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Patients with pulmonary sarcoidosis are less likely to smoke than persons of a similar age in the general population. This could be because smoking reduces the likelihood of developing sarcoidosis, or alternatively smoking could reduce the severity of the disease process so that smoking patients are underrepresented among patients with clinically overt disease. To evaluate these possibilities 64 patients with sarcoidosis of recent onset were studied at presentation and after a one year follow up period, clinical, functional, radiographic, and bronchoalveolar lavage fluid criteria being used to identify factors that might account for the lower incidence of sarcoidosis in smokers and to determine whether the disease is less severe in smoking patients. Smoking was less common in the patients with sarcoidosis (30%) than in the control subjects (46%). The study did not support the conclusion that sarcoidosis is less severe in smokers, as clinical, radiographic, and functional abnormalities were similar in smokers and non-smokers at initial evaluation and after a one year follow up period. Nevertheless, smoking did influence various indices used to assess disease "activity." Cigarette smoking was associated with a significant increase in the serum angiotensin converting enzyme activity (SACE), and patients with very high SACE and pulmonary gallium-67 uptake were smokers. Furthermore, more CD8+ (but not CD4+) lymphocytes were recovered by lavage from smoking than from non-smoking patients, giving a lower CD4: CD8 ratio in smokers. Fewer alveolar macrophages were recovered by lavage from smokers with sarcoidosis than from normal subjects with a similar smoking history. These finding support the possibility that smokers, particularly those with a prominent accumulation of alveolar macrophages in the lower respiratory tract, may be less likely to develop sarcoidosis. [ABSTRACT FROM PUBLISHER]

Quantitative and objective measurement of exposure to cigarette smoke by assays of chemical markers is desirable, especially in preventive medicine, since the negative health effects of tobacco smoke are well documented. Chemical markers include nicotine and cotinine in plasma, urine, and saliva; carbon monoxide in exhaled air; carboxyhemoglobin in blood and thiocyanate in biological fluids. Ease of use, cost, specificity, and sensitivity vary across markers. Determination of the thiocyanate/creatinine ratio in urine is a reliable, noninvasive, and inexpensive test for evaluating exposure to cigarette smoke. No marker for cumulative exposure to cigarette smoke is available to date. The plasma level of fluorescent lipoperoxides may provide an estimation of the in vivo toxicity of exposure to cigarette smoke.

After a brief review of the concepts of free radical and enzymatic lipid peroxidation, spontaneous peroxidation (initiation, propagation, termination, end-products) is described in detail on the basis of the latest published studies shedding new light on the role of this process in a wide variety of disease states. Toxic effects of lipid peroxidation and physiologic protective mechanisms are described. Currently available routine methods for evaluating lipid peroxidation, particularly in plasma, although imperfect, are nevertheless valuable in clinical practice in view of the many human disease states involving lipid peroxidation.

A simple, inexpensive spectrofluorometric ultramicroassay for determining the plasma lipid peroxidation index is described. Plasma is incubated for 60 minutes at 95 degrees C in a thiobarbituric acetate buffer medium (pH 3,5) with butylhydroxytoluene and Fe . The chromogen is then extracted in butanol 1-pyridine and quantified by spectrofluorometry (exc.: 532 nm; em: 553 nm). The mean value of the plasma thiobarbituric lipid peroxidation index determined by this method in 101 healthy non-smokers (age 39.1 +/- 8.7 years) was found to be 1.61 +/- 0.72.

A clinical, scintigraphic and hormonal study of the thyroid was performed in 50 patients with intrathoracic sarcoidosis. The patients were divided into two groups: T - : n = 32, no thyroid abnormality; T +, 18 cases, with thyroid disorders (9 moderate diffuse goitres, 2 thyroid nodules, 7 nodular goitres). All had normal T4, T3 and TSH levels, except one patient with Graves's disease. Scarce sarcoid granulomas were found in 3 out of 4 patients who underwent thyroidectomy. Dissemination, activity, type of sarcoid thoracic involvement were not different in the two groups. In contrast, T + group had higher seric IgG levels than T - group (p less than 0,05). The association of sarcoidosis and goitre is not fortuitous but thyroid enlargement and sarcoid diffusion do not seem interrelated. Auto-immune thyroiditis seems unlikely in our cases, according to the low frequency of thyroid auto-antibodies. We discuss the possible role of seric immunoglobulins in the constitution of thyroid hypertrophy with or without hyperthyroidism in sarcoidosis.

Human red cell and plasma lipids are determined in alcoholic patients with various forms of liver diseases including steatosis, cirrhosis and hepatitis. No relation between serum lipids and red cell lipids content have could be demonstrated. A relation is shown between morphology and lipids red cells content, different anatomopathologic states of liver and erythrocyte morphology. In steatosis red cells phospholipids (specially phosphatidyl choline) are increased. In cirrhosis red cells show an increased of both cholesterol and phospholipids content. Target cells show an inchanged cholesterol-phospholipids ratio when acanthocytes show and increased cholesterol phospholipids ratio by a greater increase of cholesterol than phospholipids.

In order to investigate the initial course of pulmonary sarcoidosis, the following investigations were carried out in 14 nonsmoking patients with Logfren 's syndrome 3 to 12 wk after the onset of erythema nodosum (EN): bronchoalveolar lavage (BAL) (cellular and protein components), serum assays of lgG and of the activity of angiotensin-converting enzyme (SACE), and pulmonary function tests. These results were related to the disease duration, estimated by the time lapse separating the onset of EN from the investigations. All patients but one showed a large increase in the percentage of lymphocytes (%-L) in BAL fluid (more than 30%). Although each patient was evaluated only once, and thus this work was not an actual longitudinal study, a linear relationship between lymphocyte count per milliliter of recovered fluid during BAL (L-count) and disease duration was found during the first 8 wk (r = 0.78, p less than 0.01), suggesting a fast-developing alveolitis. The delayed rise in SACE level may indicate a secondary activation of macrophages; SACE and L-count were well related, either up to 8 wk (SACE versus L-count: r = 0.84, p less than 0.01) or up to 12 wk (SACE versus L-count: r = 0.61, p less than 0.01). Serum lgG levels were found to follow the L-count (serum lgG versus L-count: r = 0.79, p less than 0.01) and appeared to be a reliable index of disease activity. Respiratory function showed a univocal pattern, with a marked decrease in all of the patients in carbon monoxide diffusing capacity (DLCO), contrasting with normal lung volumes.(ABSTRACT TRUNCATED AT 250 WORDS)

Transferrin structure, metabolism and physiological functions (iron transport, activation of cellular growth, bacteriostatic effect) are described with reference to the last informations available from the literature. This analysis results in a better understanding of the mechanisms involved in its physiopathological variations. Decreased serum transferrin levels are the result of a reduction of the biosynthesis (hepatic deficiencies, malnutrition), or an increase of catabolism (acute, chronic and malignant infections), or an increase of intestinal or renal losses, or very infrequently genetic disorders. Increased serum transferrin levels are the result of either hyposiderosis or an oestrogenic impregnation. Alcoholism and diabetes are responsible of qualitative modifications of this protein.

The carbohydrate composition of the human erythrocyte membrane was just established ten years ago. Carbohydrates have crucial functions in the membrane structures and the determination of this composition may have an important semeiological signification. In this way, reference values are necessary. The existence of possible variations of the composition with two physiological parameters: the groups in the ABO system and the age of erythrocytes have been investigated and are reported. Their repercussion on the determination of reference values is discussed.

A simple accurate and very reproducible procedure for measuring serum iron concentration without precipitating serum proteins is described. In the same time, iron is released from serum transferrin, reduced and determined at 535 mn by incubation in a water bath at 55 degrees for five minutes within a formate buffered system (pH 2,6; i = 0,05) including bathophenanthroline sulfonate. This method yields values very similar to those obtained by that of the International Committee for Standardization in Hematology (ICSH).

An original approach to reveal in Mice, the impact of some xenobiotics and drugs on the alveolo-capillary barrier...(ethanol, acetazolamide, cyclophosphamide is described. Drugs are injected I.P. during five days in subacute dose size. Concentrations of lecithines and proteins are settled in bronchoalveolar lavage fluids from animals having or not undergone an important blood loss just before the lavage.

Ghosts are adsorbed on extemporaneously formed tricalcium phosphate precipitate in lytic medium. They are free of hemoglobin and chemical characteristics are in good agreement with those obtained by Dodge (3) and Hanahan (5).