Dark liver

The increase in echogenicity (i. e. increase in density) of a homogeneous, frequently coarsened structure with decreased sound conduction in the form of a structurally dense hver is a reliable indicator of a diffuse liver disease. This increase in intensity and frequency of echoes yields the image of a bright (white) liver (e.g. fatty liver, haemachromatosis). A diffuse liver disease can also be accompanied by a decrease in echogenicity, which is why the hypoechoic liver is known as a dark liver (e. g. acute hver congestion, acute viral hepatitis, amyloidosis), (s. fig. 6.4)... 

Wistar) (G) Hepatic 1127 2255 (dark liver) gas-filled blood in intestines) 1980b... 

C. Excreted in the urine in the rare hereditary disease alkaptonuria. Homogentisic acid is easily oxidized in the air to dark-coloured polymeric products, so that urine from patients with alkaptonuria turns gradually black. It is formed from tyrosine and is an intermediate in tyrosine breakdown in the body. Alkaptonuria is due to the absence of the liver enzyme which cleaves the aromatic ring. 

ITRACONAZOLE Although rare, die patient may develop hepatitis during itraconazole administration. The nurse closely monitors die patient for signs of hepatitis, including anorexia, abdominal pain, unusual tiredness, jaundice, and dark urine. The primary healtii care provider may order periodic liver function tests. 

There is a dark side to receptor-mediated endocyto-sis in that viruses which cause such diseases as hepatitis (affecting liver cells), poliomyelitis (affecting motor neurons), and AIDS (affecting T cells) initiate their damage by this mechanism. Iron toxicity also begins with excessive uptake due to endocytosis. 

Flutamide is an androgen receptor antagonist that achieves peak concentrations approximately 2 to 4 hours after an oral dose. Flutamide is metabolized extensively, with a terminal half-life of about 8 hours. Bicalutamide achieves peak concentrations approximately 6 hours after the dose, with a terminal half-life of 6 to 10 days. Bicalutamide undergoes stereospecihc metabolism, where the S-enantiomer is cleared more rapidly by the liver than the -enantiomer. Nilutamide achieves peak serum concentrations between 1 to 4 hours after an oral dose and has a terminal half-life of 38 to 60 hours. Nilutamide is metabolized extensively, with less than 2% excreted as unchanged drug by the kidney. Side effects common to these agents are hot flashes, gynecomastia, and decreased libido. Flutamide tends to be associated with more diarrhea and requires three-times-daily administration, whereas bicalutamide is dosed once daily. Nilutamide may cause interstitial pneumonia and is associated with the visual disturbance of delayed adaptation to darkness. 

Elevated zinc levels in serum, liver, and kidney jaundice, anoxemia, anemia, vomiting, dark red urine. 

The adverse effects of antiandrogens are gynecomastia, hot flushes, GI disturbances, liver function test abnormalities, and breast tenderness. GI disturbances consist of diarrhea for flutamide and bicalutamide and nausea or constipation for nilutamide. Flutamide is also associated with methemoglobinemia, whereas nilutamide causes visual disturbances (impaired dark adaptation), alcohol intolerance, and interstitial pneumonitis. 

Late porphyria, as a rule, is accompanied by swelling of the liver, its abnormal functioning, change in color of urine to dark-orange. 

It was conclusively shown that deoxychlordiazepoxide (393) had none of the phototoxic properties of the parent drug, at least in the rat [225]. Chlordiazepoxide, demethylchlordiazepoxide, demoxepam and diazepam-4-oxide were all phototoxic to a bacterial cell preparation. There was a close relationship between the phototoxicities of the A-oxides and the toxicity in the dark of their oxaziridines. The reduced forms of the four compounds were not phototoxic [ 228 ]. Kinetic studies demonstrated that the oxaziridine (390) covalently bonds to plasma proteins. The half-life of the oxaziridine in the presence of high concentrations of protein was about 30 min. It therefore has time not only to bind to biomolecules in the skin surface, but also to attack internal organs. This was put forward as the explanation of previously observed kidney and liver damage in the rat [229]. 

Effects reported in humans following dermal exposure to phenol include liver damage, diarrhea, dark urine, and red blood cell destruction. Skin exposure to a relatively small amount of concentrated phenol has resulted in the death of humans. Small amounts of phenol applied to the skin of animals for brief periods can produce blisters and burns on the exposed surface, and spilling dilute phenol solutions on large portions of the body (greater than 25% of the body surface) can result in death. 

Chronic-Duration Exposure and Cancer. Mortality was not increased in workers occupationally exposed to phenol (Dosemeci et al. 1991). Effects reported in a case of chronic phenol poisoning, in which exposure was by both the inhalation and dermal routes, included muscle pains in the arms and legs, enlarged and tender liver with increased levels of liver enzymes in the serum, dark urine, and emaciation (Merliss 1972). 

In male rats, swelling and mild centrilobular vacuolation was observed only in the livers of rats exposed to 271 ppm. Necrosis was minimal and confined to individual hepatocytes immediately adjacent to the central vein livers were dark red and congested. The hepatocyte LI in rats were increased only at 101 and 271 ppm, 3- and 7-fold over controls, respectively. An acute-duration inhalation MRL of 0.1 ppm was based on the NOAEL of 3 ppm for hepatic effects in mice. More information on this MRL and how it was derived is located in the footnote to Table 2-1, Section 2.5 in Appendix A this profile. 

The RDI/RDA for vitamin A for adult males is 900 micrograms/day (0.9 mg/day) and for adult females 700 micrograms/day (0.7 mg/day). Children require significantly less and lactating women significantly more. There are a number of excellent sources of vitamin A fish, dairy products, liver, leafy vegetables, and dark-colored fruits. 

Necropsies for pathological study were performed promptly on moribund mice which were killed within 2 hours of injection of toxin-LR. Mouse livers were dark red, markedly enlarged, and engorged with blood. The observed 50 percent increase in fresh weight of the liver is attributed to the accumulation of about one-half of the total circulating blood in and around hepatic blood channels. The cerebral cortex was slightly swollen and pale, and a thin film of pink ascitic fluid was sometimes seen. No other abnormalities were observed. 

A laboratory technician repeatedly exposed to the vapor (unknown concentration) and to the liquid spilled on the skin developed anorexia, weight loss, weakness, muscle pain, and dark urine. During several months of nonexposure, there was gradual improvement in his condition, but, after brief reexposure, he suffered an immediate worsening of symptoms, with prompt darkening of the urine and tender enlargement of the liver. 

---