogeneity in our sample. These data again suggest the presence of a major Graves' disease susceptibilitygene (GD-1) on chromosome 14q31. This locus is close to the recently identified multinodular goiter-1 locus.

Autoimmune Diseases↗

PubMed1990

Parkinson's disease, motoneuron disease and Alzheimer's disease: origins and interrelationship.

The cause of neurodegenerative disease is considered. For Alzheimer's disease, Parkinson's disease, and motoneuron disease, accumulating evidence over the last 3 years indicates that (a) the usual etiological mechanisms involve a subclinical lesion which kills some neurons and reduces the life expectation of their surviving neighbors, and (b) there may be more than one cause for each of the idiopathic syndromes now termed AD, PD, and MND.

Alzheimer Disease↗

PubMed2005

Disease activity measurement of rheumatoid arthritis: Comparison of the simplified disease activity index (SDAI) and the disease activity score including 28 joints (DAS28) in daily routine.

OBJECTIVE: To assess the reliability and congruency of the Simplified Disease Activity Index (SDAI) compared with the Disease Activity Score including 28 joints (DAS28) in daily practice. METHODS: In 399 consecutive rheumatoid arthritis patients (307 women, 92 men), the SDAI and the DAS28 were calculated. Additionally, 115 of them were observed for 1 year and changes of both values were recorded. Joint assessments were performed by 4 experienced physicians. DAS28 and SDAI values and the respective changes were compared by correlation and regression analyses. Reliability assessment and factor analyses were performed. Disease activity categorizing was compared by the Wilcoxon's rank sum test. RESULTS: The median +/- SD scores were 3.42 +/- 1.45 for the DAS28 and 11.50 +/- 11.50 for the SDAI. Spearman's rho was 0.897 (P < 0.0001). Score changes were also significantly correlated. Reliability testing and factor analysis revealed that both scores can be regarded as monocomponent. Categorizing patients according to the European League Against Rheumatism response criteria (EULARC) or the SDAI revealed statistically significant differences between the 2 scales (P < 0.0001). CONCLUSION: SDAI values are considerably shifted to the left compared with DAS28 levels. Internal consistency and reliability of both scores are comparable. For the differences in disease activity categorizing due to the SDAI compared with the EULARC, a major limitation of the application of this newly developed disease activity score is given, unless these incongruencies can be cleared.

Adolescent↗

PubMed1992

Expression of the rheumatoid factor cross-reactive idiotype in JRA: association with disease onset subtype, disease activity and disease severity.

We previously reported that approximately one-third of patients with juvenile rheumatoid arthritis (JRA) express high concentrations of antibodies marked by the rheumatoid factor cross reactive idiotype (RCRI) in their sera (6). In order to determine if an expression of RCRI is associated with certain clinical features of the disease, we prospectively studied 49 patients with JRA over a six month period, and determined serum RCRI concentrations by inhibition ELISA. RCRI concentrations correlated significantly with the duration of morning stiffness (r = .3866, p less than .01), and the functional class (p less than .001), but not with the number of active joints. Expression of RCRI was higher in patients with systemic onset disease (p less than .03), compared to patients with pauciarticular or polyarticular disease. In patients studied on more than one occasion, the RCRI expression was relatively constant despite changes in disease activity. A subset of JRA patients with systemic onset disease, higher serum concentrations of the RCRI.

Adolescent↗

PubMed1995

Concurrence of Alzheimer's disease, Parkinson's disease, diffuse Lewy body disease, and amyotrophic lateral sclerosis.

A 71-year-old man developed signs of progressive dementia, followed by extrapyramidal and motor neuron disease symptoms, which led to death in 6 years. Neuropathological examination revealed neuritic plaques, neurofibrillary tangles, and Lewy bodies in the substantia nigra and neocortex. Atrophy and gliosis with intraneuronal ubiquitin inclusions were present in the anterior horns of the spinal cord. Overlapping of Alzheimer's disease, Parkinson's disease, diffuse Lewy body disease and amyotrophic lateral sclerosis is rare and can increase our understanding of the process of neurodegeneration.

Aged↗

PubMed2001

Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses?

Inflammatory bowel disease (IBD) comprises two chronic, tissue-destructive, clinical entities Crohn disease (CD) and ulcerative colitis (UC) both apparently caused by immunological overreaction (hypersensitivity) to commensal gut bacteria. Under normal conditions the intestinal immune system shows a down-regulating tone ('oral tolerance') against dietary antigens and the indigenous microbiota. This local homeostasis is disturbed in IBD, leading to hyperactivation of T helper 1 (Th1) cells with abundant secretion of interferon-gamma and tumor necrosis factor (TNF) and production of IgG antibodies against commensal bacteria. In addition, UC includes genetically determined autoimmunity, particularly IgG1-mediated cytotoxic epithelial attack. Breaching of the epithelium is the best-defined event underlying abrogation of oral tolerance, but immune deviation caused by cytokines fiom irritated epithelial cells or subepithelial elements (for example, mast cells, natural killer cells, macrophages) may also be involved. Endogenous infection with local hypersensitivity likewise causes periodontal disease, reflecting 'frustrated' immune elimination mechanisms entertained by antigens from dental plaque. Altogether, perturbation of a tightly controlled cytokine network, with abnormal crosstalk between several cell types, apparently explains the progressive immunopathology of chronic inflammatory mucosal diseases in general. This adverse development will be influenced by numerous immunity genes, the dosage and potential pathogeniciy of commensal bacteria, general health, nutritional status, and psychological factors. Several targets for new therapy have tentatively been identified to block immunopathological mechanisms in IBD, and inhibition of TNF has a striking beneficial effect in CD, supporting a central role of this cytokine.

Animals↗

PubMed2000

Disease outcome in inflammatory bowel disease: mortality, morbidity and therapeutic management of a 796-person inception cohort in the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD).

BACKGROUND: The course of inflammatory bowel diseases (IBD) has mainly been studied using different methods in single patient cohorts. The aim of the present study was to assess clinical aspects of disease outcome in a population-based cohort of IBD patients over a 4-year period in multiple centres across Europe. METHODS: A total of 796 patients with IBD diagnosed in 10 centres between October 1991 and October 1993, registered at the EC IBD study centre (98% of the original cohort), participated in the study. Investigators filled out a standard follow-up form containing questions on the method of follow-up, vital status of the patient, change in diagnosis, extraintestinal manifestations, medical and surgical treatment, and physician's global assessment of disease activity. RESULTS: Complete relief of the complaints was reported in 255 (48%) patients with ulcerative colitis (UC), 9 (50%) with indeterminate colitis (IC), but only in 87 (35%) of patients with Crohn disease (CD). Improvement was reported in 195 (37%) patients with UC, 113 (45%) with CD and 6 (33%) with IC. During the 4-year follow-up period, 23 patients died (14 UC, 8 CD. and 1 IC). The mean age at death was 69.3 years (s, 14.9 years). The deaths of three patients were recorded as directly due to IBD. CONCLUSIONS: With the present approach to therapeutic management the short-term outcome of patients with IBD seems to be favourable in 10 medical centres in the north and south of Europe. However, more detailed studies including both objective and subjective measures are necessary.

Adult↗

PubMed1996

Psychiatric features in diffuse Lewy body disease: a clinicopathologic study using Alzheimer's disease and Parkinson's disease comparison groups.

We conducted a retrospective study to determine the frequency of depression, hallucinations, and delusions in patients with diffuse Lewy body disease (DLBD) and to compare these findings with those in Alzheimer's disease (AD) and Parkinson's disease (PD). One hundred twelve subjects were included in the study. Of these, 28 subjects were diagnosed with DLBD, 58 with AD, and 26 with PD at autopsy. Main outcome measures included the percentages of subjects in each of the three categories in whom depression, hallucinations, or delusions were reported at any time during the course of the illness. Hallucinations and delusions were further classified by type. We found that depression was more common in DLBD (50.0%) than in AD (13.8%) (chi 2 = 13.00, p = 0.0003). There was no difference in the frequency of depression in DLBD and PD (57.7%) (chi 2 = 0.32, p = 0.57). Hallucinations were reported more frequently in DLBD (60.7%) than in AD (34.5%) (chi 2 = 5.30, p = 0.021). There was no difference in the frequency of hallucinations in DLBD and PD (53.8%) (chi 2 = 0.26, p = 0.61). Delusions were more common in DLBD (57.1%) than in PD (15.4%) (chi 2 = 10.08, p = 0.0015). There was no difference in the frequency of delusions in DLBD and AD (53.4%) (chi 2 = 0.10, p = 0.75). There was a male predominance of DLBD cases and PD cases; AD cases were predominantly women. We conclude that psychiatric features are very common in DLBD and should be a central diagnostic criterion for the disease.

Aged↗

PubMedDate not supplied

Natural history of peptic ulcer disease in Poland. Part. IX. Peptic ulcer disease and cardiovascular and respiratory system diseases.

Another analysis of the Ulcer databank was concerned with the incidence of cardiovascular diseases, respiratory diseases and pulmonary emphysema in patients with peptic ulcer. In the studied population of 5813 patients with peptic ulcer 744 (12.79%) had cardiovascular diseases, 437 (7.51%) had respiratory diseases, and 17 (0.29%) had pulmonary emphysema.

Adult↗