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No significant difference was found between the mean plasma cortisol levels in 2 groups of diabetic patients (10 with non-severe metabolic decompensation and 10 well compensated). Likewise, there was not statistical difference on considering the diurnal Cortisol/nocturnal Cortisol quotients in both groups; these quotients besides showed the persistence of the circadian rythm. No valuable difference was seen in the adrenal response to ACTH stimulus. It was found direct correlation between glycemic levels and cortisol increments after stimulus in the total series of 20 patients (r = 0.44; p < 0.05). There were also significant correlations between diurnal and nocturnal Cortisol (r = 0.63; p < 0.01) and between Cortisol levels before and after stimulus (r = 0.68; p < 0.01). No differences were found in Cortisol levels on estimating the incidence of diabetic complications (retinopathy or nephropathy). All these data suggest the tendency to adrenal hyperactivity due to the diabetic decompensation through the action of the hypothalamic-pituitary axis.

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare disease, whose origin seems to lie in a acquired defect in the membrane of the pluri-potential hematopoietic cell. Chronic or intermittent acute hemolytic syndrome is the most frequent clinical manifestation, although in the literature there are also some references to the leukocytic and immunologic disorders of this disease. In this paper, we present the case of a 63-year-old patient with NPH who developed severe neutropenia and sustained febrile syndrome. In the past four years, she had suffered frequent episodes of fever and leukopenia, which apparently disappeared spontaneously. In the physical exploration, we observed hepatosplenomegaly. The hemogram showed mild iron deficiency anemia (hemoglobin 10.8 g/dl), severe neutropenia (neutrophil 0.3 x 10(9)/l) and significant reticulocytosis (610 x 10(9)/l). Iron deposits were greatly reduced in the marrow. Simultaneously to a new febrile episode and isolation of Escherichia coli in the urine, there was a severe anemization (hemoglobin 5 g/dl) and a significant thrombopenia (platelets 30 x 10(9)) resulting in a positive hemosiderinuria and sucrose test. The study of the leukocytic function showed a defect in the neutrophil chemotaxis, although a normal phagocytic capacity and microbicidal activity. In the following nine months, the patient had several severe infections, with intense but transitory pancytopenia, which always improved when treating the infection with antibiotics. The patient died due to a septic shock twelve months after the diagnosis. Recurrent febrile episodes and severe neutropenia are very rare in the PNH (less than 4% of the cases). The cause of these disorders is still unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

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In 15 patients with chronic bronchopneumopathy (7 with polyglobulia and 8 without it), we observed that polyglobulic patients had higher average levels of sideremia and basal saturation of transferrin and lower levels of HCM, CHCM and VCM. No significant differences were observed in the average levels of ferritin between both groups. Overall, in this series of 15 patients, a significant inverse correlation was observed between sideremia and HCM (r = -0.52; p < 0.05) and between sideremia and CHCM (r = -0.55, p < 0.5), as well as a trend towards a direct correlation between sideremia and the red blood cells count (r = 0.45, N.S.). There was also a direct correlation between serum ferritin and the sedimentation rate (r = 0.72, p < 0.01) and trends towards inverse correlations although not significant, between ferritin and sideremia (r = -0.25, N.S.). These data reflect a hyperconsumption of iron in the respiratory polyglobulia, with some relative deficit, suggesting as well that serum ferritin is not a good enough criteria in these cases for the evaluation of iron deposits, because it behaves like the sedimentation rate with respect to acute phase reactants when there is inflammation.

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Complicated diabetic patients have a marked decrease of plasmatic level of T3 and a less important decrease of T4. They are caused by the alteration of the extra-thyroid T3 formation from T4 and lower TSH release. 11 patients with a different metabolic state had a basal determination of T3 and T4 and 6 hours after the administration of 5 Units of TSH intramuscular in order to see whether those changes described previously existed in any other intrinsic thyroid alteration secondary to complicated diabetes. The median increases observed were between normal limits (T3: 96%; T4: 45%) and in accordance with this, a direct correlation between glycemia and its respective rate of hormonal increase were observed as well, without any statistical significance (r = 0.56 in T4; r = 0.36 in T3). These results allow us to confirm that there is not an eventual thyroid function alteration during complicated diabetes as opposed to the afore-mentioned increase of the extra-thyroid factors.

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The plasmatic levels of TSH in 2 group of diabetic patients (7 decompensated and 8 decompensated, but in treatment) were measured at 9:30 and 23:30 hours. The mean glycemia levels were of 280 +/- 45 and 150 +/- 30 mg/dl (p less than 0.0005). There was no significant difference between daily TSH and nocturnal TSH in any of the groups, but there was a tendency for the nocturnal TSH to be higher in decompensated patients. There was no difference when comparing the TSH of the first group to the TSH of the 2nd group. The mean TSH N/TSH D was superior by 1 (1.36 in decompensated and 1,095 in treated patients). The correlation between glycemia and TSH D was negligible in all groups. The data suggests the tendency that the circadian rhythm of TSH in maintained in diabetes decompensation with shorter rhythm registered in treated patients. This shows a certain normality in the suprahypophysary area in charge of the rhythm and is similar to the minor liberation of TSH after TRH stimulus that other authors have described as happening in the decompensation of diabetes mellitus.

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42 patients with chronic bronchopneumopathy were divided into 2 groups: one with polyemia (15 patients) and the other without polyemia (27 patients). There was no statistical significant differences in median age, clinical evolution nor basal medium arterial PO2 value (43 +/- 12 and 48 +/- 11 mm Hg); while there was an increase of median basal PCO2 in patients with polyemia (54 +/- 8.4 and 48 +/- 9.3; P < 0.025). There was direct correlation between PCO2 and Hb levels in the whole series (r = 0.42; P < 0.01) and equal correlation in the limit of statistical signification between PCO2 and red cells (r = 0.29; P = 0.05). The correlation between these hematic values and the PO2 values of the whole series was not significant, this taking into account the logical inverse relation between them, because of the important role of hypoxia in developing polyemia. The correlation between PO2 and PCO2 was inverse and significant (r = -0.33; P < 0.05). These findings show the apparent influence of CO2 retention to produce polyemia, apart from the effects of hypoxia, being the opposite of the results in experimental studies which showed a stoppage of the erythropoietin production by CO2 effects. The probable explanation is that patients with more PCO2 had more intense respiratory malfunction than lower PCO2 patients, producing night episodes of more basal hypoxia, this being a major stimulus of polyemia.

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