Hypocarotenemia in patients fed enterally with commercial liquid diets

We have found that 12 patients requiring permanent enteral feeding secondary to cerebrovascular accident with adequate Vitamin A nutritional status had serum concentrations of various carotenoids which were only 8-17% of sex- and age-matched healthy controls. Their serum retinol levels were normal, but only 61% of their controls despite receiving two to three times the recommended daily allowance (RDA) in retinol equivalents. Commercial enteral formulas were found to contain only negligible quantities of the carotenoids and were the cause of the hypocarotenemia. To assess the ability of these patients to absorb beta-carotene, nine tube-fed patients were given 15 mg of beta-carotene (2.5 times the RDA) in a single dose. Serum concentration time curves showed that only four patients absorbed significant quantities of the beta-carotene and absorption was delayed compared to previously studied subjects taking enteral formulas as meals. These studies suggest that the efficiency of absorption of the fat soluble vitamins may be lower in tube-fed patients and that patients receiving long-term tube feeding are denied the possible protective effects of the carotenoids normally contained in the American diet.     

An evaluation of the trends in analytical performance of international apolipoprotein A-1 and B assays

Two international apolipoprotein A-1 and B (apoA-1 and apoB) surveys were conducted in 1983 and 1986 with use of a lyophilized serum measured by 55 and 91 participants, respectively. The chief source of variability in both surveys was among laboratories, but among-method variation was significant for apoB. Comparing the 1986 with the 1983 findings, we saw a 60% decrease in apoA-1 variability among laboratories, and a similar decrease (53%) was found for apoB. Evaluation of individual measurements suggests that some collaborators may have adjusted their calibrators toward the consensus values published in 1983.     

A rapid digestion method for analysis of nickel compounds in tissue by electrothermal atomic absorption spectrometry

Quantification of nickel in animal soft tissue is of toxicological interest. A digestion method applying the use of microwave ovens for irradiating samples in Teflon digesters was developed. An acid mixture containing nitric acid (16 M, 1.0 ml g-1 tissue), hydrochloric acid (6 M, 0.5 ml g-1 tissue) and H2O2 (30%, 1.0 ml g-1 tissue) and irradiation at 600 W for 5 min were required for complete dissolution of tissue matrices and nickel compounds. Analyses of Ni in National Bureau of Standards Reference Material 1566 oyster tissue gave 0.87 +/- 0.24 micrograms g 1(mean +/- SD, n = 5), which was in agreement with the NBS certified value of 1.03 +/- 0.19 micrograms g-1. Recoveries of 1-300 micrograms Ni added as nickel sulfate (highly soluble), nickel subsulfide (moderately soluble in biological fluids and acid) or nickel oxide (green high-temperature oxide, low solubility in biological fluids and acid) to lung, liver, lymph node and kidney were quantitative, except in the case of nickel sulfate added to kidney, where recovery was less than quantitative for 1-10 micrograms Ni. The method appears effective for digestion of a variety of tissues requiring Ni analyses.     

Arthroscopic stabilization of the anterior shoulder

The arthroscopic stabilization of the shoulder is in its infancy. Soon, improvements in technique and equipment may make it the standard, thus reducing morbidity and time loss from full function.     

Priapism Following Trazodone Overdose with Cocaine Use

Priapism is a urologic disorder and medical emergency with a variety of known etiologies including the use of psychotropic medications. The antidepressant trazodone is the agent most frequently implicated in the precipitation of priapism. Additionally, a number of drugs of abuse including marijuana, ethanol, and cocaine have been known to cause the disorder. It is unknown if drugs may act in an additive or a synergistic manner to cause priapism. We report a case of priapism which occurred following trazodone overdose in an individual actively using cocaine. This case suggests that combined trazodone and cocaine use may pose an additional risk of priapism. Since trazodone is commonly employed as a hypnotic and often chosen for polysubstance abusers due to its low abuse potential, clinicians should be aware of the possible additive risk of priapism in this patient population.     

Acute renal failure due to xanthine stones

A 9-month-old child with the skeletal abnormalities of Fuhrmann's syndrome presented with acute renal failure secondary to bilateral renal calculi. Hereditary xanthinuria was shown to be the underlying metabolic defect. Treatment with allopurinol was unsuccessful at reducing the xanthine excretion.     

NGF Augmentation rescues trigeminal ganglion and principalis neurons,but not brainstem or cortical whisker patterns,after infraorbital nerve injury at birth

Prior studies indicate that neonatal nerve injury kills many trigeminal (V) first- and second-order cells, and interrupts pattern formation in the brainstem and cerebral cortex. Yet it is not known whether effects upon cell survival and pattern formation are causally related. To determine whether axotomized V ganglion cells can be rescued by an exogenous trophic agent, rats received 5 mg/kg of nerve growth factor (NGF) prior to, and every day after, infraorbital nerve section on the day of birth until sacrifice on postnatal day (PND) 1, 3, 5, 7, or 14. Other animals received identical lesions without NGF. Ganglion cell numbers were significantly reduced by PNDl in pups not given NGF, while NGF-treated rats displayed no significant cell loss through PND7. However, NGF did not permanently rescue V neurons because ganglion cell numbers were reliably reduced by PND14. Cell numbers in V nucleus principalis were reduced by PNDl in pups not given NGF, while NGF-treated animals displayed no cell loss through PND14. NGF's rescue of second-order cells is probably an indirect effect of NGF actions upon V ganglion cells because, in other newborns, NGF failed to maintain principalis cells after direct lesion of the left V ganglion. To determine whether preventing cell death permits whisker-related pattern formation, other rats also received NGF prior to and after infraorbital nerve section at birth. After 3–14 days, patterns were assessed in the brainstem and cortex with cytochrome oxidase histochemistry and serotonin immunocytochemistry. Whisker-related patterns failed to develop as in cases not given NGF. These data indicate that communication with the periphery is necessary for the maintenance of central whisker-related patterns. They also suggest that V ganglion cells can be rescued, albeit temporarily, from rapid injury-induced death by NGF, thereby delaying injury-induced cell death in nucleus principalis. However, the mechanism(s) responsible for injury-induced pattern alterations in the developing V system remains to be elucidated. © 1993 Wiley-Liss, Inc.