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O Dolva

Publications and source records attributed to O Dolva.

6 recordsLinked to original sources

Adrenal autoantibodies and organ-specific autoimmunity in patients with Addison's disease.

OBJECTIVE: Autoimmune destruction of the adrenal gland is the major cause of Idiopathic Addison's disease, but the significance of 21-hydroxylase autoantibodies and their correlation with the presence of other autoantibodies have not so far been investigated in a larger population of patients with Addison's disease. We have now characterized a cohort of patients with idiopathic Addison's disease (n = 97) regarding the specificity of autoantibodies against the adrenal cortex and, as Addison's disease can be either an isolated condition or part of a polyendocrine disorder, we investigated the presence of organ-specific polyendocrine autoimmunity in this patient population. DESIGN: Cross-sectional study. MEASUREMENTS: Autoantibodies were analysed with indirect immunofluorescence (IF) on tissue preparations, ELISA and in Western blots using bacterially expressed proteins. RESULTS: Eighty-four per cent (81/97) of the patient sera recognized the steroid-producing cells of the adrenal cortex in indirect IF. The antigen was identified as 21-hydroxylase by 72% (70/97) of the patient sera in Western blots. Seven sera that were negative on adrenocortical IF identified 21-hydroxylase on Western blot, while eight IF-positive sera were 21-hydroxylase-negative. Five sera weakly recognized 17 alpha-hydroxylase in Western blots, but all of these were also positive for 21-hydroxylase. In 13 cases (12 women), the sera also reacted with testicular Leydig cells, and nine of these identified the side-chain cleavage (SCC) enzyme. Other clinically evident organ-specific autoimmune disorders were present in 40% of the 97 patients and abnormal titres of organ-specific antibodies were found in 60% of the patients. CONCLUSIONS: In idiopathic Addison's disease, auto-antibodies against 21-hydroxylase are found in a majority of cases and this represents an important diagnostic tool. The enzyme 17 alpha-hydroxylase does not seem to constitute a major autoantigen in Addison's disease. In a subgroup of patients with autoantibodies to gonads, antibodies to SCC are produced, often in parallel with antibodies to 21-hydroxylase. In yet another subgroup the specificity of autoantibodies giving positive immunofluorescence is still unknown. Three patients revealed a polyendocrine syndrome which clinically resembles autoimmune polyendocrine syndrome (APS) type I, but serologically corresponds to APS type II. Polyendocrine disorders are often associated with Addison's disease, and screening, including quantification of autoantibodies, may help to identify those at risk of developing associated autoimmune disorders.

Addison Disease↗

[Lung damage in amiodarone therapy].

Amiodarone pulmonary toxicity is the most serious side effect of amiodarone therapy. We describe a patient who died of this adverse effect. The clinical presentation is most often that of an indolent illness, with cough and/or fever. The diagnosis is made by careful exclusion of other causes of the observed illness and the finding of clinical, radiographic, physiologic, and pathologic abnormalities compatible with amiodarone toxicity. Examination prior to drug therapy, including lung function tests, is recommended for later controls. Of the therapeutic options, discontinuation of amiodarone is most frequent. However, for some patients with life-threatening ventricular arrhythmias this is the only effective therapy.

Aged↗

Thyrotrophin-releasing hormone in human ejaculate.

Immunoassayable TRH in human ejaculate was eluted from a gel column in a form with a molecular weight larger than that of the native peptide. With reverse-phase high-performance liquid chromatography (HPLC) the same activity co-eluted with standard TRH. Incubation of ejaculates at room temperature for 8 h was associated with a time-related increase in the total immunoassayable TRH. Analysis by HPLC of ejaculates after 12 h of incubation at room temperature indicated that, whereas the levels of the peptide co-eluting with native TRH declined with time, there was a concomitant increase in the concentration of a molecular species which also cross-reacted with the TRH antiserum, but which was more hydrophobic. The latter species is presumably identical to the tetrapeptide recently described by others and which may arise from the proteolytic degradation of secretory macromolecules. Although immunological activity was present in all six fractions of split ejaculates, the bulk of the peptide was associated with the later portions, implying a major vesicular contribution. However, secretions isolated from surgical preparations of the seminal vesicles contained undetectable levels of peptide, suggesting that the ejaculation process may represent a stimulus for its appearance in the semen. This study is further support for a local involvement of TRH in male reproductive function.

Chromatography, Gel↗

Actions of thyrotropin-releasing-hormone on gastrointestinal function in man. I. Inhibition of glucose and xylose absorption from the gut.

We studied serum glucose levels following a peroral glucose test in 6 healthy subjects on 2 alternate days in random order; with or without an i.v. TRH infusion for 3 hours (0.66 mg/hour). TRH infusion reduced serum glucose levels following oral glucose in all 6 subjects investigated. Serum insulin levels were reduced accordingly. Furthermore, serum xylose levels following peroral xylose were studied in the same 6 subjects. TRH infusion i.v. reduced serum xylose levels in all 6 subjects studied. I.v. glucose tolerance tests with or without an i.v. TRH infusion (0.66 mg/h) for 3 hours were studied in 4 healthy subjects. No change in serum glucose or insulin levels following TRH infusion was observed. We conclude that an i.v. infusion of TRH reduces serum levels of glucose following a peroral xylose load. TRH thus has marked actions on gastro-intestinal function in man inhibiting and/or retarding the absorption of glucose and xylose from the gut.

Adult↗