Thursday, September 22, 2011
Wednesday, July 8, 2009
الكبد الدهنى
الكبد الدهنى
ما هو الكبد الدهني؟
زيادة الدهون في خلايا الكبد بحيث تزيد الدهون في الكبد على 5 % من وزنه
ما هي أسباب حدوث الكبد الدهني ؟
الأسباب المشهورة التي تؤدي للكبد الدهني هي
تناول المشروبات الكحولية .
السمنة وزيادة الوزن .
مرض السكر .
زيادة الدهون في الدم .
سوء التغذية .
بعض الأدوية مثل أقراص منع الحمل .
ما هي أعراض الكبد الدهني ؟
عادة لا يؤدي الكبد الدهني لأي أعراض ولكن في أحوال قليلة قد يحس المريض بألم بسيط في الجزء الأيمن العلوي من البطن
كيف يتم تشخيص حالات الكبد الدهني ؟
يتم اكتشاف الحالة عندما يفحص الطبيب المريض لأي سبب من الأسباب فيجد عنده تضخم بالكبد فيقوم بطلب أشعه بالموجات الصوتية للبطن وهنا قد يقوم بعض الأطباء بالتشخيص أن الحالة دهون على الكبد ولكن هذا التشخيص غير دقيق لأن التهاب الكبد يؤدي لنفس الصورة بالضبط لذلك فان تشخيص دهون على الكبد يعتمد أساسا على فحص عينة من خلايا الكبد يتبين بها وجود نسبة الدهون فيها
ما هى الأبحاثات المطلوبه للكبد الدهني ؟
أشعه بالموجات الصوتية للبطن
تحليل وظائف الكبد ( أنزيمات الكبد ) حيث إنها قد ترتفع بشكل بسيط في حالات الكبد الدهني ولكنها ترتفع بشكل أكبر في حالة التهاب الكبد
التحاليل الخاصة بالفيروسات (س ؛ ب) ليعرف إذا كان المريض مصابا بالفيروسات الكبدية أم لا
تحليل الأجسام المضادة لتشخيص حالات التهاب الكبد المناعي
تحليل عينة من خلايا الكبد للتفرقة بين التهاب الكبد والكبد الدهن
هل هناك خطورة من الكبد الدهني ؟
أغلب حالات الكبد الدهني ليس لها خطورة أو مضاعفات فقد يتم الشفاء الكامل لهم
ولكن وجد حديثا أن بعض حالات الكبد الدهنى نادرا ما قد يصاحبها التهاب بالكبد او قد يحدث بها تليف للكبد
ما هو علاج الكبد الدهني ؟
-يتم علاج السبب أولا بمعنى
يتوقف المريض عن تناول المشروبات الكحولية
التغذية الصحيحه للمرضى الذين يعانون من سوء التغذية
عمل نظام غذائي لتقليل مرض السمنة وزيادة الوزن
علاج مرض السكر
إعطاء أدوية لتقليل الدهون في الدم في المرضى الذين يعانون من زيادتها
وبالإضافة إلى هذا يتم إعطاء المريض مضادات الأكسدة التي تحافظ على خلايا الكبد وينصح المريض بتناول الخضراوات الطازجة والفاكهة حيث إنها تحتوي على الكثير من مضادات الأكسدة وتساعد على تنظيم الوزن
Tuesday, July 7, 2009
GB VIRUS C (GBV-C)
GB virus C (GBV-C) is a species of virus in the Flaviviridae family which has not yet been assigned to a genus, is known to infect humans, but is not known to cause human disease.
There have been reports that HIV patients coinfected with GBV-C can survive longer than those without GBV-C, but the patients may be different in other ways.
There is current active research into the virus' effects on the immune system in patients coinfected with GBV-C and HIV
History
Hepatitis G virus and GB virus C (GBV-C) are RNA viruses that were independently identified in 1995, and were subsequently found to be two isolates of the same virus.
Although GBV-C was initially thought to be associated with chronic hepatitis, extensive investigation failed to identify any association between this virus and any clinical illness.
Taxonomy
GBV-C is a member of the Flaviviridae family and is phylogenetically related to hepatitis C virus but appears to replicate primarily in lymphocytes, and poorly if at all in hepatocytes.
GBV-A and GBV-B are probably Tamarin viruses, while GBV-C infects humans.
Human infection
The majority of immune-competent individuals appear to clear GBV-C viraemia within the first few years following infection and although the time interval between GBV-C infection and clearance of viraemia (detection of GBV-C RNA in plasma) is not known, infection may persist for decades in some individuals.
Approximately 2% of healthy US blood donors are viraemic with GBV-C, and up to 13% of blood donors have antibodies to E2 protein, indicating prior infection.
Parenteral, sexual and vertical transmission of GBV-C have all been documented, and because of shared modes of transmission, individuals infected with HIV are commonly co-infected with GBV-C. Among people with HIV infection, the prevalence of GBV-C viraemia ranges from 14 to 43%.
Some studies have suggested that co-infection with GBV-C will actually slow the progression of HIV disease.
There have been reports that HIV patients coinfected with GBV-C can survive longer than those without GBV-C, but the patients may be different in other ways.
There is current active research into the virus' effects on the immune system in patients coinfected with GBV-C and HIV
History
Hepatitis G virus and GB virus C (GBV-C) are RNA viruses that were independently identified in 1995, and were subsequently found to be two isolates of the same virus.
Although GBV-C was initially thought to be associated with chronic hepatitis, extensive investigation failed to identify any association between this virus and any clinical illness.
Taxonomy
GBV-C is a member of the Flaviviridae family and is phylogenetically related to hepatitis C virus but appears to replicate primarily in lymphocytes, and poorly if at all in hepatocytes.
GBV-A and GBV-B are probably Tamarin viruses, while GBV-C infects humans.
Human infection
The majority of immune-competent individuals appear to clear GBV-C viraemia within the first few years following infection and although the time interval between GBV-C infection and clearance of viraemia (detection of GBV-C RNA in plasma) is not known, infection may persist for decades in some individuals.
Approximately 2% of healthy US blood donors are viraemic with GBV-C, and up to 13% of blood donors have antibodies to E2 protein, indicating prior infection.
Parenteral, sexual and vertical transmission of GBV-C have all been documented, and because of shared modes of transmission, individuals infected with HIV are commonly co-infected with GBV-C. Among people with HIV infection, the prevalence of GBV-C viraemia ranges from 14 to 43%.
Some studies have suggested that co-infection with GBV-C will actually slow the progression of HIV disease.
HEPATITIS F
Hepatitis F is a hypothetical virus linked to hepatitis. Several hepatitis F candidates emerged in the 1990s; none of these reports have been substantiated.
Most recently, in 1994 Deka et al. reported that novel viral particles had been discovered in the stool of post-transfusion, non-hepatitis A, non-hepatitis B, non-hepatitis C, non-hepatitis E patients.
Injection of these particles, into the bloodstream of Indian rhesus monkeys caused hepatitis, and the virus was named hepatitis F, or Toga virus.
Further investigations failed to confirm the existence of the virus, and it was delisted as a cause for infectious hepatitis.
A subsequently-discovered virus thought to cause hepatitis was named Hepatitis G, though its role in hepatitis has not been confirmed and it is now considered synonymous with GB virus C and is an "orphan virus" with no causal links to any human disease
Most recently, in 1994 Deka et al. reported that novel viral particles had been discovered in the stool of post-transfusion, non-hepatitis A, non-hepatitis B, non-hepatitis C, non-hepatitis E patients.
Injection of these particles, into the bloodstream of Indian rhesus monkeys caused hepatitis, and the virus was named hepatitis F, or Toga virus.
Further investigations failed to confirm the existence of the virus, and it was delisted as a cause for infectious hepatitis.
A subsequently-discovered virus thought to cause hepatitis was named Hepatitis G, though its role in hepatitis has not been confirmed and it is now considered synonymous with GB virus C and is an "orphan virus" with no causal links to any human disease
HEPATITIS E
Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a virus called hepatitis E virus (HEV).
HEV virus is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kb genome.
HEV has a fecal-oral transmission route.
Infection with this virus was first documented in 1955 during an outbreak in New Delhi, India.
Molecular biology
Although it was originally classified in the Caliciviridae family, the virus has since been classified into the genus Hepevirus of the family Hepeviridae. The virus itself is a small non-enveloped particle.
The genome is approximately 7200 bases in length, is a polyadenylated single-strand RNA molecule that contains three discontinuous and partially overlapping open reading frames (ORFs) along with 5' and 3' cis-acting elements, which have important roles in HEV replication and transcription. ORF1 encode a methyltransferase, protease, helicase and replicase; ORF2 encode the capsid protein and ORF3 encodes a protein of undefined function.
There are currently (2009) approximately 1,600 sequences of HEV that are already available of both human and animal isolates.
Although there is one serotype of this virus, four distinct genotypes have been reported. Genotypes 1 and 2 are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions.
Genotypes 3 and 4 infect humans, pigs and other animal species and have been responsible for sporadic cases of hepatitis E in both developing and industrialized countries.
An avian virus has been described that is associated with Hepatitis-Splenomegaly syndrome in chickens.
This virus is genetically and antigenically related to mammalian HEV and probably represents a new genus in the family.
Replicative virus has been found in the small intestine, lymph nodes, colon as well as the liver of experimentally infected pigs.
An in vitro culture system is not yet available.
Despite this difficulty a number of vaccine candidates are under investigation.
Epidemiology
The incidence of hepatitis E is highest in adults between the ages of 15 and 40.
Though children often contract this infection as well, they less frequently become symptomatic. Mortality rates are generally low, for Hepatitis E is a “self-limiting” disease, in that it usually goes away by itself and the patient recovers.
However, during the duration of the infection (usually several weeks), the disease severely impairs a person’s ability to work, care for family members, and obtain food.
Hepatitis E occasionally develops into an acute severe liver disease, and is fatal in about 2% of all cases.
Clinically, it is comparable to hepatitis A, but in pregnant women the disease is more often severe and is associated with a clinical syndrome called fulminant hepatic failure.
Pregnant women, especially those in the third trimester, suffer an elevated mortality rate from the disease ~20%.
Patterns
Hepatitis E is prevalent in most developing countries, and common in any country with a hot climate.
It is widespread in Southeast Asia, northern and central Africa, India, and Central America.
It is spread mainly through fecal contamination of water supplies or food; person-to-person transmission is uncommon.
Outbreaks of epidemic Hepatitis E most commonly occur after heavy rainfalls and monsoons because of their disruption of water supplies.
Major outbreaks have occurred in New Delhi, India (30,000 cases in 1955-1956), Burma (20,000 cases in 1976-1977), Kashmir, India (52,000 cases in 1978), Kanpur, India (79,000 cases in 1991), and China (100,000 cases between 1986 and 1988).
Animals as a reservoir
Domestic animals have been reported as a reservoir for the hepatitis E virus, with some surveys showing infection rates exceeding 95% among domestic pigs.
Transmission after consumption of wild boar meat and uncooked deer meat has been reported as well.
The rate of transmission to humans by this route and the public health importance of this are however still unclear.
A number of rodents have been identified as potential reservoirs: the Lesser Bandicoot Rat (Bandicota bengalensis), the Black Rat (Rattus rattus brunneusculus) and the Asian House Shrew (Suncus murinus).
Recent outbreaks
In 2004, there were two major outbreaks, both of them in sub-Saharan Africa.
There was an outbreak in Chad in which, as of September 27 there were 1,442 reported cases and 46 deaths.
In Sudan, which has been troubled with conflict recently (see, Darfur conflict), they are also suffering from a severe Hepatitis E epidemic.
As of September 28, there were 6,861 cases and 87 deaths, mainly in the West Darfur Region.
UNICEF, Doctors Without Borders, the Red Cross, and other international health organizations are currently working to increase the availability of soap, dig new wells, and chlorinate water supplies and reserves. However, the existing resources are still not enough, and more personnel and funds are severely needed in the region to assure the health and welfare of the people.
Increasingly, hepatitis E is being seen in developed nations with reports of cases in the UK, US and Japan. The disease is thought to be a zoonosis in that animals are thought to be the source. Both deer and pigs have been implicated.
Prevention
Improving sanitation is the most important measure, which consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures and sanitary food preparation.
Thus, prevention strategies of this disease are similar to those of many others that plague developing nations, and they require large-scale international financing of water supply and water treatment projects.
A vaccine based on recombinant viral proteins has been developed and recently tested in a high-risk population (military personnel of a developing country).
The vaccine appeared to be effective and safe, but further studies are needed to assess the long-term protection and the cost-effectiveness of hepatitis E vaccination.
HEV virus is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kb genome.
HEV has a fecal-oral transmission route.
Infection with this virus was first documented in 1955 during an outbreak in New Delhi, India.
Molecular biology
Although it was originally classified in the Caliciviridae family, the virus has since been classified into the genus Hepevirus of the family Hepeviridae. The virus itself is a small non-enveloped particle.
The genome is approximately 7200 bases in length, is a polyadenylated single-strand RNA molecule that contains three discontinuous and partially overlapping open reading frames (ORFs) along with 5' and 3' cis-acting elements, which have important roles in HEV replication and transcription. ORF1 encode a methyltransferase, protease, helicase and replicase; ORF2 encode the capsid protein and ORF3 encodes a protein of undefined function.
There are currently (2009) approximately 1,600 sequences of HEV that are already available of both human and animal isolates.
Although there is one serotype of this virus, four distinct genotypes have been reported. Genotypes 1 and 2 are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions.
Genotypes 3 and 4 infect humans, pigs and other animal species and have been responsible for sporadic cases of hepatitis E in both developing and industrialized countries.
An avian virus has been described that is associated with Hepatitis-Splenomegaly syndrome in chickens.
This virus is genetically and antigenically related to mammalian HEV and probably represents a new genus in the family.
Replicative virus has been found in the small intestine, lymph nodes, colon as well as the liver of experimentally infected pigs.
An in vitro culture system is not yet available.
Despite this difficulty a number of vaccine candidates are under investigation.
Epidemiology
The incidence of hepatitis E is highest in adults between the ages of 15 and 40.
Though children often contract this infection as well, they less frequently become symptomatic. Mortality rates are generally low, for Hepatitis E is a “self-limiting” disease, in that it usually goes away by itself and the patient recovers.
However, during the duration of the infection (usually several weeks), the disease severely impairs a person’s ability to work, care for family members, and obtain food.
Hepatitis E occasionally develops into an acute severe liver disease, and is fatal in about 2% of all cases.
Clinically, it is comparable to hepatitis A, but in pregnant women the disease is more often severe and is associated with a clinical syndrome called fulminant hepatic failure.
Pregnant women, especially those in the third trimester, suffer an elevated mortality rate from the disease ~20%.
Patterns
Hepatitis E is prevalent in most developing countries, and common in any country with a hot climate.
It is widespread in Southeast Asia, northern and central Africa, India, and Central America.
It is spread mainly through fecal contamination of water supplies or food; person-to-person transmission is uncommon.
Outbreaks of epidemic Hepatitis E most commonly occur after heavy rainfalls and monsoons because of their disruption of water supplies.
Major outbreaks have occurred in New Delhi, India (30,000 cases in 1955-1956), Burma (20,000 cases in 1976-1977), Kashmir, India (52,000 cases in 1978), Kanpur, India (79,000 cases in 1991), and China (100,000 cases between 1986 and 1988).
Animals as a reservoir
Domestic animals have been reported as a reservoir for the hepatitis E virus, with some surveys showing infection rates exceeding 95% among domestic pigs.
Transmission after consumption of wild boar meat and uncooked deer meat has been reported as well.
The rate of transmission to humans by this route and the public health importance of this are however still unclear.
A number of rodents have been identified as potential reservoirs: the Lesser Bandicoot Rat (Bandicota bengalensis), the Black Rat (Rattus rattus brunneusculus) and the Asian House Shrew (Suncus murinus).
Recent outbreaks
In 2004, there were two major outbreaks, both of them in sub-Saharan Africa.
There was an outbreak in Chad in which, as of September 27 there were 1,442 reported cases and 46 deaths.
In Sudan, which has been troubled with conflict recently (see, Darfur conflict), they are also suffering from a severe Hepatitis E epidemic.
As of September 28, there were 6,861 cases and 87 deaths, mainly in the West Darfur Region.
UNICEF, Doctors Without Borders, the Red Cross, and other international health organizations are currently working to increase the availability of soap, dig new wells, and chlorinate water supplies and reserves. However, the existing resources are still not enough, and more personnel and funds are severely needed in the region to assure the health and welfare of the people.
Increasingly, hepatitis E is being seen in developed nations with reports of cases in the UK, US and Japan. The disease is thought to be a zoonosis in that animals are thought to be the source. Both deer and pigs have been implicated.
Prevention
Improving sanitation is the most important measure, which consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures and sanitary food preparation.
Thus, prevention strategies of this disease are similar to those of many others that plague developing nations, and they require large-scale international financing of water supply and water treatment projects.
A vaccine based on recombinant viral proteins has been developed and recently tested in a high-risk population (military personnel of a developing country).
The vaccine appeared to be effective and safe, but further studies are needed to assess the long-term protection and the cost-effectiveness of hepatitis E vaccination.
HEPATITIS D
Hepatitis D, also referred to as Hepatitis D virus (HDV) and classified as Hepatitis delta virus, is a disease caused by a small circular RNA virus.
HDV is considered to be a subviral satellite because it can propagate only in the presence of another virus, the Hepatitis B virus (HBV).
Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or via infection of an individual previously infected with HBV (superinfection).
Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone.
These complications include a greater likelihood of experiencing liver failure in acute infections and a greater likelihood of developing liver cancer in chronic infections.
In combination with hepatitis B virus, hepatitis D has the highest mortality rate of all the hepatitis infections of 20%.
Genome
The HDV genome exists as a negative sense, single-stranded, closed circular RNA.
Because of a nucleotide sequence that is 70% self-complementary, the HDV genome forms a partially double stranded RNA structure that is described as rod-like.
With a genome of approximately 1700 nucleotides, HDV is the smallest "virus" known to infect animals.
It has been proposed that HDV may have originated from a class of plant viruses called viroids.
Evidence in support of this hypothesis stems from the fact that both HDV and viroids exist as single-stranded, closed circular RNAs that have rod-like structures.
Likewise, both HDV and viroids contain RNA sequences that can assume catalytically active structures called ribozymes.
During viral replication, these catalytic RNAs are required in order to produce unit length copies of the genome from longer RNA concatamers.
Finally, neither HDV nor viroids encode their own polymerase.
Instead, replication of HDV and viroids requires a host polymerase that can utilize RNA as a template.
RNA polymerase II has been implicated as the polymerase responsible for the replication of HDV.
Normally RNA polymerase II utilizes DNA as a template and produces mRNA.
Consequently, if HDV indeed utilizes RNA polymerase II during replication, it would be the only known pathogen capable of using a DNA-dependent polymerase as an RNA-dependent polymerase.
Delta antigens
A significant difference between viroids and HDV is that, while viroids produce no proteins, HDV produces two proteins called the small and large delta antigens (HDAg-S and HDAg-L, respectively).
These two proteins are produced from a single open reading frame.
They are identical for 195 amino acids and differ only by the presence of an additional 19 amino acids at the C-terminus of HDAg-L. Despite having 90% identical sequences, these two proteins play diverging roles during the course of an infection.
HDAg-S is produced in the early stages of an infection and is required for viral replication.
HDAg-L, in contrast, is produced during the later stages of an infection, acts as an inhibitor of viral replication, and is required for assembly of viral particles.
Transmission
HDV is rare in most developed countries, and is mostly associated with intravenous drug abuse.
However HDV is much more common in Mediterranean countries, sub-Saharan Africa, the Middle East, and countries in the northern part of South America.
In all, about 20 million people may be infected with HDV.
HDV is considered to be a subviral satellite because it can propagate only in the presence of another virus, the Hepatitis B virus (HBV).
Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or via infection of an individual previously infected with HBV (superinfection).
Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone.
These complications include a greater likelihood of experiencing liver failure in acute infections and a greater likelihood of developing liver cancer in chronic infections.
In combination with hepatitis B virus, hepatitis D has the highest mortality rate of all the hepatitis infections of 20%.
Genome
The HDV genome exists as a negative sense, single-stranded, closed circular RNA.
Because of a nucleotide sequence that is 70% self-complementary, the HDV genome forms a partially double stranded RNA structure that is described as rod-like.
With a genome of approximately 1700 nucleotides, HDV is the smallest "virus" known to infect animals.
It has been proposed that HDV may have originated from a class of plant viruses called viroids.
Evidence in support of this hypothesis stems from the fact that both HDV and viroids exist as single-stranded, closed circular RNAs that have rod-like structures.
Likewise, both HDV and viroids contain RNA sequences that can assume catalytically active structures called ribozymes.
During viral replication, these catalytic RNAs are required in order to produce unit length copies of the genome from longer RNA concatamers.
Finally, neither HDV nor viroids encode their own polymerase.
Instead, replication of HDV and viroids requires a host polymerase that can utilize RNA as a template.
RNA polymerase II has been implicated as the polymerase responsible for the replication of HDV.
Normally RNA polymerase II utilizes DNA as a template and produces mRNA.
Consequently, if HDV indeed utilizes RNA polymerase II during replication, it would be the only known pathogen capable of using a DNA-dependent polymerase as an RNA-dependent polymerase.
Delta antigens
A significant difference between viroids and HDV is that, while viroids produce no proteins, HDV produces two proteins called the small and large delta antigens (HDAg-S and HDAg-L, respectively).
These two proteins are produced from a single open reading frame.
They are identical for 195 amino acids and differ only by the presence of an additional 19 amino acids at the C-terminus of HDAg-L. Despite having 90% identical sequences, these two proteins play diverging roles during the course of an infection.
HDAg-S is produced in the early stages of an infection and is required for viral replication.
HDAg-L, in contrast, is produced during the later stages of an infection, acts as an inhibitor of viral replication, and is required for assembly of viral particles.
Transmission
HDV is rare in most developed countries, and is mostly associated with intravenous drug abuse.
However HDV is much more common in Mediterranean countries, sub-Saharan Africa, the Middle East, and countries in the northern part of South America.
In all, about 20 million people may be infected with HDV.
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