Emphysema vs asthma with antitrypsin deficiency.
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Biomedical subjects
Publications and source records attributed to J Lieberman.
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Measurement of serum angiotensin-converting-enzyme (SACE) is the most useful test for diagnosing and monitoring disease activity in sarcoidosis. Because elevated levels of SACE are not specific for sarcoidosis, other conditions in which SACE levels are also elevated are examined.
The presence of an intrinsic inhibitor of ACE in blood of approximately 25% of sera submitted for serum ACE assay in the diagnosis and evaluation of patients with sarcoidosis, and the common use of ACE inhibitors (captopril and enalapril) in the treatment of hypertension and congestive heart failure, stimulated these studies to compare the effects of the intrinsic and medicinal inhibitors upon serum ACE activity. Since the intrinsic ACE inhibitor in man is affected by serum dilution (inhibition is reversed) and by dialysis (inhibition becomes irreversible), these manipulations were also studied with medicinal inhibitors to provide guidelines for suspecting their presence in submitted serum samples without an accompanying history. Enalapril was found to have delayed onset of action after oral administration (1-2 hours), and was even further delayed (4 hours) when the intrinsic inhibitor also happened to be present. Inhibition by enalapril was not attenuated with refrigerated storage, with dilution or with dialysis of the serum. Captopril had a more rapid time of onset of ACE inhibition, but its inhibitory activity was markedly reduced with refrigerated storage of the serum; patients showed either a short half-life for the effect (1-4 days) or a prolonged half-life (10-17 days). Inhibitory activity of captopril was reversed following dilution of serum or following dialysis. The reversal of inhibition by captopril following dialysis, therefore, differed from the effect of dialysis on the intrinsic ACE inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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Sixty-nine male patients participated in a self-evaluation survey measuring their satisfaction with maxillary and mandibular dentures. Patients generally had a high evaluation of their dentures, with the highest scores given to appearance. Age was not a significant predictor of denture success. Patients receiving their first dentures consistently had more difficulties in all categories of function, comfort, and appearance than patients with past experience with dentures.
Based on the results of two preliminary studies, we concluded that late-developing persistent drug-induced movement disorders are pharmacologically heterogeneous, and this heterogeneity is seen between individual patients (and groups of patients) as well as within body areas of individual patients; dystonic pathology has a distinct and more consistent response to pharmacologic stimulation than does nondystonic tardive dyskinesia (TD); and, although disturbances in dopamine and acetylcholine appear to be involved in these disorders, they do not in all cases exist in functionally opposite relationships. The observed pharmacologic heterogeneity in TD response reflects the limitations of the dopamine/acetylcholine model of TD, which oversimplifies the neuroanatomy of the basal ganglia and the pathophysiology of TD. The chemical and anatomical complexity of this region suggests that other neurotransmitter systems and neuronal circuits within and extending from the basal ganglia may be disturbed in the pathogenesis of TD.
Generalized lymphadenopathy in intravenous drug abusers (IVDAs) at risk for AIDS has not been well studied. We have retrospectively analyzed the results of lymph node biopsies obtained from 27 patients referred to the Infectious Diseases Service for evaluation of generalized lymphadenopathy and suspected AIDS during a recent 18-month period. Fourteen of the patients were heterosexual IVDAs, 7 were male homosexual IVDAs, and 6 were male homosexual non-IVDAs. All of the patients were residents of the Bronx, New York. Mycobacterium tuberculosis (TB) was the most frequent diagnosis established on lymph node biopsies from IVDAs, in 12 out of 21 (57%). Tuberculous adenitis was not diagnosed in the 6 non-IVDAs. All TB patients were febrile, 11 (91%) had lost weight, and 10 (84%) had an abnormal chest roentgenogram. The 5TU PPD skin test, however, was reactive in only 2 (16%) of 12 patients. Tuberculosis is important to consider in patient populations with exposure histories to both AIDS and TB. The alarmingly high prevalence of TB in this drug addict population emphasizes the importance of lymph node biopsies with acid-fast smears and mycobacterial cultures in symptomatic IVDAs. Preventive antituberculosis therapy for HIV-positive persons, especially IVDAs, with a history of positive tuberculin reactions or of recent household contact should be seriously considered.
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Although there continues to be some debate as to the extent to which neuroleptic drug treatment is either necessary or sufficient to produce abnormal involuntary movements in various psychiatric populations, the consensus at present is that neuroleptics do play a major role in producing, precipitating or evoking abnormal involuntary movements. No doubt a variety of other factors play a critical role in predisposing particular individuals to the development of the condition. Numerous prevalence surveys have been conducted and extensively reviewed. In general, prevalence surveys have helped to identify populations at particular risk, to suggest factors which contribute to risk and to establish the overall scope of the problem. The strategy of estimating prevalence in a specific population has limitations, however, and further advances in our understanding of tardive dyskinesia (TD) will require a different type of methodology. Important progress has been made in the last several years involving prospective studies of TD development. Current estimates of incidence suggest that TD develops in about 5% of patients with each year of cumulative neuroleptic exposure. These data are derived from relatively young patients (average age 28); the incidence in older individuals is likely to be higher. Further data on the epidemiology of TD will be presented.
Despite increased attention to the problem of tardive dyskinesia (TD), many questions remain unresolved. There is a consensus that neuroleptics play a substantial role in its development, but other variables must also contribute. Prevalence surveys have helped to define the scope of the problem and suggest risk factors for further study. Their usefulness has been limited by methodological problems including the difficulty of estimating false-negative (masked) dyskinesia and false-positive (movements caused by other neuromedical conditions) rates. A recent large scale survey reported an overall rate of abnormal involuntary movements of 23.4% among neuroleptic-treated psychiatric patients; the range was from 12.3% among outpatients at a Veterans Administration hospital to 37.4% among state hospital inpatients. Rates of covert dyskinesia, obtained by withdrawing medication from 70 TD negative cases, ranged from 17% for the Veterans Administration to 67% at the state hospital (overall rate, 34%). Very few clear false-positive cases were found. The incidence of TD, based on a large prospective study of young adult patients, is 19% after 4 years of cumulative neuroleptic exposure. Higher incidence rates have been found in prospective studies of older patient samples. Age remains the risk factor most consistently associated with TD development; it may also relate to increased persistence. Female sex among older populations, diagnosis of affective disorder, and evidence of neuroleptic-induced pseudoparkinsonism also relate to increased risk. Further work is needed to elucidate the role of dosage and length of neuroleptic treatment, as well as other potential contributory factors.
Tardive dyskinesia (TD) occurs in approximately 20% of patients treated chronically with antipsychotic drugs and constitutes a major public health problem. The cause of this disorder remains unknown, and no effective treatment has yet been found. The major etiologic theory (dopamine [DA] supersensitivity hypothesis) suggests that TD is the pharmacologic opposite of Parkinson's disease and implies that all patients with TD should respond uniformly to specific pharmacologic agents. Clinical research, however, has not borne this out. To evaluate pharmacologic response in TD syndromes, 15 patients underwent single dose acute administration of four different drugs: a DA agonist (bromocriptine 5 mg orally), a DA antagonist (haloperidol 5 mg intravenously), a cholinergic agonist (physostigmine 2 mg intravenously) and a cholinergic antagonist (benztropine 4 mg intravenously), individually in separate procedures at weekly intervals for four consecutive weeks in randomized order and under controlled double-blind conditions. Patients were evaluated for their clinical and endocrine responses. Pre- and post-drug administration TD exams were blindly rated. Results were not consistent with the DA supersensitivity theory; instead they demonstrated marked inter- and intrasubject variability in pharmacologic responses. Greatest uniformity in response was found among the tardive dystonic subjects, although this also was not consistent with a DA supersensitivity hypothesis. TD appears to be a pharmacologically heterogeneous condition, which may reflect the neurochemical complexity of the basal ganglia.
A case of necrotizing sialometaplasia in a 29-year-old man is reported. Characterized by large, deep, well-demarcated ulcerations on the hard palate and other areas where salivary gland tissue is found, the condition is benign and resolves spontaneously. The cause is believed to be infarctive.
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Serum angiotensin converting enzyme levels were measured in 184 subjects having either MM, MZ, ZZ, or MS Pi-types of alpha 1-antitrypsin. Elevated angiotensin converting enzyme levels were detected in 31 percent of the patients with the MZ Pi-type, 20 percent of the patients with the ZZ Pi-type, and 20 percent of the patients with the MS Pi-type compared with 1.33 percent of those with normal MM Pi-type. The mean serum angiotensin converting enzyme levels were also significantly higher in those with the MZ, ZZ, and MS Pi-types. Multiple family members of two families were found to have both the Z variant and angiotensin converting enzyme elevations, suggesting the possibility of a genetic linkage. Alpha 1-antitrypsin deficiency must be added to the list of disease states potentially associated with elevated serum angiotensin converting enzyme levels.