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Biomedical subjects

D Vollmer

Publications and source records attributed to D Vollmer.

At least 19 recordsLinked to original sources
PubMed1995

Successful use of the nocturnal urine alarm for diurnal enuresis.

We report the effects of using a urine alarm, typically employed for nocturnal enuresis, to treat chronic diurnal enuresis in a 15-year-old female resident at Boys' Town. The results of an ABAB reversal design indicate that the alarm eliminated wetting in both treatment phases and that continence was maintained at 3- and 6-month follow-up.

Adolescent↗
PubMed1994

Impairment of adrenocortical function associated with increased plasma tumor necrosis factor-alpha and interleukin-6 concentrations in African trypanosomiasis.

African sleeping sickness (SS) is a severe, potentially lethal parasitic disease. The treatments of choice are the antiparasitic agents suramin, which is adrenotoxic, and/or melarsoprol. We evaluated the functional integrity of the hypothalamic-pituitary-adrenal (HPA) axis of patients with SS before, during, and after therapy with suramin and/or melarsoprol, in two sequential stages. First, we employed the standard adrenocorticotropic hormone (ACTH) 1-24 stimulation test (250 micrograms i.v.) to assess the maximal adrenocortical responsiveness of 69 patients with SS and 38 normal controls. We demonstrated paradoxically subnormal cortisol responses before suramin therapy [net cortisol response 60 min after stimulation: 10.5 +/- 2.9 (mean +/- SE) vs. 17.5 +/- 1.0 micrograms/dl for controls, p = 0.004], with 27% of the patients falling within the adrenal insufficiency range (stimulated cortisol concentration < 20 micrograms/dl). These responses subsequently and unexpectedly improved with suramin and/or melarsoprol therapy. Second, we performed a human corticotropin-releasing hormone (hCRH) test (100 micrograms i.v.) in 68 additional patients with SS and 14 control subjects to examine whether the glucocorticoid deficiency observed was primary and/or secondary. Compared to controls, the ACTH and cortisol responses to hCRH were blunted (ACTH after 60 min: 29 +/- 7 vs. 58 +/- 8 pg/ml in controls, p = 0.014; cortisol: 15.2 +/- 1.5 vs. 19.6 +/- 0.7 micrograms/dl, p = 0.018), suggesting the presence of secondary adrenal insufficiency. There was improvement of both ACTH and cortisol responsiveness to hCRH with therapy, with cortisol recovery occurring before ACTH, suggesting an additional primary component of adrenal dysfunction in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Hypothalamic chordoma. Case report.

The case is reported of a 51-year-old woman found to have a hypothalamic mass with the histological features typical of chordoma. This represents the first description of a chordoma arising within the brain.

Chordoma↗
PubMed1993

Thyroid dysfunction in African trypanosomiasis: a possible role for inflammatory cytokines.

OBJECTIVE: Sleeping sickness (African trypanosomiasis) is an anthropozoonosis transmitted by the tsetse fly. The treatments of choice are the antiparasitic agents suramin and/or melarsoprol. Experimental infection of animals with Trypanosoma brucei results in inflammatory lesions in the pituitary and/or the thyroid gland. In biochemical terms, these animals have hypothyroidism. We evaluated the functional integrity of the hypothalamic-pituitary-thyroid axis in patients with African trypanosomiasis before, during and after specific therapy. DESIGN: Prospective, controlled, cross-sectional study. PATIENTS AND MEASUREMENTS: Sixty-five patients with sleeping sickness (31 female, 34 male; aged 18-66; 32 with haemolymphatic sleeping sickness receiving suramin i.v., 33 with cerebral sleeping sickness receiving melarsoprol) and 13 control subjects (6 female, 7 male; aged 21-60) were enrolled in a cross-sectional study after giving informed consent. Fourteen patients were studied shortly after admission for sleeping sickness, 19 in the middle of the course of treatment, 18 at the end of the 5-week treatment period, and 14 patients after cure. All subjects underwent a TRH stimulation test at 1200 with bolus injection of 400 micrograms TRH i.v. Blood was drawn for determination of fT3, fT4, TSH, rT3, TNF-alpha, IL-1 and IL-6 at 0 minutes and TSH at 60 minutes. All hormones and cytokines were determined by RIA or ELISA. RESULTS: Baseline TSH concentrations (mean +/- SEM) were elevated in unmedicated patients with sleeping sickness compared to normal subjects (2.6 +/- 0.4 vs 1.4 +/- 0.2 mU/l; P = 0.01), whereas fT3 (2.7 +/- 0.5 vs 5.8 +/- 0.3 pmol/l; P = 0.0002) and fT4 concentrations (10.3 +/- 1.2 vs 15.4 + 0.8 pmol/l; P = 0.007) were low. Stimulated TSH concentrations did not significantly differ from normal controls. Reverse T3 concentration in patients with sleeping sickness were normal (2.2 +/- 0.3 vs 2.4 +/- 0.2 nmol/l; P = NS). During the course of treatment, baseline TSH, fT3 and fT4 concentrations slowly returned to normal and were indistinguishable from controls after cure. Plasma concentrations of TNF-alpha (16.0 +/- 4.1 vs 2.9 +/- 1.4 ng/l in controls; P = 0.003) and interleukin-6 (19.2 +/- 7.3 vs 1.3 +/- 0.2 ng/l; P = 0.0001), but not interleukin-1 beta (2.0 +/- 0.2 vs 0.9 +/- 0.2, ng/l P = NS), were elevated, when thyroid function impairment and disease activity were at their maximum, but gradually decreased into the normal range with therapy. We found a negative correlation between baseline cytokine concentrations and fT3 concentrations (TNF-alpha: r = -0.34, P = 0.003; IL-6: r = -0.43, P = 0.0001). CONCLUSIONS: We conclude that unmedicated sleeping sickness is associated with significant impairment of thyroid function, which is reversed with specific therapy. Elevated TSH concentrations and low fT3 and fT4 concentrations suggest primary hypothyroidism in patients with sleeping sickness. However, an additional pituitary and/or hypothalamic component cannot be excluded. This impairment may be due to the elevated plasma cytokine concentrations found in these patients or may be the result of parasitic thyroiditis.

Adolescent↗
PubMed1987

An evaluation of a new test kit to screen for galactosemia.

A new galactosemia screening kit has been evaluated. The kit employs the Yoshida modification of the Paigen et al. Escherichia coli bacteriophage assay and is produced by Eiken Co. Ltd. of Japan. The assay estimates galactose and galactose-1-phosphate in dried blood specimens. The kit is sufficiently sensitive to detect possible heterozygotes as well as possible homozygotes.

Biological Assay↗
PubMed1987

"Defasciculation" with metocurine prevents succinylcholine-induced increases in intracranial pressure.

In order to determine whether a small, "defasciculating" dose of metocurine could prevent increases in intracranial pressure (ICP) induced by succinylcholine (Sch), the authors studied 12 patients (ages 25-79 yr) undergoing craniotomy for excision of malignant supratentorial gliomas. After insertion of a subarachnoid bolt for ICP monitoring and a radial arterial cannula for determination of blood pressure and blood gas tensions, six patients (group I) were randomly allocated to receive MTC 0.03 mg/kg 3 min before induction of general anesthesia with thiopental 4 mg/kg and nitrous oxide 70% in O2. Six other patients (group II) received saline 0.015 ml/kg instead of MTC, followed by the same induction sequence. After induction of anesthesia, ventilation was controlled by mask (PaCO2 = 40 mmHg +/- 2 SE), and arterial and intracranial pressures were allowed to stabilize. Four minutes after thiopental administration (7 min after MTC), after a 1-min period of relatively stable arterial pressure and ICP, Sch 1 mg/kg was administered as a bolus. ICP and blood pressure were recorded continuously until normal twitch tension was restored. In group I (MTC pretreatment), ICP did not change significantly from the mean value observed before Sch, 14 mmHg +/- 2 SE. In group II (saline pretreatment), ICP increased from 11 mmHg +/- 2 SE to 23 mmHg +/- 4 SE (P less than .05). This study not only confirms previous work showing that Sch may induce marked ICP increases in lightly anesthetized patients with intracranial mass lesions, but also indicates that pretreatment with a "defasciculating" dose of MTC can prevent these potentially deleterious ICP increases in patients known to be at risk.

Adult↗