Clinical and biochemical correlates of male hypogonadism in type 2 diabetes.

The origin of hypogonadism, a condition including both symptoms and biochemical criteria of androgen deficiency, in type 2 diabetes is poorly known. In a cross-sectional study of 267 unselected patients, we analyzed the potential correlation of several clinical and biochemical variables as well as chronic micro- and macrovascular diabetic complications with hypogonadism. Hypogonadism was present in 46 patients (17.2%) using a cutoff of total testosterone 10.4 nmol/L and in 31 (11.6%) with a cutoff of 8 nmol/L. Among these patients, hypogonadotropic hypogonadism was the most prevalent form (82.6%). Compared to eugonadal subjects, hypogonadal men had significantly lower glomerular filtration rate (67.1 ± 23.4 vs. 78.4 ± 24.6 mL/min/1.73 m2 , p = 0.005) and higher prevalence of chronic kidney disease (43.5% vs. 20.4%, p = 0.002), abnormal liver function tests (26.7% vs. 12%, p = 0.019), and psychiatric treatment (23.9% vs. 10.4%, p = 0.025). Total testosterone levels correlated inversely with age (R = -0.164, p = 0.007), fasting blood glucose (R = -0.127, p = 0.037), and triglycerides (R = -0.134, p = 0.029) and directly with glomerular filtration rate (R = 0.148, p = 0.015). Calculated free testosterone and bioavailable testosterone correlated directly with hemoglobin (R = 0.171, p = 0.015 and R = 0.234, p = 0.001, respectively). Multivariate logistic regression analysis, after adjusting for relevant confounding variables, showed that age >60 years (OR = 3.58, CI 95% = 1.48-8.69, p = 0.005), body mass index >27 kg/m2 (OR = 2.85, CI 95% = 1.14-7.11, p = 0.025), hypertriglyceridemia (OR = 2.16, CI 95% = 1.05-4.41, p = 0.035), glomerular filtration rate <60 mL/min/1.73 m2 (OR = 2.51, CI 95% = 1.19-5.29, p = 0.015), and abnormal liver function tests (OR = 3.57, CI 95% = 1.48-8.60, p = 0.005) were independently associated with male hypogonadism. Although older age, body mass index, and hypertriglyceridemia have been previously related to hypogonadism, our results describe that chronic kidney disease and abnormal liver function tests are independently correlated with hypogonadism in type 2 diabetic men.

Plurihormonal Cosecretion by a Case of Adrenocortical Oncocytic Neoplasm.

Adrenocortical oncocytic neoplasms (oncocytomas) are extremely rare; only approximately 159 cases have been described so far. The majority are nonfunctional and benign. We describe an unusual case of a functional oncocytoma secreting an excess of glucocorticoids (cortisol) and androgens (androstenedione and DHEAS), a pattern of plurihormonal cosecretion previously not reported in men, presenting with endocrine manifestations of Cushing's syndrome. The neoplasm was considered to be of uncertain malignant potential (borderline) according to the Lin-Weiss-Bisceglia criteria.

Testosterone replacement therapy in hypogonadal men is associated with increased expression of LAMP-2 (CD107b) by circulating monocytes and dendritic cells.

BACKGROUND: Accumulated experimental data indicates that androgen therapy has effects on inflammation and protects from autoimmune disorders. Despite this, the in vivo effects of testosterone replacement therapy on human antigen-presenting cells-for example, monocytes and dendritic cells- remain unknown. OBJECTIVE, DESIGN AND PATIENTS: We monitored the effects of testosterone replacement therapy on the number and the functionality -as assessed by the expression of CD107b (lysosome-associated membrane protein 2, LAMP-2)- of resting and in vitro-stimulated peripheral blood (classical and nonclassical) monocytes and dendritic cells (myeloid and plasmacytoid) from hypogonadal men. RESULTS: Our results show that testosterone replacement therapy induces overexpression of CD107b by circulating monocytes and dendritic cells from hypogonadal men, both under resting (i.e. nonstimulated) conditions and after in vitro stimulation. CD107b overexpression mostly involved monocytes and in vitro stimulation with CpG oligodeoxynucleotides. Of note, a strong correlation was found between CD107b expression on monocytes and serum gonadotrophins levels. CONCLUSION: These results support the existence of an effect of testosterone therapy, and potentially also of gonadotrophins, on circulating antigen-presenting cells.

[Tethered cord syndrome in the adult]. / Síndrome de médula anclada en el adulto.

INTRODUCTION: The tethered cord syndrome (TCS) is a congenital malformation with a pathologic fixation of the spinal cord in the spinal canal. It presents clinically as musculoskeletal, cutaneous, urological and neurological manifestations. The diagnosis is based on the clinical manifestations and on the MRI (Magnetic Resonance Imaging) of the lumbar spine. It is usually diagnosed in childhood, but the symptoms can appear in adult life. METHOD: We reviewed all the cases of TCS in the adult diagnosed in our hospital between 1998 and 2005. The following parameters were evaluated: mean age at onset, initial symptoms, signs, MRI findings and outcome. RESULTS: Four 22 to 72 year old patients were diagnosed. The age at onset varied from 16 to 52 years old and the diagnosis took between 2 and 20 years to be established. The most frequent initial symptoms were the muscular atrophy and the motor weakness in the lower extremities. Two patients exhibited cutaneous stigmata (one had hypertrichosis and the other one a lipoma in the sacrum area) and one a partial agenesis of the sacrum. The most frequent MRI finding was a low lying cord with a lipoma in the sacrum area. In three patients the cord was detethered surgically, but only two of them improved. CONCLUSIONS: The TCS is an uncommon disease in adult, which is usually diagnosed very late in the adult. Because of its insidious and non specific symptomatology, and of its potential surgical treatment, it should be considered in the differential diagnosis of medullar syndromes and polyneuropathies.

Trocar site hernia after laparoscopic ventral hernia repair.

BACKGROUND: The incidence of trocar site hernia (TSH) after laparoscopic ventral hernia repair (LVHR) is reported to be low. The present study investigates the associated risk factors, with a view to preventing this complication. METHODS: A retrospective study was made of the incidence of TSH in a personal series of LVHR, recording anthropometric and clinical data on the patients. Risk factors were assessed by bivariate and multivariate analyses. The patients were subjected to clinical and telephone follow-up. RESULTS: In a series of 27 LVHR, the incidence of TSH was 22% (6 patients). The use of meshes larger than 10 x 15 cm for LVHR was the only TSH risk factor to reach statistical significance. Female gender and diabetes showed a higher incidence in the TSH group. CONCLUSIONS: The use of large meshes may be a risk factor for TSH. We believe this to be due to dilatation of the trocar orifice during introduction of the mesh, and also to postoperative retraction of the mesh.

Linfangiosarcoma sobre un linfedema crónico postmastectomía: síndrome de Stewart-Treves / No disponible

En 1948, Stewart y Treves comunicaron la aparición de unlinfangiosarcoma en el brazo edematoso de 6 pacientes sometidasa mastectomía radical por cáncer de mama. El síndromede Stewart-Treves describe la presentación de un linfangiosarcomao de un hemangiosarcoma sobre un linfedema crónico.Comunicamos el caso de una mujer de 74 años que fue sometidaa mastectomía radical derecha con radioterapia 23 añosantes y que consultó por la aparición de lesiones cutáneas enforma de placas violáceas en el brazo homolateral que llegarona hacerse nodulares. Tras la biopsia, el análisis histopatológicoconfirmó el diagnóstico de linfangiosarcoma. El estudio de extensiónfue negativo para metástasis. Se decidió la amputaciónde la extremidad. Seis meses más tarde, se diagnosticóuna metástasis cerebral y la paciente falleció poco tiempo después.Las opciones terapéuticas en estos casos (amputación,radioterapia y quimioterapia) son muy agresivas y ofrecen pobresresultados. Sólo un diagnóstico muy precoz, basado en lasospecha clínica, puede mejorar el pronóstico de esta complicaciónde la linfadenectomía axilar. La biopsia es obligatoriaante cualquier lesión sospechosa(AU)

In 1948, Stewart and Treves reported a lymphangiosarcomain 6 patient’s edematous arm after radical mastectomy forbreast cancer. Stewart-Treves syndrome describes a cutaneouslymphangiosarcoma or hemangiosarcoma that develops inlong-standing chronic lymphedema. We report a 74-year-oldwoman who was submitted to a right mastectomy and radiotherapy23 years before. She developed a chronic lymphedemain the same limb and fast-growing purplish lesions on thearm. These lesions became nodular. After the biopsy examinationthey were diagnosed as lymphangiosarcoma. The studyfor metastatic extension was negative. It was decided the amputationof the limb. Six months after the treatment, a brainmetastasis was diagnosed and the patient died. The therapeuticpossibilities (amputation, radiotherapy, chemotherapy) arevery aggresive and offer poor results. The physician mustmaintain a high index of suspicion in diagnosing this complicationof lymphadenectomy. If there is any doubt, biopsy is mandatory(AU)

Androgen-replacement therapy depresses the ex vivo production of inflammatory cytokines by circulating antigen-presenting cells in aging type-2 diabetic men with partial androgen deficiency.

Androgens are considered to have immunomodulatory effects but their cellular mechanisms of action remain largely unknown. In the present study we prospectively analyzed the serial effects of androgen-replacement therapy on both the distribution of peripheral blood lymphocytes, monocytes and dendritic cells as well as on the production of interleukin (IL)-1beta, IL-6 and tumor necrosis factor alpha (TNFalpha) inflammatory cytokines by circulating monocytes and CD33 myeloid, CD16 and plasmacytoid dendritic cell subsets, the most potent antigen-presenting cells (APCs) in type-2 diabetic men with partial androgen deficiency. Analyses were performed before therapy and at 1, 3, 6 and 12 months after treatment with 150 mg testosterone enanthate every 2 weeks in a group of 13 type-2 diabetic men. Our results show for the first time that testosterone-replacement therapy is associated with a reduction or complete abrogation of spontaneous ex vivo production of IL-1beta, IL-6 and TNFalpha by APCs. Meanwhile, the in vitro production of inflammatory cytokines by these cells after stimulation with lipopolysaccharide plus recombinant human interferon-gamma remained unchanged, suggesting that APCs preserve their constitutive machinery to produce inflammatory cytokines under androgen treatment. These results confirm and extend previous observations about the anti-inflammatory effects of androgen therapy on APCs in a new, previously unexplored model of androgen deficiency; namely, aging type-2 diabetic men. A decreased production of inflammatory cytokines by APCs might have important consequences for sex differences in susceptibility to autoimmune diseases, inflammatory response to injury and atheromatosis.

Hiperandrogenismo / Hyperandrogenism

El hiperandrogenismo es un problema endocrinológico frecuente en mujeres adultas. Su manifestación más habitual es el hirsutismo, acompañado o no de trastornos menstruales y con menor frecuencia de virilización. Se presenta un caso clínico de hiperandrogenismo con amenorrea secundaria y virilización en una mujer en edad fértil. Se evalúa el papel de las diferentes determinaciones hormonales y técnicas de imagen en el diagnóstico etiológico de este cuadro

Hyperandrogenism is one of the most common endocrine diseases affecting adult women. Clinical presentation includes hirsutism, with or without menstrual disturbances (oligomenorrhea, amenorrhea) and, less frequently, virilization. We report the case of a woman of reproductive age with hyperandrogenism, secondary amenorrhea, and virilization. The diagnostic role of laboratory tests and imaging techniques is discussed

Partial androgen deficiency in aging type 2 diabetic men and its relationship to glycemic control.

Aging in the male is associated with both a higher incidence of type 2 diabetes and hypogonadism. However, little information is available about the complex of symptoms and hormonal changes related to partial androgen deficiency in aging (called andropause) in type 2 diabetic men. Here, for the first time, we used a combination of clinical and hormonal criteria to define andropause and to analyze the relationships between the androgen environment and glucose metabolism in 55 type 2 diabetic men (63.6 +/- 7.9 years, mean +/- SD). Low plasma levels of total testosterone (< or =3.4 ng/mL) and free testosterone (< or =11 pg/mL) were found in 20% and 54.5%, respectively, of the diabetic men. The fraction of diabetic men with subnormal levels of total testosterone increased with aging: 14.2% (50 to 59 years), 17.4% (60 to 69 years) and 36% (> 70 years). The corresponding figures for subnormal values of free testosterone were 38%, 69.6%, and 54.5%, respectively. In the whole group of type 2 diabetic men, no significant linear correlations between total or free testosterone with fasting plasma glucose, insulin, C-peptide, or fructosamine values could be established. Total testosterone was positively correlated with glycosylated haemoglobin (HbA(1c)) levels (r =.322, P =.01). Although fasting plasma glucose was marginally higher in aging type 2 diabetic patients with andropause than in those without andropause (162 +/- 6.9 v 139 +/- 8.9, mean +/- SEM, P =.05), there were no differences between both subgroups for plasma fasting insulin, C-peptide, fructosamine, or HbA(1c) levels. Replacement therapy (150 mg intramuscular [IM] of enanthate of testosterone every 14 days for 6 months) was applied in 10 type 2 diabetic men with clinical features of andropause associated with subnormal concentrations of serum testosterone. The treatment induced significant increases in total plasma testosterone (baseline: 3.9 +/- 0.3; at 6 months: 7.1 +/- 0.9 ng/mL, mean +/- SEM, P =.003) and free testosterone (baseline: 9.3 +/- 0.6; at 6 months 17.6 +/- 2.4 pg/mL, P =.003), but had a neutral effect on overall glycemic control. These data show a high prevalence of andropause in aging type 2 diabetic men and suggest that the endogenous androgen environment, as well as correction of the partial androgen deficiency, do not have a meaningful effect on glycemic control.

Adenoma ovárico de células de Leydig: una rara causa devirilización asociada a factores de riesgo cardiovascular / Leydig cell ovarian adenoma: a rare cause of virilization associated with cardiovascular risk factors

La masculinización de la mujer adulta ovirilismo es un trastorno endocrino infrecuente debido a un exceso de secreción androgénica causado por tumores adrenales u ováricos 1. Dentro de estos últimos, los más comunes son los de células de Sertoli-Leydig (androblastomas), si bien otros tipos patológicos, como los tumores de la granulosa-teca, de células hiliares, de células lipoideas y de restos adrenales, también pueden generar el cuadro1. Presentamos un caso clínico de virilización debido a un adenoma de células de Leydig, un tumor ovárico raro que sólo representa un 0,1% de los tumores ováricos. Describimos su asociación con factores de riesgo cardiovascular y el efecto de la corrección permanente del hiperandrogenismo sobre los mismos (AU)

Abnormal expression of acid glycosidases in seminal plasma and spermatozoa from infertile men with varicocele.

The activities of acid beta-glucuronidase, alpha-mannosidase, alpha-glucosidase, alpha-galactosidase, beta-galactosidase and beta-N-acetylglucosaminidase were analysed in seminal plasma and spermatozoa from 26 infertile men with varicocele and from 36 men of normal fertility. Semen samples from ten men with non-obstructive azoospermia were used as control specimens that contained the other components of semen. Spermatozoa were solubilized by both physical (homogenization) and chemical (Triton-X100) methods to obtain the soluble and non-soluble fractions. The activities of several glycosidases measured both in seminal plasma and spermatozoa were directly correlated with the numbers of spermatozoa and sperm motility, confirming previous studies. As some infertile patients with varicocele have normal semen parameters, whereas others have low numbers of spermatozoa and low sperm motility, the varicocele patients were prospectively divided into two groups: one (n = 15) with normal spermiograms and the other (n = 11) with abnormal spermiograms. The activities (expressed in mU ml(-1)) of alpha-mannosidase, beta-galactosidase and beta-N-acetylglucosaminidase in seminal plasma of normozoospermic infertile patients with varicocele were significantly higher than those of fertile controls, but not when expressed in U per 10(8) spermatozoa. The activities of beta-glucuronidase, alpha-mannosidase, beta-galactosidase and beta-N-acetylglucosaminidase in seminal plasma when expressed in U per 10(8) spermatozoa in varicocele patients with abnormal spermiograms were significantly higher than in those of men of normal fertility. The activity of alpha-mannosidase in the soluble fraction of sperm homogenates, expressed as U per 10(8) spermatozoa, was significantly higher in infertile patients with varicocele and abnormal spermiograms than in controls. In the non-soluble fraction of spermatozoa from infertile patients with varicocele, there was an increase in the expression of beta-galactosidase and beta-N-acetylglucosaminidase activities compared with the fraction of spermatozoa from fertile subjects. In summary, infertile patients with varicocele displayed an overexpression of acid alpha-mannosidase, beta-galactosidase and beta-N-acetylglucosaminidase activities in seminal plasma and spermatozoa that may be associated with functional defects in spermatozoa as these glycosidases play an important role in mammalian fertilization.

Edema agudo de pulmón en una mujer joven con masa suprarrenal / Acute pulmonary edema in a young woman with an adrenal mass

El feocromocitoma es un tumor neuroendocrino responsable del 0,05-0,1 por ciento de las hipertensiones secundarias, asociándose en ocasiones con normotensión. La miocardiopatía es una complicación rara, inducida por el exceso de catecolaminas. Presentamos el caso de una mujer joven que inició con cuadro de edema agudo de pulmón no cardiogénico sin hipertensión arterial asociada, debido a una miocardiopatía hipertrófica obstructiva grave. La paciente presentaba niveles elevados de catecolaminas y un tumor localizado en la glándula suprarrenal derecha. Después del comienzo del tratamiento alfa-beta bloqueante, se observó mejoría clínica y ecocardiográfica de la miocardiopatía, y la normalización posterior de los diámetros ventriculares tras la extirpación del feocromocitoma (AU)

Abnormalities in sperm acid glycosidases from infertile men with idiopathic oligoasthenoteratozoospermia.

OBJECTIVE: To analyze and compare acid beta-glucuronidase, alpha-mannosidase, alpha-glycosidase, alpha-galactosidase, beta-galactosidase, and beta-N-acetylglucosaminidase activities in fertile and infertile patients. DESIGN: An observational, controlled, clinical study. SETTING: A university tertiary hospital. PATIENT(S): Thirty-six fertile controls, 24 infertile oligoasthenoteratozoospermic (OAT) patients, and 10 azoospermic patients, who served as negative controls. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Analysis of the six glycosidase activities in seminal plasma and in solubilized spermatozoa. RESULT(S): alpha-galactosidase and beta-galactosidase activities in spermatozoa were significantly correlated with the serum levels of gonadotropins both in fertile controls and in OAT patients. The relative contribution of alpha-galactosidase and beta-galactosidase from the soluble fraction of spermatozoa to the total activity measured in the ejaculate of OAT patients was significantly lower than in fertile controls. The activities of beta-galactosidase and beta-N-acetylglucosaminidase in the soluble fraction of spermatozoa from OAT patients were significantly lower than in fertile controls. In seminal plasma, the activity of alpha-mannosidase from OAT patients was significantly higher than in fertile controls. The activity of beta-N-acetylglucosaminidase in the nonsoluble fraction of spermatozoa from OAT patients was three times higher than in fertile controls. CONCLUSION(S): The abnormalities in the distributions and contents of alpha-galactosidase, beta-galactosidase, and beta-N-acetylglucosaminidase in sperm suggest possible functional defects in spermatozoa from OAT infertile patients.

Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: relationship with disease activity.

Growing evidence points to the involvement of cytokines in the pathogenesis of some autoimmune diseases. To investigate the possible role of interleukin 2 (IL-2) and interleukin 6 (IL-6) on the pathogenesis of Graves disease (GD), the binding of both exogenous IL-2 and IL-6 and the expression of the IL-2 receptor subunit p55 (CD25) were evaluated by flow cytometry in peripheral blood T and B cells from 70 GD patients, in different states of the disease, and from 19 age- and sex-matched healthy volunteers. Serum levels of total T3 and T4, of free T4, and of anti-TSH receptor antibodies were also simultaneously determined. All GD patients displayed significantly increased numbers of B cells bound to IL-2. Hyperthyroid untreated GD patients had significantly higher numbers of T and B cells expressing the IL-2 receptor subunit p55 as compared to euthyroid patients in long-term remission. In addition, serum anti-TSH receptor antibody levels were directly correlated with the absolute numbers of T cells bound to IL-2 (r = 0.565, P < 0.05) and to IL-6 (r = 0.653), P = 0.02) in the hyperthyroid untreated patients, but not in long-term remission euthyroid GD patients or in patients treated with methimazole. The serum levels of total T3 and free T4 were significantly correlated with the absolute numbers of circulating T cells binding IL-2 (r = 0.720, P < 0.01 and r = 0.783, P < 0.002, respectively) as well as with the absolute numbers of circulating T cells binding IL-6 (r = 0.671, P < 0.02 and r = 0.626, P < 0.02, respectively). The serum levels of total T3 were also correlated with both the absolute numbers of B cells binding to IL-2 (r = 0.586, P < 0.05) and to IL-6 (r = 0.757, P < 0.001). These findings suggest that IL-2 and IL-6 may play a role in the pathogenesis of GD.

Methimazole therapy in Graves' disease influences the abnormal expression of CD69 (early activation antigen) on T cells.

At present, the in vivo response of T, B and natural killer (NK) cells to antithyroid drug therapy remains largely unknown. In the present study, we have prospectively analyzed the in vivo effects of methimazole treatment on a large number of circulating T and NK cell subsets, some of them expressing cell surface activation antigens involved in the very early phase of the immune response, in a group of 17 hyperthyroid, untreated patients with Graves' disease (GD). As one of the first events during T cell activation is the expression of interleukin (IL) receptors, we also studied the binding of IL-2 and IL-6 to T cells. Patients with Graves' disease were sequentially studied at diagnosis/before treatment (day 0) and 7, 14, 30, 90 and 180 days after methimazole therapy. The results were compared with both a group of 19 age- and sex-matched control volunteers and a group of 20 untreated/euthyroid patients with Graves' disease in long-term remission. The combination of flow cytometry and three-color immunofluorescence revealed a clear (P < 0.01) decrease in the percentage of NK cells before and during the whole course of therapy with respect to both controls and patients with Graves' disease who were in long-term remission. Before therapy, a marked increase (P < 0.001) in the ratio of B to NK cells was also observed; thereafter, a slight decrease in this ratio was observed, although normal values were detected only in patients in long-term remission. Expression of the CD69 early activation antigen in the hyperthyroid untreated patients with Graves' disease was clearly increased (P < 0.01) with respect to both controls and patients with Graves' disease who were in long-term remission. This abnormal CD69 expression was found to be significantly reduced (P < 0.001) by methimazole therapy, and this represents a new effect of the drug. Expression of the low-affinity receptor for IL-2 (CD25)--another early T cell activation marker--was not altered in Graves' disease, but the binding of IL-2 and IL-6 to T cells exhibited a progressive and parallel increase during the first 30 days of therapy, decreasing thereafter. Our results show that methimazole therapy downregulates the abnormally high expression of the CD69 early activation antigen on T cells, being less effective on inducing changes in other T cell activation markers and in NK cells.

CD5+ B cells in Graves' disease: correlation with disease activity.

In the present paper the distribution of peripheral blood CD5+/CD19+ (CD5+B) and CD5-/CD19+ (CD5-B) B-lymphocytes in Graves' disease (GD) patients is analyzed in order to correlate them with disease activity, interleukin-2 (IL-2) and IL-6 binding to T and B cells as well as with anti-thyrotropin (TSH) receptor antibodies and the thyroid hormone serum levels. The combination of flow cytometry and 3-color immunofluorescence revealed a remarkable increase in the absolute numbers of CD5+ B cells in hyperthyroid-untreated GD patients (218 +/- 137 x 10(6)/l vs. 66 +/- 69 x 10(6)/l in healthy subjects, p < 0.01) that gradually fell to normal values once hyperthyroidism had been controlled by methimazole. However, relative numbers of CD5+ B cells persisted at a relatively stable but increased level in GD patients in long term remission of an average of 3.1 years. This was also confirmed in a follow-up study of a group of 12 newly diagnosed patients during the first 90 days of anti-thyroid drug therapy with methimazole. No correlation was observed between either CD5+ B cells or CD5- B cells and the serum levels of pathogenic anti-TSH receptor antibodies. Increased numbers of CD5+ B cells were related to the increased free thyroxine and total triiodothyronine serum levels. In addition, a strong correlation between both the absolute levels of B cells binding to exogenous IL-2 and IL-6 and the absolute number of CD5+ B cells in hyperthyroid GD patients (LR = 0.798, p < 0.001; LR = 0.569, p < 0.01, respectively) was observed. These results suggest that CD5+ B cells in GD are partly regulated by thyroid hormone serum levels as well as by IL-2 and IL-6 binding to B cells. Nevertheless, they are not involved, at least directly, in the production of anti-TSH receptor antibodies.

The relationship between hyperthyroidism and the distribution of peripheral blood T, NK and B-lymphocytes in multinodular goiter.

Peripheral blood T, NK and B-cell subsets were analyzed in 18 patients with nontoxic multinodular goiter (NMG) and 11 patients with toxic multinodular goiter (TMG) in order to evaluate whether hyperthyroidism modifies the distribution of these cell populations. As a control group, 26 age and sex-matched healthy individuals were included in the study. Lymphoid subsets were analyzed with flow cytometry by double staining immunofluorescence techniques using a large panel of monoclonal antibodies. No differences were found in the absolute or relative numbers in any of the cell populations analyzed in both groups--NMG and TMG--, with the exception of a significant decrease in CD19+ cells in TMG. However, patients with multinodular goiter showed important abnormalities in the distribution of T, NK and B lymphocytes with respect to the control subjects. The pattern of abnormalities detected was characterized by a marked increase in the absolute and relative counts of activated T-lymphocytes (CD3+/HLA-DR+), cytotoxic T-cells (CD57+/CD8+) and of cells expressing NK-related antigens. None of these alterations were related to the serum levels of T3, T4 or TSH. Our results point to the existence of important abnormalities in the distribution of several lymphoid subsets in multinodular goiter, regardless of whether the subjects are euthyroid or hyperthyroid.

Urinary prostaglandins (PGE2 and PGI2) in hyporeninaemic hypoaldosteronism in diabetic patients with chronic renal failure.

The present work studies the urinary excretion of PGE2 and PGI2 (6-keto PGF 1 alpha) in 11 insulin-dependent diabetic patients with chronic renal failure with a glomerular filtration rate of 33.9 +/- 9.03 ml/min who had hyporeninaemic hypoaldosteronism to evaluate the influence of these prostaglandins on the appearance of this latter process. The results obtained in this group of patients were compared with those of a control group of healthy individuals, another group of nine non-diabetic patients with CRF, and a last group of eight insulin-dependent diabetic patients with normal renal function to evaluate to what extent the possible variations in prostaglandin excretion could be related to the diabetes, CRF, or a conjunction of both processes. The results of the groups of diabetic patients with CRF were Ccr 33.9 +/- 9.03 ml/min, decreased (P < 0.0001) with respect to the control group and with no difference with the CRF group without diabetes; plasma potassium (4.7 +/- 0.4 mEq/l), increased (P < 0.005) with respect to the values found in the control group; plasma bicarbonate (17.8 +/- 1.8 mEq/l), decreased (P < 0.005) with respect to the control group and also, though not significantly, with respect to the group of non-diabetic patients with CRF. Plasma aldosterone (pg/ml): resting 44.3 +/- 14.9; standing 65.7 +/- 63.5 and post-frusemide 65.5 +/- 58.6, decreased (P < 0.01) with respect to the other three groups. Plasma renin activity (PRA) (ng/ml/h): resting 0.34 +/- 0.3; standing 0.6 +/- 0.4, post-frusemide 0.9 +/- 0.5, decreased significantly with respect to the other three groups.(ABSTRACT TRUNCATED AT 250 WORDS)