[Diagnostic image (104) Purple discoloration of the urine bag]. / Diagnose in beeld (104). Paarse verkleuring van de urinezak. Paarse-urinezaksyndroom.

In a 65-year-old woman who had a suprapubic catheter for nine years, purple urine bag syndrome was diagnosed.

[Hyponatremia caused by thiazide diuretics: be aware of drug combinations which enhance this effect]. / Hyponatriëmie bij gebruik van thiazidediuretica: let op combinaties van geneesmiddelen die dit effect versterken.

In 3 patients, two women aged 88 and 82 and a man aged 76, the consciousness became disrupted due to a severe hyponatraemia, after a thiazide diuretic had been combined with another drug without laboratory control. After a change in medication, the laboratory values and the patients' conditions normalised. Severe hyponatraemia is a well known but rare complication of thiazide therapy. It has a significant mortality and morbidity rate. The risk is greater for elderly women. This effect on serum sodium can be enhanced by the use of other drugs like furosemide, carbamazepine, paroxetine and NSAIDs. That a patient uses a thiazide is sometimes overlooked when a combined preparation of other drugs is prescribed. Diuretic serum electrolytes should be monitored once treatment with thiazide has been started, especially in elderly patients taking other drugs.

Clinical and biochemical changes following 131I therapy for hyperthyroidism in patients not pretreated with antithyroid drugs.

BACKGROUND: Radioiodine therapy (131I) for the treatment of hyperthyroidism has been shown to be effective and safe. Despite the extensive experience with radioiodine therapy, the necessity for pretreatment with antithyroid drugs is controversial. Pretreatment is partly based on the concept that antithyroid drugs deplete the thyroidal hormonal stores, thereby reducing the risk of a radioiodine-induced aggravation of hyperthyroidism or thyroid storm. Few data are available on the frequency of clinically significant exacerbations of hyperthyroidism following 131I therapy without prior treatment with antithyroid drugs. The aim of the present study was to determine prospectively the early clinical and biochemical changes after 131I therapy in patients who were not pretreated with antithyroid drugs. METHODS: Patients with Graves' disease (n = 21), toxic multinodular goiter (n = 11) or toxic adenoma (n = 2) were studied before and after 131I therapy. Clinical and biochemical parameters of thyroid function were investigated before and 1, 2, 8, 11, 18 and 25 days after 131I treatment. Patients were given no antithyroid drugs prior to 131I therapy, all patients received beta-blocking agents for symptomatic relief. RESULTS: In 19 of 34 patients, a transient increase in thyroid hormone levels was observed, predominantly in the first week following 131I therapy. None of these patients experienced worsening of thyrotoxic symptoms. This transient increase in thyroid hormone levels was demonstrated in all patients with toxic multinodular goiter, whereas it was found in only six of 21 patients with Graves' disease. This difference could not readily be explained by differences in pretreatment thyroid hormone levels, administered dose or effectively absorbed dose of 131I. CONCLUSIONS: 131I treatment of hyperthyroidism without pretreatment with antithyroid drugs may cause a transient increase in thyroid hormone levels. Clinically significant exacerbations of hyperthyroidism were, however, not observed in our study population. Increased hormone levels following 131I therapy were more often seen in patients with toxic multinodular goiter than in patients with Graves' disease.

Mineralocorticoid excess due to precursors only in a patient with adrenal cortical carcinoma.

A patient with carcinoma of the adrenal cortex presented with mineralocorticoid excess due to hypersecretion of deoxycorticosterone, which is exceedingly rare. Backache was the only symptom and an unexplained hypokalaemia was the only sign. Because of the abnormal synthesis of steroid precursors in these tumours a urinary steroid profile may be helpful as a diagnostic tool in such cases.

Heerlen polymorphism of protein S, an immunologic polymorphism due to dimorphism of residue 460.

We recently developed an enzyme-linked immunosorbent assay (ELISA) for total protein S (PS) antigen using the monoclonal antibody S-12. During the screening of thrombophilic patients we identified a patient, who was using marcoumar, with 0% PS by monoclonal ELISA and 23% PS by polyclonal ELISA. Further analysis of this patient and his family showed that the patient was a compound heterozygote for type 1 PS deficiency and for an abnormal PS molecule (PS-Heerlen) that was not recognized by the S-12 antibody. Similar observations were made in two sisters from an unrelated Dutch family. Subsequent studies showed that PS Heerlen has a slightly lower molecular weight (71,000) than normal PS (73,000), binds normally to C4b-binding protein, and retains full activated protein C cofactor activity. The alteration in the PS Heerlen molecule was identified as a substitution of Ser460 by Pro, which is due to a unique T---C transition in exon 13 of the active PS-alpha gene. The substitution occurs in the consensus sequence for the potential N-linked glycosylation of Asn458. Digestion with N-glycanase showed that normal PS probably contains three N-linked oligosaccharide side chains, while PS Heerlen contains only two (Asn458 not glycosylated?). Segregation analysis in the two original families showed that the presence of the genetic abnormality was always associated with the PS-Heerlen phenotype. The frequency of the PS-Heerlen allele was found to be 0.52% in the general population and 0.67% in a population of patients with unexplained thrombophilia. There is no evidence that the PS Heerlen allele is associated with an increased risk for thrombosis.

Effects of chlorthalidone on serum and total body potassium in hypertensive patients.

Total body potassium has been estimated in 26 hypertensive patients who were hypokalaemic as a result of long-term chlorthalidone treatment (mean 20.5 months), while they were on chlorthalidone and 4 weeks after this had been discontinued. The mean difference amounted to only 95 mEq (not significant). In 6 additional patients not previously treated with chlorthalidone, serial total body potassium estimations revealed a mean potassium deficiency of 245 mEq after 33 days and of 106 mEq after 100 days. These results suggest that the mechanism causing the initial potassium loss is partly reversed or compensated later on. In patients with uncomplicated hypertension, no significant potassium deficiency was detected during long-term treatment. Eighteen of our patients received 39 mEq potassium chloride supplements daily for 4 weeks; this caused a mean rise in serum potassium from 3.23 mEq/l to 3.38 mEq/l (not significant). Total body potassium did not change at all. We conclude that potassium chloride supplements are not an effective treatment of hypokalaemia in this condition. Correction of the extracellular pH by ammonium chloride in 6 patients on chlorthalidone, who demonstrated a slight metabolic alkalosis, gave rise to a mean increase in plasma potassium from 2.78 mEq/l to 2.96 mEq/l (not significant). The hypokalaemia in hypertensive patients on long-term chlorthalidone treatment cannot be explained by either a potassium deficiency or the change in extracellular pH.