Acute phase

The goals of treatment during the acute phase of illness are to reduce the positive symptoms of schizophrenia and to plan for extended treatment during the maintenance phase. Reducing the positive symptoms quickly is important for at least two reasons. First, the erratic behavior of an acutely psychotic patient can take a tremendous toll, risking arrest, loss of job, suicide, and the alienation of friends and family. Second, there is some evidence that psychosis itself is harmful to the brain. In other words, it may be that the longer the patient is actively psychotic, the worse the prognosis becomes. 

It usually takes several days to a few weeks before the symptoms of psychosis noticeably improve. During that period, benzodiazepines (usually lorazepam or clonazepam) can also be used to cahn the agitated patient. 

An adequate trial of an antipsychotic is defined as treatment with a demonstrable therapeutic dose for at least 6 weeks. We generally recommend a full 6 week trial of an antipsychotic before switching to another antipsychotic when the response is unsatisfactory. One exception may be the rare circumstances when there is absolutely no improvement after 2-3 weeks of treatment. In this case, we believe that it often makes sense to go ahead and switch to another antipsychotic rather than wait the full 6 weeks. 

Subsequent Acute Exacerbations. When a patient with schizophrenia experiences another acute phase of illness, two questions must be answered. First, is hospitalization needed Second, why has this happened  

The decision regarding hospitalization depends on the severity of the episode. If the illness is seriously threatening the patient s well-being, then the patient should be hospitalized. 

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Acute phase reactants (e.g., C-reactive protein) are proteins that increase during inflammation and are deposited in damaged tissues. They were first discovered in the serum, but are now known to be involved in inflammatory processes in the brain (e.g., found in the brain of Alzheimer patients and associated with amyloid plaques). 

A number of adipokines are linked to inflammation and immunity (Fig. 1). This includes both leptin and adiponectin, and also a number of other key inflammatory proteins, particularly cytokines and chemokines [1]. The cytokines and chemokines encompass interleukin-1(3 (EL-1 (3), IL-6, DL-10, TNFa, monocyte chemoattractant protein-1 (MCP-1), and macrophage migration inhibitory factor (MIF). Other major inflammation-related adipokines include nerve growth factor (NGF), and acute phase proteins such as serum amyloid A and haptoglobin. In addition, adipocytes secrete plasminogen activator inhibitor-1 (PAI-1), which is an important thrombotic factor as well as an acute phase protein. 

An acute-phase reactant protein, the plasma concentration of which increases in inflammatory states. 

Release of SP from neurons in the AP, NTS and dorsal vagal motor nucleus may play a role in vomiting induced by cytotoxics. Based on the relative effectiveness of selective antagonists of 5-HT3 receptors and NKi receptors against acute and delayed phases of cisplatin-induced vomiting, it has been suggested that serotonin has a greater role in the acute phase whereas SP has the major role in the delayed phase. 

Fever. Table 2 Some characteristic physiological responses to infectious pathogens or their products (the acute-phase reaction )... 

Family of transcription factors that modulate the expression of genes which control immune, inflammatory, and acute-phase responses, as well as cell growth, responses to stress, apoptosis, and oncogenesis. All members of this family have a Rel-homology domain that contains sequences responsible for dimerization and DNA binding. In vertebrates, this family includes NF-kB1 (also known as p50), NF-kB2 (also known as p52), Rel (also known as cRel), Rel-A (also known as p65), and Rel-B. 

LITHIUM The dosage of lithium is individualized according to serum levels and clinical response to the drug. The desirable serum lithium levels are 0.6 to 1.2 mEq/L Blood samples are drawn immediately before die next dose of lithium (8-12 hours after the last dose) when lithium levels are relatively stable During die acute phase die nurse monitors serum lithium levels twice weekly or until die patient s manic phase is under control. During maintenance therapy, the serum lidiium levels are monitored every 2 to 4 months. 

On occasion, it may be necessary to postpone the regular immunization schedule, particularly for children. This is of special concern to parents. The decision to delay immunization because of illness or for other reasons must be discussed with the primary health care provider. However, the decision to administer or delay vaccination because of febrile illness (illness causing an elevated temperature) depends on the severity of the symptoms and the specific disorder. In general, all vaccines can be administered to those with minor illness, such as a cold virus and to those with a low-grade fever. However, moderate or severe febrile illness is a contraindication. hi instances of moderate or severe febrile illness, vaccination is done as soon as the acute phase of... 

One of the questions confronting investigators in the HS field is whether fever or other acute phase reactants can induce HS gene expression. In vitro studies utilize extraordinary temperatures of 42 °C and higher. Core body temperatures may approach 40 °C as a result of fever. In most in vitro systems, this temperature does not lead to the HS response. However, there are reports that fever induces the increased synthesis of hsps in peripheral blood lymphocytes (Ciavarra, 1990). This response was observed in mononuclear cells exposed to febrile temperatures and in cells isolated from a medical intern who developed fever. 

Morimoto, A., Murakami, M., Takada, M., Teshirogti, S., Watanabe, T. (1987). Fever and the acute phase response induced in rabbits by human recombinant interferon. J. Physiol. 391, 209-218. 

HCV infection is rarefy diagnosed in the acute phase, as most acutely infected individuals are asymptomatic. Between 50% and 90% of patients develop chronic infection, however, and this warrants early therapy. After occupational exposure with a known date, treatment should not be started before the acute episode characterized by alanine aminotransferase elevation, but it should always be started within 24 weeks after the onset of symptoms. The optimal treatment schedule for acute hepatitis C is controversial. Pegylated IFN-a monotherapy at the standard dose for 24 weeks yielded SVR rates close to 100% in symptomatic patients referred to tertiary care centers (De Rosa et al. 2006 Jaeckel et al. 2001 Santantonio et al. 2005 Wiegand et al. 2006). Shorter therapy may be envisaged (Calleri et al. 2007). Combination with ribavirin is recommended if a first course of pegylated IFN-a monotherapy fails to eradicate the infection. Viral elimination appears to be independent of the HCV genotype and the HCV RNA level (Calleri et al. 2007 De Rosa et al. 2006 Jaeckel et al. 2001). 

These proteins are called acute phase proteins (or reactants) and include C-reactive protein (CRP, so-named because it reacts with the C polysaccharide of pneumococci), ai-antitrypsin, haptoglobin, aj-acid glycoprotein, and fibrinogen. The elevations of the levels of these proteins vary from as little as 50% to as much as 1000-fold in the case of CRP. Their levels are also usually elevated during chronic inflammatory states and in patients with cancer. These proteins are believed to play a role in the body s response to inflammation. For example, C-reactive protein can stimulate the classic complement pathway, and ai-antitrypsin can neutralize certain proteases released during the acute inflammatory state. CRP is used as a marker of tissue injury, infection, and inflammation, and there is considerable interest in its use as a predictor of certain types of cardiovascular conditions secondary to atherosclerosis. Interleukin-1 (IL-1), a polypeptide released from mononuclear phagocytic cells, is the principal—but not the sole—stimulator of the synthesis of the majority of acute phase reactants by hepatocytes. Additional molecules such as IL-6 are involved, and they as well as IL-1 appear to work at the level of gene transcription. 

Acute phase response proteins (eg, C-reactive protein, a,-acid glycoprotein [orosomucoid])... 

Gabay C, Kushner I Acute-phase proteins and other systemic responses to inflammation. New Engl J Med 1999 340 448. 

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