Self-report and urine drug screen concordance among women with co-occurring PTSD and substance use disorders participating in a clinical trial: Impact of drug type and participant characteristics.

BACKGROUND: Self-report measures are important in substance use assessment, yet they are susceptible to reporting errors. Urine drug screens (UDS) are often considered a more valid alternative. However, collecting in-person UDS may not always be feasible, contributing to the need to understand factors that influence the validity of self-reported substance use. METHODS: In this secondary analysis of data from 295 women with co-occurring PTSD and substance use disorders (SUD) who participated in a clinical trial testing behavioral interventions, we examined concordance and discordance between self-reported drug use and associated UDS results. Generalized linear mixed models were used to examine the impact of treatment type and participant characteristics on the associations between self-reported drug use and UDS results. RESULTS: Findings revealed higher disagreement between self-report and UDS for opioids and sedatives (ranging from.77 to.90) and lower disagreement rates for cannabis and cocaine (ranging from.26 to.33). Treatment type was not a significant moderator of the associations between self-report and UDS across all drugs. Among those with a positive opioid UDS, those who reported employment in the past three years were more likely to self-report no opioid use compared to their counterparts without employment in the past three years. CONCLUSIONS: Findings add to the literature that supports the validity of self-reported cannabis and cocaine use. The greater discrepancies between self-report and UDS test results of opioids and sedatives suggest adjunctive UDS may be required, although a variety of factors other than inaccurate self-report may be associated with this discrepancy.

[Rocky Mountain spotted fever in an American tourist]. / 'Rocky mountain spotted fever' bij een Amerikaanse toerist.

In a 28-year-old male American tourist who presented in the hospital with fever, cold shivers, headache, nausea, myalgia and arthralgia, Rocky Mountain spotted fever was suspected, partly because he came from an endemic region (the state of Georgia). The patient was treated with doxycycline, 100 mg b.i.d.; 9 days after the first appearance of the symptoms, the diagnosis was confirmed by the report of a positive antibody titre against Rickettsia rickettsii. The patient did not have exanthema. He was discharged in good general condition after two weeks of treatment. Rocky Mountain spotted fever, caused by the Gram-negative bacterium R. rickettsii, is a serious rickettsiosis. The disease is seen only sporadically in the Netherlands because the ticks in the Netherlands do not carry the bacterium. The travel history is still not a standard component of the anamnesis and is therefore often forgotten. This can lead to under-diagnosis and delayed treatment of diseases that were formerly limited to the continent. The early recognition and treatment of Rocky Mountain spotted fever is important since delayed treatment is associated with a clear increase in both morbidity and mortality.

Handling of iodothyronines by the liver and kidney in patients with chronic liver disease.

Possible arterio-venous gradients of T4, T3, rT3 and 3,3'-diiodothyronine (3,3'-T2) across the liver and the kidneys were measured in 9 patients with varying degrees of liver failure undergoing diagnostic catheterization. Plasma iodothyronine levels were measured in peripheral, hepatic and renal veins before and at 10-min intervals until 60 min after iv injection of 400 micrograms of TRH. In 2 patients estimated hepatic plasma flow and effective renal plasma flow were determined as well. In these 2 patients, no significant differences between iodothyronine levels in arterial and peripheral venous plasma were found. T4 and T3 levels were not significantly different between peripheral, renal and hepatic veins. Hepatic vein rT3 and 3,3'-T2 concentrations were 10.7 +/- 8.3% (mean +/- SD, P less than 0.005) and 36 +/- 18% (P less than 0.001) lower than those in the peripheral vein (N = 9). Renal vein rT3 was just (6.2 +/- 7.5%, P less than 0.05) lower than rT3 in peripheral vein, whereas 3,3'-T2 was not different between the two veins. Estimates of hepatic and renal plasma flow were in agreement with values from the literature. On the basis of these data approximate hepatic clearance rates of 110 and 380 1/day for rT3 and 3,3'-T2 and a renal clearance rate of about 35 1/day for rT3 were calculated. Sixty min after TRH, plasma T3 was increased to 147 +/- 56% (P less than 0.05) and 3,3'-T2 in peripheral plasma was increased to 142 +/- 36% (P less than 0.025), whereas plasma T4 and rT3 did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Seizures associated with oxamniquine therapy.

Three patients who were treated for schistosomiasis mansoni with oxamniquine suffered generalized seizures. We suggest that this side effect may be more common than previously reported. Specific ethnic groups may be particularly at risk.

Hyperprolactinemia in hepatic encephalopathy: the effect of infusion of an amino acid mixture with excess branched chain amino acids.

Prolactin levels are elevated in patients with liver cirrhosis and hepatic encephalopathy. Patients with hepatic encephalopathy also have an abnormal plasma amino acid composition, with a relative excess of aromatic amino acids, and a relative decrease in branched chain amino acid levels. In order to study the effect of the plasma amino acid composition on prolactin release, we measured plasma PRL at 0, 10, 20, 30, 40, 50 and 60 minutes after 400 micrograms TRH, both after infusion of a conventional amino acid mixture and after a branched chain amino acid enriched mixture (BCAA) in 5 patients with cirrhosis of the liver and hepatic encephalopathy. After conventional amino acid infusion, a depressed branched chain/aromatic amino acid ratio was found in all patients, together with an increased PRL response to TRH. After BCAA infusion the branched chain/aromatic amino acid ratio normalized. At the same time the excessive PRL response to TRH stimulation was significantly lower in all patients. This suggests that the elevated PRL levels in hepatic encephalopathy are caused by a disturbance of hypothalamic neurotransmitter systems, due to altered amino acid-neurotransmitter precursor levels.

hyperprolactinemia of portal hypertension in rats.

Plasma prolactin levels are often raised in patients with liver cirrhosis and portal hypertension. To obtain more insight into the underlying mechanisms we examined the synthesis and release of prolactin in male rats with partially ligated portal veins. Portal hypertension led to an increase in pituitary prolactin, plasma prolactin, and plasma 17 beta-estradiol, and a decrease in hypophyseal stalk dopamine levels. Castration decreased plasma prolactin levels and prevented the induction of hyperprolactinemia by portal hypertension. Administration of dihydrotestosterone to castrated animals did not affect prolactin levels in the pituitary gland or in the plasma. Plasma tryptophan and tyrosine concentrations did not change in portal hypertension. A low protein diet caused a decrease in plasma tryptophan and an increase in plasma tyrosine levels without affecting prolactin levels in either controls or portal hypertensive rats. The hyperprolactinemia of portal hypertension is probably caused by elevated estrogen levels which interfere with hypothalamic dopamine release. Changes in plasma amino acid levels are of little importance in the regulation of prolactin release in portal hypertensive rats.U

Peripheral elimination of growth hormone in chronic liver disease.

Chronic liver disease is associated with raised basal and TRH-stimulated PRL and GH levels. In a recent study we found the kidney to be the main site of prolactin elimination in patients with liver disease. In order to determine whether this is specific for PRL or a more general mechanism for polypeptide removal, we studied the elimination of GH, which resembles PRL in molecular weight and primary amino acid sequence, in 5 patients with portal hypertension and hepatic cirrhosis and 5 patients with noncirrhotic portal hypertension. Plasma GH levels were measured before and after TRH in peripheral, hepatic and renal vein samples, taken during diagnostic hepatic vein catheterization. An excessive paradoxical increase of GH after THR stimulation was found in 4 out of 5 cirrhotic patients but in none of the noncirrhotic individuals (p less than 0.025). After TRH the mean hepatic venous levels were significantly lower than the peripheral venous levels in 4 out of 5 noncirrhotic patients but in only 1 of the 5 cirrhotic patients (p less than 0.05). The mean renal vein GH levels were significantly lower than the peripheral levels in 3 out of 5 noncirrhotic patients and in none of the cirrhotic patients. In 2 patients in whom renal and hepatic plasma flow was measured, renal extraction of GH was found to be 0 to 6.4 micrograms, while liver extraction amounted to 22.1 and 34.7 micrograms of GH during the same 60-min period. Despite the similarity in molecular weight and primary amino acid sequence between PRL and GH, GH appears to be mainly taken up by the liver while PRL is mainly eliminated by the kidney in this group of patients with portal hypertension. This suggests that the renal elimination of prolactin is not solely dependent on glomerular filtration. The selective hepatic removal of growth hormone is probably related to a specific action of growth hormone on liver metabolism.