Chronic compensated

Based on their pharmacokinetic profile alone, the safest statins in chronic compensated liver disease and a history of decompensation are prohahly pravastatin and rosnvastatin. However, clinical experience with rosnvastatin in liver disease is lacking, and so it cannot be recommended. In addition, the true rate of post-marketing adverse drug reactions is not yet clear. Pravastatin is therefore the drug of choice in these patients, where treatment is deemed necessary. It should, however, be avoided in acute episodes until liver function or transaminases stabilise/return to normal. 

Hjqiochloremia is common in gastrointestinal disease (Svendsen et al 1979), because of the loss of gastric hydrochloric acid in high volume reflux from the stomach (in proximal enteritis and grass sickness) and the secretion and/or lack of absorption of chloride in severe colitis. It may also occur in exhausted horse syndrome, chronic compensated respiratory acidosis and following furosemide (frusemide) administration. Hypochloremia in the absence of hyponatremia results in a metabolic alkalosis (Corley Marr 1998). The alkalosis associated with hypochloremia may also result in increased cellular uptake of potassium, leading to hypokalemia (Schaer 1999). 

Juvenile Gout and Hyperuricosuria Due to Chronic Compensated Hemolytic Syndrome... 

In this communication we present the case report of the patient with juvenile gout due to chronic compensated hemolytic syndrome as well as data presently available on the other patients suspected of being similarly affected. 

Toxic effects often disappear after the cessation of the exposure, but they can also be permanent. The tissue s ability to regenerate is one of the most important factors that determines the nature of toxic effects. For example, liver tissue has a remarkable capacity to regenerate, and therefore liver injur> is often reversible. On the other hand, neuronal cells do not regenerate at all, thus neuronal injury is irreversible. It is true that neuronal cells can compensate for possible losses, but only to a minor degree. In particular, chronic effects tend to be irreversible. ... 

Once an acute diarrheal situation ensues, patients typically eat less as they become focused on the diarrhea. Both children and adults should attempt to maintain nutritional intake. Food provides not only nutrients but also fluid volume that helps replace what is lost. However, food-related fluid may not be enough to compensate for diarrheal losses. Some foods may be inappropriate if they irritate the gastrointestinal tract or if they are implicated as the cause of the diarrhea. Patients with chronic diarrhea may find that increasing bulk in the diet may help (e.g., rice, bananas, whole-wheat, and bran). 

Changes that follow the primary disorder and attempt to restore the blood pH to normal are referred to as compensatory changes. It should be stressed that compensation never normalizes the pH. Because all metabolic acid-base disorders are chronic and the normal respiratory system can quickly alter the PaC02, essentially all metabolic disorders are accompanied by some degree of respiratory compensation.3 Similarly, chronic respiratory acid-base disorders are typically accompanied by attempts at metabolic compensation.4,5 However, with acute respiratory acid-base disorders there is insufficient time for the metabolic pathways to compensate significantly.6 As such, acute respiratory derangements are essentially uncompensated. 

It is critical to differentiate acute and chronic respiratory acidosis, as the acute form is often a medical emergency that requires intubation and mechanical ventilation, whereas the chronic form is typically a stable condition. The blood gases in Case Study 2 came from a patient with advanced emphysema who is a "C02 retainer" due to ineffective ventilation. Because this patient s disease is chronic, the elevated PaC02 developed very slowly and allowed for metabolic compensation. 

Now consider a psychiatric patient who presents with a pH of 7.50, a PaC02 of 20 mm Hg (2.7 kFh), an HC03 of 16 mEq/L (mmol/L), a sodium concentration of 140 mEq/L (mmol/L), and a chloride level of 103 mEq/L (mmol/L). Because this person is alkalemic, the low PaC02 is the primary disturbance and represents respiratory alkalosis. If this disturbance is a chronic respiratory alkalosis with metabolic compensation, the expected AHC03 is 0.4 x APaC02 (in millimeters of mercury) or 0.4 x 20, which is 8 mEq/L (mmol/L). As such, the predicted HC03 concentration should be 24 mEq/L (mmol/L) [normal] - 8 mEq/L (mmol/L) [expected compensation] or 16 mEq/L (16 mmol/L). 

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. 

Data on nonfatal injuries or chronic diseases caused by chemicals are very difficult to collect. Far too often, it is gathered from reports of compensation Commissions or court decisions in which legal rather than scientific proof prevails. One might venture the guess that at least as many injuries and chronic conditions are caused by synthetic medicaments used improperly, or without adequate medical control, as are caused by the ordinary products of the chemical manufacturing industry. 

Radiation causes dominant lethal mutations in the medaka (Oryzias latipes) (Shima and Shimada 1991). Mosquitofish (Gambusia spp.) from radionuclide-contaminated ponds in South Carolina differed from conspecifics in reference ponds, as judged by the frequency of DNA markers, and this is consistent with the hypothesis that these DNA markers may originate from genetic elements that provide a selective advantage in contaminated habitats (Theodorakis et al. 1998). Ionizing radiation at low-level chronic exposure reportedly has no deleterious genetic effects on aquatic populations because exposure is compensated by density-dependent responses in fecundity (IAEA 1976). However, this needs verification. 

Treatment for HCV infection is necessary because a high percentage of acutely infected patients develop chronic infections. Treatment is indicated in patients previously untreated who have chronic HCV, circulating HCV RNA, increased alanine transaminases levels, evidence on biopsy of moderate to severe hepatic grade and stage, and compensated liver disease. 

Some patients lose the ability to increase the rate or depth or respiration in response to persistent hypoxemia. This decreased ventilatory drive may be due to abnormal peripheral or central respiratory receptor responses. This relative hypoventilation leads to hypercapnia in this situation the central respiratory response to a chronically increased PaC02 can be blunted. Because these changes in Pa02 and PaC02 are subtle and progress over many years, the pH is usually near normal because the kidneys compensate by retaining bicarbonate. 

Chronic hepatitis C with compensated liver disease after a-IFN Jan. 1998... 

Consistent with this observation is the fact, perhaps, that in the British experience, to date, chronic bronchitis is not compensable under the jurisdiction of the byssinosls scheme. The British Ministry of Pensions has Issued a statement denying occupational significance to chronic bronchitis occurring in textile workers (18). 

Chronic HCV- In combination with peginterferon alfa-2a for the treatment of adults with chronic HCV infection who have compensated liver disease and have not been previously treated with interferon alpha. Patients in whom efficacy was demonstrated included patients with compensated liver disease and histological evidence of cirrhosis (Child-Pugh class A). 

Chronic HCV- In combination with interferon alfa-2b injection for the treatment of chronic HCV in patients 3 years of age (oral solution) or 5 years of age (capsules) and older with compensated liver disease previously untreated with alpha interferon or in patients who have relapsed following alpha interferon therapy. Note Ribaspheres is only indicated in combination with interferon alfa-2b in patients 18 years of age and older. 

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