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Time course and sequence of pathological changes in the cerebellum of microsphere-embolized rats.

Ischemia is a major cause of damage to the central nervous system as a consequence of stroke or trauma. Here, we analyzed with high temporal resolution the time course of pathological changes in the neurons (granule and Purkinje cells) and glia (Bergmann and astroglia cells) in the cerebellar cortex and white matter. The period studied ranged from 30 min to 7 days after a microsphere-induced embolism used as a model of stroke and multi-infarct dementia. Some pathological changes in the neurons in the cerebellar cortex were identified early, that is, beginning at 3 h after the microsphere-induced embolism, and glial pathology appeared only later. The pathological changes in the white matter also appeared slightly later, that is, 6 h after embolism and were less pronounced than those in the cerebellar cortex. This suggests that neuronal pathology is induced more rapidly and/or more easily than the glial pathology. In addition, BrdU staining shows that cell proliferation is limited to a 1-day period beginning about 1 day after the embolism. These data demonstrate that changes after an ischemic lesion of the cerebellum proceeds from upper cerebellar cortex to deeper cerebellar cortex or white matter and also that microsphere-induced changes proceed from neuronal to glial pathology.

Animals↗

Incidence of unexpected pathology in routine adenoidectomy specimens.

OBJECTIVE: The aim of this study was to determine the incidence of unexpected pathologies in adenoidectomy specimens and necessity for histopathologic evaluation of adenoid tissue. MATERIALS AND METHODS: All patients younger than 16 years who underwent routine adenoidectomy were reviewed. Patients were excluded if the primary surgery was other than routine adenoidectomy such as nasopharyngeal biopsy for suspicion of malignancy or other pathology. RESULTS: One thousand one hundred eighty-four patients (683 males, 501 females) were involved in this study. The mean age was 7.53+/-3.24 years, ranging between 2 and 16 years. There was no patient with unexpected pathology among 1184 routine and primary adenoidectomy procedures. However, one patient had unexpected pathology among 33 revision adenoidectomy procedures (3%). CONCLUSIONS: There was no occult pathology in routine primary adenoidectomy. The incidence of unexpected pathology in revision adenoidectomy was 3%. Microscopic evaluation of adenoid tissue gives some knowledge about histological properties and rarely some unexpected pathologies. Searching for malignancy is unnecessary in routine primary adenoidectomy cases without any other clinical, radiological and laboratory findings.

Adenoidectomy↗

The prevalence of fimbrial pathology in patients with early stages of endometriosis.

STUDY OBJECTIVE: The presence of fimbrial pathology in advanced endometriosis is clearly understood. However, little is known about the prevalence of fimbrial pathology in early stages of endometriosis. The purpose of this study is to determine the prevalence of fimbrial pathology in patients with infertility with early stages of endometriosis. DESIGN: Historical cohort study (Canadian Task Force classification II/III). SETTING: Tertiary referral center. PATIENTS: The study group (Group 1) consisted of 315 infertile women who were found to have stage I or stage II endometriosis, and the control group (Group 2) consisted of 152 infertile women without endometriosis (Group 2). INTERVENTION: Laparoscopic evaluation for the presence and type of fimbrial pathology. MEASUREMENTS AND MAIN RESULTS: The prevalence of fimbrial pathology was significantly higher in infertile patients with early stages of endometriosis (50.2%) compared with infertile patients with no endometriosis (17.8%, p <.0001). CONCLUSION: These preliminary data suggest the presence of fimbrial pathology in many patients with early stages of endometriosis. Such pathology may act as a mechanical factor interfering with the ovum pick-up mechanism.

Cohort Studies↗

Investigation of Lewy pathology in the visual pathway of brains of dementia with Lewy bodies.

We examined 19 autopsied cases of dementia with Lewy bodies (DLB) using pathological and alpha-synuclein-immunohistochemical methods, and investigated Lewy pathology in the primary visual pathway (lateral geniculate body and Brodmann's area 17), secondary visual pathway (pulvinar, Brodmann's areas 18 and 19, and inferior temporal cortex), amygdala and substantia nigra, to clarify the relationship between visual misidentification and Lewy pathology in the visual pathway. Consequently, the secondary visual pathway revealed significantly severer Lewy pathology than the primary visual pathway, suggesting that the degeneration of the secondary visual pathway induces dysfunction in the recognition of objects shape and color. In addition, the amygdala revealed significantly severer Lewy pathology and neuronal loss than the primary and secondary visual pathways, suggesting that the degeneration of the amygdala, which receives the afferent connections from the substantia nigra, fails to modulate the visual processing according to cognition and emotion. These findings suggest that Lewy pathologies in the secondary visual pathway and amygdala may cause the dysfunction of the visuo-amygdaloid pathway and participate in visual misidentification in DLB patients. In addition, we compared Lewy pathology between cases with and without visual hallucinations, and showed no significant differences between the two groups.

Aged↗

CSF monoamine patterns in pathological gamblers and healthy controls.

Previous reports on compounds in the cerebrospinal fluid (CSF) of pathological gamblers have focused on disturbed NA, DA and 5-HT function in the central nervous system. We have analysed precursors, transmitters and transmitter metabolites in 3 x 6 ml of CSF obtained from one female and 11 male pathological gamblers and 11 healthy male controls lumbar punctured at the L4-5 level after 8 h of fasting without preceding strict bedrest. Pathological gamblers displayed lower CSF levels of tryptophan and 5-HT while the opposite was the case for 5-HIAA, tyrosine, DA, HVA, DOPAC and HMPG. In contrast to previous studies, the NA level did not differ between pathological gamblers and healthy controls. A disrupted CSF gradient was noted for tryptophan, 5-HT, DA, HVA, DOPAC, NA and HMPG, but only in pathological gamblers. A disrupted gradient was found for 5-HIAA in both pathological gamblers and healthy controls. The results are in line with the presence of altered indoleamine and catecholamine function in pathological gamblers as well as an altered CSF transport from the brain to the lumbar compartment in such gamblers.

Adult↗

Pathogenesis of partial tear of the rotator cuff: a clinical and pathologic study.

This prospective study investigated the clinical and pathologic results in 66 patients with partial tears of the rotator cuff from January 1996 to December 1998. The pathologic change in the rotator cuff was graded from the magnetic resonance images by using the criteria described by Zlatkin and Iannotti. A modified grading system from Ozaki and Panni was used for pathologic grading of the anterior acromion. The functional score of Constant and Murley was used for clinical assessment. The pathologic change in the rotator cuff revealed by the magnetic resonance imaging study was more severe in patients with articular side tears compared with patients who had bursal side tears. On the contrary, the pathologic changes in the acromion were significantly milder in patients with articular side tears compared with bursal side tears. These observations indicate that articular side tears of the rotator cuff are mainly associated with intrinsic pathologic changes of the rotator cuff, whereas bursal side tears are associated with subacromial impingement on an underlying milder pathologic change of the rotator cuff.

Acromion↗

Two commonly used neoadjuvant chemoradiotherapy regimens for locally advanced stage III non-small cell lung carcinoma: long-term results and associations with pathologic response.

BACKGROUND: We performed this study to determine the outcomes (pathologic response, survival, local-regional control, and toxicity) in patients treated with neoadjuvant chemoradiotherapy and planned operation for stage IIIA non-small cell lung carcinoma. METHODS: Patients treated from 1993 to 2000 with neoadjuvant chemoradiotherapy and a predetermined plan for subsequent surgical resection for stage III non-small cell lung carcinoma were analyzed. All patients underwent pretreatment evaluation at the university's Multidisciplinary Lung Cancer Center. Most patients (87%) had complete mediastinoscopy staging, and all were believed to be poor candidates for up-front operation because of bulky extent of disease. The radiotherapy program used conventional, 2-dimensionally planned treatment to 45 to 54 Gy in 1.8- to 2-Gy fraction size. Concurrent chemotherapy consisted of etoposide/cisplatin or carboplatin/paclitaxel. Study end points included resectability, pathologic response, local-regional control, survival, and toxicity. An exploratory comparison between pathologic response and long-term survival was performed. An exploratory comparison between older chemotherapy (etoposide/cisplatin) and third-generation chemotherapy (carboplatin/paclitaxel) was also performed. RESULTS: Of 53 patients, 45 (85%) were deemed surgical candidates after induction therapy. Twenty-two (42% of the initial cohort) patients had a major pathologic response to stage 0, I, or II disease. The 5-year actuarial survival was 31%. Major pathologic response was associated with improved survival (48% vs 24%; P =.027). The overall rate of early death potentially related to therapy in this series was 9%; this mostly occurred in patients who underwent right pneumonectomy. There was no difference in efficacy or mortality between etoposide/cisplatin and radiotherapy versus carboplatin/paclitaxel and radiotherapy, although the latter regimen was associated with less grade 3 or higher acute toxicity necessitating interruption or hospitalization during neoadjuvant treatment (P =.02). In-field local control was achieved in 83% of all patients (90% of the patients who underwent resection). Brain metastases as the first site of treatment failure occurred in 23% of all patients. CONCLUSIONS: Neoadjuvant concurrent chemoradiation delivers high resectability, major pathologic response rate, and excellent local-regional control, with encouraging long-term survival considering the patient population studied. Major pathologic response correlates with long-term survival. Neoadjuvant carboplatin/paclitaxel and radiotherapy is an appropriate framework on which to add new therapies.

Aged↗

Is biopsy Gleason score independently associated with biochemical progression following radical prostatectomy after adjusting for pathological Gleason score?

PURPOSE: Biopsy Gleason score is known to be associated with prostate specific antigen failure following radical prostatectomy. However, it is unclear whether it remains associated with outcome after surgery when the pathological Gleason score is known. MATERIALS AND METHODS: We determined the association between biopsy Gleason score and biochemical progression after correcting for preoperative and postoperative characteristics, including pathological Gleason score, in 1,931 men treated with radical prostatectomy between 1988 and 2005 in the Shared Equal Access Regional Cancer Hospital Database Study Group database. Gleason score was examined as a categorical variable of 2 to 6, 3 + 4 and 4 + 3 or greater. RESULTS: Higher biopsy Gleason scores were positively associated with extracapsular extension (p <0.001), positive surgical margins (p <0.001), seminal vesicle invasion (p <0.001), positive lymph nodes (p <0.001) and biochemical progression (log rank p <0.001). After adjusting for only preoperative characteristics biopsy Gleason 3 + 4 and 4 + 3 or greater were associated with increased risk of biochemical progression compared to biopsy Gleason 6 or less (p = 0.001 and <0.001, respectively). After further adjusting for multiple pathological characteristics, including pathological Gleason score, the association between higher biopsy Gleason score and progression was little changed, in that men with biopsy Gleason 3 + 4 and 4 + 3 or greater were significantly more likely to experience progression (p = 0.001 and <0.001, respectively). Furthermore, when stratified by pathological Gleason score, higher biopsy Gleason scores were associated with an increased risk of biochemical progression in each pathological Gleason score category (log rank p </=0.007). CONCLUSIONS: Biopsy Gleason score remained strongly associated with progression even when the pathological Gleason score was known and controlled for. If confirmed at other centers, incorporation of biopsy Gleason score into postoperative nomograms designed to estimate the progression risk might improve model precision.

Aged↗

Evaluation of voice pathology based on the estimation of vocal fold biomechanical parameters.

Voice disorders are a source of increasing concern as normal voice quality is a social demand for at least one third of the population in developed countries in cases where voice is an essential resource in professional exercise. In addition, the growing exposure to certain pathogenic factors such as smoking, alcohol abuse, air pollution, and acoustic contamination, and other problems such as gastro-esopharyngeal reflux or allergy as well as aging, aggravate voice disorders. Voice pathologies justify the assignment of larger resources to prevention policies, early detection, and less aggressive treatments. Traditional pathology detection relies on perceptive evaluation methods (GRABS), acoustic analysis, and visual inspection (indirect laryngoscopy, and modern fibro-endo-stroboscopy). This article describes a method for voice pathology detection based on the noninvasive estimation of vocal cord biomechanical parameters derived from voice using specific signal processing methods. Preliminary results using records from patients showing four frequent causes of voice pathology (nodules, polyps, chronic laryngitis, and Reinke's edema) are given. The results show that the alteration (distortion, unbalance, or deviation) of cord biomechanical parameters may serve as an indicator of pathology. Statistical methods based on hierarchical clustering and principal component analysis reveal that combining biomechanical estimates with classic perturbation parameters increases the accuracy of acoustic analysis, improving the detection of voice pathology. This research could open new possibilities for noninvasive screening of vocal fold pathologies and could be used in the implantation of e-health voice care services.

Biomechanical Phenomena↗

Insular Alzheimer's disease pathology as a cause of "age-related" autonomic dysfunction and mortality in the non-demented elderly.

Only a few brain structures have been implicated in the autonomic control of blood pressure and heart rate. Among them are heteromodal association areas in the cortex, especially the insular cortex. Ischemic insular lesions have been associated with both cardiac arrhythmias and mortality. However, stroke may not be the only insular pathology with the potential to disrupt autonomic function. Alzheimer's disease (AD) is associated with both insular pathology and autonomic dysfunction. Alzheimer's dementia is merely the final stage of a pathological process that spans decades. Recent studies have demonstrated a hierarchichal sequence of AD pathology that includes the insular cortex. This may explain why AD has effects on BP and central autonomic cardio-regulatory functions. However, AD reaches the insular cortex at a "preclinical" stage in its development (i.e., before "dementia" can be diagnosed). Thus, AD pathology should also be considered as a possible explanation for autonomic morbidity and mortality in non-demented elderly persons. We hypothesize that autonomic dyscontrol, commonly seen in non-demented well elderly persons without significant cardiovascular disease (CVD), reflects subclinical stages of AD pathology affecting the insular cortex. If true, then preclinical AD pathology should be considered as a possible explanation for arrhythmia/fall related morbidity and mortality in non-demented elderly persons.

Aged↗

Pathology of presynaptic proteins in Alzheimer's disease: more than simple loss of terminals.

Synaptic pathology is receiving increased attention in the study of the pathophysiology of Alzheimer's disease. A review of the literature on synaptic pathology in Alzheimer's disease was undertaken, focused on five areas. First, concerning the molecular substrates of presynaptic terminal changes, not all proteins are equally affected. Second, all brain regions in Alzheimer's disease do not show equivalent presynaptic protein pathology, hippocampus tended to be most affected. Third, relationships between presynaptic and neurofibrillary tangle pathology tended to be stronger than relationships with plaques. Fourth, broadly speaking, more severe cognitive impairment was associated with more severe presynaptic pathology. Finally, the relationship of presynaptic pathology and stage of illness appeared complex, with some reports of increased presynaptic proteins in earlier phases of illness, but consistent decreases in later phases. Detailed studies of presynaptic pathology in transgenic mouse models related to Alzheimer's disease may provide important insights concerning these observations.

Alzheimer Disease↗

Probability of biochemical recurrence by analysis of pathologic stage, Gleason score, and margin status for localized prostate cancer.

OBJECTIVES: The Partin tables provide pretreatment information regarding the probability of various pathologic stages (eg, organ confined, extraprostatic extension, and seminal vesicle or lymph node involvement). Although the pathologic stage serves as an excellent surrogate for outcome after radical prostatectomy (RRP), many patients and physicians want to know how the predictions made from the Partin tables can be translated into long-term biochemical recurrence-free survival. In this work, we go beyond the pathologic outcomes predicted by the Partin nomograms to provide long-term biochemical recurrence-free estimates on the basis of the pathologic data obtained at RRP to help counsel patients after surgery for prostate cancer. METHODS: The study group comprised 1955 men treated by one surgeon with RRP and pelvic lymph node dissection for clinically localized disease (1989 to 2001). The patients were followed up for at least 1 year postoperatively, and the disease-free survival rates were determined using Kaplan-Meier analysis. RESULTS: The pathologic stages were as follows: organ confined in 57%, extraprostatic extension in 35%, seminal vesicle involvement in 4%, and lymph node involvement in 4%. The prostatectomy Gleason score distribution was as follows: 2 to 4 in 1%, 5 to 6 in 63%, 7 in 30%, and 8 to 10 in 6%. Overall, a positive surgical margin was present in 9.8%. On the basis of the prostatectomy Gleason score, pathologic stage, and surgical margin status, the probability of long-term biochemical recurrence-free survival was divided into four groups: excellent, good, moderate, and low. CONCLUSIONS: These simple to use and explain risk groups can be used to predict long-term biochemical recurrence-free survival from pathologic stage data obtained at surgery or predicted from the Partin tables, along with surgical margin status and Gleason score information obtained at RRP.

Adenocarcinoma↗

Adjuvant radiotherapy in patients with pathologic Stage C (pT3N0) adenocarcinoma of the prostate.

OBJECTIVES: This report is an update on the outcomes in the management of pathologic Stage C (T3N0) prostate cancer (CaP) with postoperative irradiation. METHODS: Between 1976 and 1994, 311 patients with pathologic Stage C CaP were treated with radical prostatectomy. Pathologic stage was as follows: C1, 60 patients (19%), C2, 146 patients (47%), and C3, 105 patients (34%). Gleason score was 2 to 4 in 10 patients (3.2%), 5 to 6 in 121 (39%), 7 in 101 (32%), and 8 to 10 in 76 (24%); median prostate-specific antigen (PSA) level was 11.9 ng/mL. Postoperative irradiation consisted of a median dose of 48 Gy. Follow-up was up to 18 years (median 5). RESULTS: The 10-year actuarial survival was 81% and 10-year disease-free survival was 51%. Pathologic stage and Gleason score were independently predictive of recurrence, each with P >0.001 after controlling for the other. Patients with pathologic Stage C3 and Gleason score 7 to 10 were in the worst prognostic category and had 5.4 times the risk of recurrence compared with patients with pathologic Stage C1-C2, Gleason score 2 to 6. Preoperative PSA was a good (P = 0.02) predictor of disease-free survival. Clinical recurrence was seen in 28 patients (9%), including 10 (3.2%) with local recurrence. PSA recurrence (PSA greater than 0.05 ng/mL) developed in 68 patients (22%). CONCLUSIONS: With the known limitations of a nonrandomized clinical trial, on the basis of the experience of this study we recommend the use of moderate dose, limited-field postoperative radiotherapy in patients with pathologic Stage C disease with Gleason score greater than 4.

Actuarial Analysis↗

"Auditory neuropathy": physiologic and pathologic evidence calls for more diagnostic specificity.

The term "auditory neuropathy" is being used in a rapidly increasing number of papers in the audiology/otolaryngology literature for a variety of individuals (mostly children) who fulfill the following criteria: (1) understanding of speech worse than predicted from the degree of hearing loss on their behavioral audiograms; (2) recordable otoacoustic emissions and/or cochlear microphonic; together with (3) absent or atypical auditory brain stem responses. Because of the general lack of anatomic foundation for the label "auditory neuropathy" as currently used, we review the anatomy of the auditory pathway, the definition of neuropathy and its demyelinating, axonal, and mixed variants. We submit that the diagnostic term "auditory neuropathy" is anatomically inappropriate unless patients have documented evidence for selective involvement of either the spiral ganglion cells or their axons, or of the 8th nerve as a whole. In view of biologic differences between peripheral nerves and white matter tracts in the brain, the term "auditory neuropathy" is inappropriate for pathologies affecting the central auditory pathway in the brainstem and brain selectively. Published reports of patients with "auditory neuropathy" indicate that they are extremely heterogeneous in underlying medical diagnosis, age, severity, test results, and that only a small number have undergone the detailed investigations that would enable a more precise diagnosis of the locus of their pathologies. The electrophysiology of peripheral neuropathies and the deficits expected with pathologies affecting the hair cells, spiral ganglion cells and their axons (auditory neuropathy sensu stricto), and brain stem relays are reviewed. In order to serve patients adequately, including potential candidates for cochlear implants, and to increase knowledge of auditory pathologies, we make a plea for more comprehensive evaluation of patients who fulfill the currently used audiologic criteria for "auditory neuropathy" in an effort to pinpoint the site of their pathologies. We suggest that the term auditory neuropathy be limited to cases in which the locus of pathology is limited to the spiral ganglion cells, their processes, or the 8th nerve, and that the term neural hearing loss be considered for pathologies that affect all higher levels of the auditory pathway, from the brainstem to the auditory cortex.

Audiology↗

The role of bile salt composition in liver pathology of mdr2 (-/-) mice: differences between males and females.

BACKGROUND/AIMS: The mouse mdr2 gene encodes a P-glycoprotein expressed in the canalicular membrane of the hepatocyte. Mice in which this gene has been inactivated (mdr2 -/-) show a defect in biliary phospholipid and cholesterol secretion and develop non-suppurative cholangitis. We hypothesized that secretion of bile salts without lipids initiates this liver disease. METHODS: To delineate the pathologic process, mdr2 (-/-) mice were fed different bile salt-supplemented diets for 22 weeks after weaning. Aspects of liver pathology including eosinophilic bodies, portal inflammation, ductular proliferation, mitotic activity and fibrosis were semi-quantitatively scored. RESULTS: It was observed that liver pathology was more severe in female than in male mice when fed a purified control diet. This correlated with a more hydrophobic bile salt composition of female vs. male bile. When increasing amounts of cholate were added to the diet (0.01% and 0.1%), the secretion of taurocholate increased and this was accompanied by a more severe liver pathology. At the high dose of cholate (0.1%), the bile salt compositions of male and female mice became similar, as did the severity of the histological score. Addition of cholate to the diet did not induce liver pathology in (+/+) mice. Addition of ursodeoxycholate to the diet (0.5%) led to a near complete replacement of biliary bile salts by tauroursodeoxycholate and this reduced pathology and dissipated the difference between males and females. CONCLUSIONS: These observations support our hypothesis that liver pathology in the mdr2 (-/-) mouse is caused by bile salts and depends on the hydrophobicity c.q. cytotoxicity of biliary bile salts.

Animals↗

Psychopharmacologic treatment of pathologic aggression.

Several drugs are apparently effective in treating pathologic anger and aggression. Because many of the studies on aggressive populations allowed the use of concomitant medications, it is unclear whether the efficacy of each drug in a particular population is dependent on the presence of other medications, such as antipsychotic agents. Finally, one needs to be circumspect in inferring efficacy of a particular drug in aggressive patients with neuropsychiatric conditions other than the ones in which some efficacy has been established. Lithium appears to be an effective treatment of aggression among nonepileptic prison inmates, mentally retarded and handicapped patients, and among conduct-disordered children with explosive behavior. Certainly, lithium would be the treatment of choice in bipolar patients with excessive irritability and anger outbursts, and it has been shown to be effective in this population. Anticonvulsant medications are the treatment of choice for patients with outbursts of rage and abnormal EEG findings. The efficacy of these drugs in patients without a seizure disorder, however, remains to be established, with the exception perhaps of valproate and carbamazepine. In fact, dyphenylhydantoin did not appear to be effective in treating aggressive behavior in children with temper tantrums and was found to be effective in only a prison population. There is some evidence for the efficacy of carbamazepine and valproate in treating pathologic aggression in patients with dementia, organic brain syndrome, psychosis, and personality disorders. As Yudofsky et al point out in their review of the literature, although traditional antipsychotic drugs have been used widely to treat aggression, there is little evidence for their effectiveness in treating aggression beyond their sedative effect in agitated patients or their antiaggressive effect among patients whose aggression is related to active psychosis. Antipsychotic agents appear to be effective in treating psychotic aggressive patients, conduct-disordered children, and mentally retarded patients, with only modest effects in the management of pathologic aggression in patients with dementia. Furthermore, at least in one study, these drugs were found to be associated with increased aggressiveness in mentally retarded subjects. On the other hand, atypical antipsychotic agents (i.e., clozapine, risperidone, and olanzapine) may be more effective than traditional antipsychotic drugs in aggressive and violent populations, as they have shown efficacy in patients with dementia, brain injury, mental retardation, and personality disorders. Similarly, benzodiazepines can reduce agitation and irritability in elderly and demented populations, but they also can induce behavioral disinhibition. Therefore, one should be careful in using this class of drugs in patients with pathologic aggression. Beta-blockers appear to be effective in many different neuropsychiatric conditions. These drugs seem effective in reducing violent and assaultive behavior in patients with dementia, brain injury, schizophrenia, mental retardation, and organic brain syndrome. As pointed out by Campbell et al in their review of the literature, however, systematic research is lacking, and little is known about the efficacy and safety of beta-blockers in children and adolescents with pathologic aggression. Although widely used in the management of pathologic aggression, the use of this class of drugs has been limited partially by marked hypotension and bradycardia, which are side effects common at the higher doses. The usefulness of the antihypertensive drug clonidine in the treatment of pathologic aggression has not been assessed adequately, and only marginal benefits were observed with this drug in irritable autistic and conduct disorder children. Psychostimulants seem to be effective in reducing aggressiveness in brain-injured patients as well as in violent adolescents with oppositional or conduct disorders, particu

Adrenergic beta-Antagonists↗

[Functional thyroid pathology in the elderly].

OBJECTIVE: To describe the prevalence of functional thyroid pathology (FTP) and pathologies associated with it in an elderly population. DESIGN: Descriptive, cross-sectional study. SETTING: Urban primary care centre. PATIENTS: Representative sample of the entire population attended that was 60 years old or over. MAIN MEASUREMENTS: Demographic variables, clinical history of thyroid pathology and pathology associated with it, Body Mass Index, small tests for diagnosing depression and anxiety, the mini-mental test, electrocardiogram, determination of total cholesterol and LDL cholesterol, and of free thyrotrophin and thyroxin if it is disturbed. RESULTS: 192 people were studied, 56% women, 53% between 60 and 69 and 12% over 79 years old. 10% had a history of previous FTP. Prevalence of active FTP was 13% (10.41% sub-clinical hypothyroidism, 0.52% clinical hypothyroidism, 1.56% sub-clinical hyperthyroidism, and 0.52% clinical hyperthyroidism). Prevalence of new diagnoses of FTP was 4.1% (7 with hypothyroidism and 1 with hyperthyroidism, all sub-clinical). During the study the following pathology was detected in hypothyroidism sufferers: 43% anxiety disorder, 38% depressive syndrome, 28.5% cognitive deterioration, 9.5% dementia, 26% electrocardiographic disturbances, 47.6% obesity, and 28.5% with total cholesterol > or =250 mg/dL. In hyperthyroidism, 50% with depressive syndrome, 25% with cognitive deterioration, 25% with electrocardiographic disturbances, and 50% with obesity were detected. CONCLUSIONS: FTP is more prevalent among the elderly than in the population as a whole, with predominance of hypothyroidism, subclinical pathology and among women. In terms of pathology traditionally linked to thyroid malfunction, few differences were found between the population affected with FTP and those not affected. Primary care doctors are important in reducing under-diagnosis.

Aged↗

[The levels of IgG subclasses in respiratory allergic pathology in the childhood].

OBJECTIVES: To assess the existence of immunologic alterations, referring to IgG subclasses, in the respiratory allergic pathology in the childhood. MATERIAL AND METHODS: This is a prospective study that compares the IgG subclasses levels in a sample of patient with allergic breathing illness (n = 169) and a group control (n = 130) with ages range from one month to 13 years old. The statistical analysis includes a descriptive statistic and a comparative statistic carrying out comparison of means between both groups with the Welch test and the Student's T test. RESULTS: The mean rate of IgG1 in the group with breathing allergic pathology being of 578,1 mg/dl and in the control group, being of 632,78 mg/dl. The mean rate of IgG2 in the group with breathing allergic pathology being of 106,12 mg/dl and in the control group, being of 142,38 mg/dl. The mean rate of IgG3 in the group with breathing allergic pathology being of 53,73 mg/dl and in the control group, being of 63,78 mg/dl. The children with breathing allergic pathology have significantly decreased IgG1, IgG2, IgG3 levels in comparison to the control group (p < 0.001). The mean rate of IgG4 in the group with breathing allergic pathology being of 25,86 mg/dl and in the control group, being of 13,89 mg/dl. The children with breathing allergic pathology have significantly elevated IgG4 levels in comparison to the control group (p < 0.001). CONCLUSIONS: The findings obtained suggest that an relation exists in the breathing allergic processes with the IgG subclasses levels disturbances and also that there is an alteration of the immune response maturation in relation to subclasses IgG1, IgG2, IgG3. The valuation of the levels of these immunoglobulins can be useful in the pathogenic diagnosis of the allergic processes.

Adolescent↗