samo da kazem da je u pitanju alkoholicar koji je trazio da ide na lecenje
evo rezultata
Hb 149
erci 4.46
Lkci 3.4
trobociti 139
MCT 44
Seg WB 0.58
Ly 0.35
Eo manje od 0.7
Mo manje od 0.7
SE 21/36
glukoza 5.9
ureoa 2.7
kreatinin 77
bilirubin ukupni 18.4
holesterol 6.3
trigliceridi 1.24
AST 257
ALT 182
yGT 1346 nije pogresno napisano
ALP 244
nalaz urina PH 6.0
relativna gustina 20
ostalo 0
Molim za realno misljenje, na UZ jetre pre 6 meseci nije bilo znakova ciroze, jetra blago uvecana
Ozbiljno mi je potrebno tumacenje jer tek u utorak ima zakazano kod lekara ko da ceka do tad
VERUJEM da ce neko pomoci
alkoholicarski hepatitis ili .....HITNOOOOO
Moderatori: mr ph. Silvio, ModeratA, moderato, admin, vlada99
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majja
- Stalni član
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Pozdrav!!
Za pocetak, nisam cula za alkoholicarski hepatitis, i da bi se hepatitis ustanovio, mora da se uradi analiza krvi na sve hepatitise pa tek onda da se prica o postojanju nekog od hepatitisa.
Ove analize ukazuju da jetra ne radi kako treba, ali jedino se biopsijom moze doci do tacnog uvida u stanje jetre, da li i koliki stepen fibroze (ostecenja) postoji i u kakvom je ona stanju. UZ za to na zalost, nije merodavan!
Sta god da je u pitanju, kada su ovakvi nalazi, obavezna je dijeta, bez svinjskog mesa, masnoca, alkohola, gaziranih pica.........
Najbolje se strpite do odlaska kod lekara, pa onda sledite njegove upute. Ovako, na osnovu ovih rezultata, niko ne moze da Vam kaze sta je u pitanju, osim da jetra ne radi kako treba, pa cete zato morati da uradite jos nekoliko dodatnih analiza (biopsija, hepatitisi, alkalna fosfataza, protrombinsko vreme..........).
Samo hrabro, i javite kako je bilo kod lekara!!
Pozdrav i sve najbolje, Majja
Za pocetak, nisam cula za alkoholicarski hepatitis, i da bi se hepatitis ustanovio, mora da se uradi analiza krvi na sve hepatitise pa tek onda da se prica o postojanju nekog od hepatitisa.
Ove analize ukazuju da jetra ne radi kako treba, ali jedino se biopsijom moze doci do tacnog uvida u stanje jetre, da li i koliki stepen fibroze (ostecenja) postoji i u kakvom je ona stanju. UZ za to na zalost, nije merodavan!
Sta god da je u pitanju, kada su ovakvi nalazi, obavezna je dijeta, bez svinjskog mesa, masnoca, alkohola, gaziranih pica.........
Najbolje se strpite do odlaska kod lekara, pa onda sledite njegove upute. Ovako, na osnovu ovih rezultata, niko ne moze da Vam kaze sta je u pitanju, osim da jetra ne radi kako treba, pa cete zato morati da uradite jos nekoliko dodatnih analiza (biopsija, hepatitisi, alkalna fosfataza, protrombinsko vreme..........).
Samo hrabro, i javite kako je bilo kod lekara!!
Pozdrav i sve najbolje, Majja
nadam se da znas engleski..kako da nema alkoholni hepatitis. hepatitis je upala jetre i nista drugo. razlozi mogu da budu , virus (b,c,d,e, itd) a isto tako moze da bude uslovljen alkohiolom
http://en.wikipedia.org/wiki/Hepatitis# ... _hepatitis
Alcoholic hepatitis
Ethanol, mostly in alcoholic beverages, is an important cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.
Roughly one in four people that consume more than three drinks per day during a period of ten to fifteen years will experience some level of alcoholic hepatitis.
Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C. The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis in Western countries.
Drug induced hepatitis
A large number of drugs can cause hepatitis. The anti-diabetic drug troglitazone was withdrawn in 2000 for causing hepatitis. Other drugs associated with hepatitis[1]:
Halothane (a specific type of anesthetic gas)
Methyldopa (antihypertensive)
Isoniazid (INH), rifampicin, and pyrazinamide (tuberculosis-specific antibiotics)
Phenytoin and valproic acid (antiepileptics)
Zidovudine (antiretroviral i.e. against AIDS)
Ketoconazole (antifungal)
Nifedipine (antihypertensive)
Ibuprofen and indomethacin (NSAIDs)
Amitriptyline (antidepressant)
Amiodarone (antiarrhythmic)
Nitrofurantoin (antibiotic)
Oral contraceptives
Allopurinol
Azathioprine [2] [3]
Some herbs and nutritional supplements
The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Oral contraceptives can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.
Other toxins that cause hepatitis
Toxins and drugs can cause hepatitis:
Amatoxin-containing mushrooms, including the Death Cap (Amanita phalloides), the Destroying Angel (Amanita ocreata), and some species of Galerina. A portion of a single mushroom can be enough to be lethal (10 mg or less of α-amanitin).
Yellow phosphorus is an industrial toxin.
Paracetamol (acetaminophen in the United States) can cause hepatitis when taken in an overdose. The severity of liver damage can be limited by prompt administration of acetylcysteine.
Carbon tetrachloride ("tetra", a dry cleaning agent), chloroform, and trichloroethylene, all chlorinated hydrocarbons, cause steatohepatitis (hepatitis with fatty liver).
[edit]
Metabolic disorders
Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.
See below for non-alcoholic steatohepatitis (NASH), effectively a consequence of metabolic syndrome.
Obstructive
"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding it leads to destruction and inflammation of liver tissue.
Autoimmune
Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes—possibly due to genetic predisposition or acute liver infection—causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.
Autoimmune hepatitis has a prevalence of 1-2 per 1000. As with most other autoimmune diseases, it affects women much more often than men (8:1). Liver enzymes are elevated, as is bilirubin. Autoimmune Hepatitis can progress to cirrhosis. Treatment is with steroids and disease-modifying antirheumatic drugs (DMARDs).
The diagnosis of autoimmune Hepatitis is best achieved with a combination of clinical and laboratory findings. A number of specific antibodies found in the blood (antinuclear antibody (ANA), smooth muscle antibody (SMA), Liver/kidney microsomal antibody (LKM-1) and anti-mitochondrial antibody (AMA)) are of use, as is finding an increased Immunoglobulin G level. However, the diagnosis of autoimmune hepatitis always requires a liver biopsy. In complex cases a scoring system can be used to help determine if a patient has autoimmune hepatitis, which combines clinical and laboratory features of a given case.
Four subtypes are recognised, but the clinical utility of distinguishing subtypes is limited.
Positive ANA and SMA, raised immunoglobulin G
Positive LKM-1 (typically children and teenagers; disease can be severe)
All antibodies negative, positive antibodies against soluble liver antigen (SLA)
No autoantibodies detected
[edit]
Alpha 1-antitrypsin deficiency
In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.
Nonalcoholic steatohepatitis
Non-alcoholic steatohepatitis (NASH) is a type of hepatitis which resembles alcoholic hepatitis on liver biopsy (fat droplets, inflammatory cells, but usually no Mallory's hyalin) but occurs in patients who have no known history of alcohol abuse. NASH is more common in women and the most common cause is obesity or the metabolic syndrome. A related but less serious condition is called "fatty liver" (steatosis hepatis), which occurs in up to 80% of all clinically obese people. A liver biopsy for fatty liver shows fat droplets throughout the liver, but no signs of inflammation or Mallory's hyalin.
The diagnosis depends on history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is radiologic imaging including ultrasound, computed tomographic imaging, or magnetic resonance imaging. However, radiologic imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow -up blood tests and a repeat liver biopsy are required.
NASH is becoming recognized as the most important cause of liver disease
. The clinical diagnosis of alcoholic hepatitis can be made in alcoholics with associated fever, leukocytosis, jaundice and tender hepatomegaly. Associated laboratory abnormalities may include leukocytosis or leukopenia, anemia, a prolonged prothrombin time and elevated liver enzymes, including aspartate amino-transferase (AST), alanine aminotransferase (ALT), alkaline phosphatase and bilirubin. An AST-to-ALT ratio greater than 2 is common in patients with alcoholic hepatitis. Liver biopsy may be required to establish the diagnosis and to identify other pathology, such as cirrhosis. Histologic diagnosis of alcoholic hepatitis requires the presence of liver cell damage, an inflammatory infiltrate and fibrosis. Biopsy-proven cirrhosis with alcoholic hepatitis or a significantly elevated total bilirubin level and prolonged prothrombin time are associated with a worse prognosis. Abstinence from alcohol, nutritional supplementation and corticosteroids are the mainstays of treatment for severe alcoholic hepatitis.
http://en.wikipedia.org/wiki/Hepatitis# ... _hepatitis
Alcoholic hepatitis
Ethanol, mostly in alcoholic beverages, is an important cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.
Roughly one in four people that consume more than three drinks per day during a period of ten to fifteen years will experience some level of alcoholic hepatitis.
Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C. The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis in Western countries.
Drug induced hepatitis
A large number of drugs can cause hepatitis. The anti-diabetic drug troglitazone was withdrawn in 2000 for causing hepatitis. Other drugs associated with hepatitis[1]:
Halothane (a specific type of anesthetic gas)
Methyldopa (antihypertensive)
Isoniazid (INH), rifampicin, and pyrazinamide (tuberculosis-specific antibiotics)
Phenytoin and valproic acid (antiepileptics)
Zidovudine (antiretroviral i.e. against AIDS)
Ketoconazole (antifungal)
Nifedipine (antihypertensive)
Ibuprofen and indomethacin (NSAIDs)
Amitriptyline (antidepressant)
Amiodarone (antiarrhythmic)
Nitrofurantoin (antibiotic)
Oral contraceptives
Allopurinol
Azathioprine [2] [3]
Some herbs and nutritional supplements
The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Oral contraceptives can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.
Other toxins that cause hepatitis
Toxins and drugs can cause hepatitis:
Amatoxin-containing mushrooms, including the Death Cap (Amanita phalloides), the Destroying Angel (Amanita ocreata), and some species of Galerina. A portion of a single mushroom can be enough to be lethal (10 mg or less of α-amanitin).
Yellow phosphorus is an industrial toxin.
Paracetamol (acetaminophen in the United States) can cause hepatitis when taken in an overdose. The severity of liver damage can be limited by prompt administration of acetylcysteine.
Carbon tetrachloride ("tetra", a dry cleaning agent), chloroform, and trichloroethylene, all chlorinated hydrocarbons, cause steatohepatitis (hepatitis with fatty liver).
[edit]
Metabolic disorders
Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.
See below for non-alcoholic steatohepatitis (NASH), effectively a consequence of metabolic syndrome.
Obstructive
"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding it leads to destruction and inflammation of liver tissue.
Autoimmune
Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes—possibly due to genetic predisposition or acute liver infection—causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.
Autoimmune hepatitis has a prevalence of 1-2 per 1000. As with most other autoimmune diseases, it affects women much more often than men (8:1). Liver enzymes are elevated, as is bilirubin. Autoimmune Hepatitis can progress to cirrhosis. Treatment is with steroids and disease-modifying antirheumatic drugs (DMARDs).
The diagnosis of autoimmune Hepatitis is best achieved with a combination of clinical and laboratory findings. A number of specific antibodies found in the blood (antinuclear antibody (ANA), smooth muscle antibody (SMA), Liver/kidney microsomal antibody (LKM-1) and anti-mitochondrial antibody (AMA)) are of use, as is finding an increased Immunoglobulin G level. However, the diagnosis of autoimmune hepatitis always requires a liver biopsy. In complex cases a scoring system can be used to help determine if a patient has autoimmune hepatitis, which combines clinical and laboratory features of a given case.
Four subtypes are recognised, but the clinical utility of distinguishing subtypes is limited.
Positive ANA and SMA, raised immunoglobulin G
Positive LKM-1 (typically children and teenagers; disease can be severe)
All antibodies negative, positive antibodies against soluble liver antigen (SLA)
No autoantibodies detected
[edit]
Alpha 1-antitrypsin deficiency
In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.
Nonalcoholic steatohepatitis
Non-alcoholic steatohepatitis (NASH) is a type of hepatitis which resembles alcoholic hepatitis on liver biopsy (fat droplets, inflammatory cells, but usually no Mallory's hyalin) but occurs in patients who have no known history of alcohol abuse. NASH is more common in women and the most common cause is obesity or the metabolic syndrome. A related but less serious condition is called "fatty liver" (steatosis hepatis), which occurs in up to 80% of all clinically obese people. A liver biopsy for fatty liver shows fat droplets throughout the liver, but no signs of inflammation or Mallory's hyalin.
The diagnosis depends on history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is radiologic imaging including ultrasound, computed tomographic imaging, or magnetic resonance imaging. However, radiologic imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow -up blood tests and a repeat liver biopsy are required.
NASH is becoming recognized as the most important cause of liver disease
. The clinical diagnosis of alcoholic hepatitis can be made in alcoholics with associated fever, leukocytosis, jaundice and tender hepatomegaly. Associated laboratory abnormalities may include leukocytosis or leukopenia, anemia, a prolonged prothrombin time and elevated liver enzymes, including aspartate amino-transferase (AST), alanine aminotransferase (ALT), alkaline phosphatase and bilirubin. An AST-to-ALT ratio greater than 2 is common in patients with alcoholic hepatitis. Liver biopsy may be required to establish the diagnosis and to identify other pathology, such as cirrhosis. Histologic diagnosis of alcoholic hepatitis requires the presence of liver cell damage, an inflammatory infiltrate and fibrosis. Biopsy-proven cirrhosis with alcoholic hepatitis or a significantly elevated total bilirubin level and prolonged prothrombin time are associated with a worse prognosis. Abstinence from alcohol, nutritional supplementation and corticosteroids are the mainstays of treatment for severe alcoholic hepatitis.
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majja
- Stalni član
- Postovi: 3256
- Pridružio se: Čet Jan 26, 2006 10:57 pm
- Koliki je zbir brojeva cetiri i pet: 5
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Izgleda da sam se bacila bas samo na nas problem, pa te stvari izostavila....u svakom slucaju hvala na obavestenju!!
Poslednja izmena od majja u Sub Jul 15, 2006 12:45 am, izmenjeno 1 put ukupno.
nije da nisam nasla i ja ovo na engleskom ,ali ne znam toliko da bih se upustila u prevod a strah me da ne pogresim , ipak nije svejdno , pokusala sam da se skoncentrisem i prevedem koliko mogu
Pa sad , ne znam , nije mi jasno da li u Palmoticevoj imaju i lekare koji lece jetru ili rade samo psihoterapije, saznacu uskoro
Mozda odemo u ponedeljak kod dr. Perisic na UZ za svaki slucaj , ona moze da vidi da li ima znakova ciroze zar ne?
pokusacu jos negde da potrazim koji podatak
hvala svima
Pa sad , ne znam , nije mi jasno da li u Palmoticevoj imaju i lekare koji lece jetru ili rade samo psihoterapije, saznacu uskoro
Mozda odemo u ponedeljak kod dr. Perisic na UZ za svaki slucaj , ona moze da vidi da li ima znakova ciroze zar ne?
pokusacu jos negde da potrazim koji podatak
hvala svima
-
majja
- Stalni član
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Dr Perisic je sjajna, ima odlican aparat, vrlo je ljubazna i za nju imam samo reci hvale!! 
I mi smo bili kod nje, i stvarno mislim da je ona pun pogodak!!!
Ali, ako sto ti rekoh, UZ je samo jedna od metoda za dijagnosticiranje....na kojoj se mogu videti promene na porti, samoj jetri, protoku krvi, nekim ostecenjima.......Probaj, vidi sta ce ona da kaze, ali svakako idi i kod infektologa, a za pocetak, obavezna dijeta......
Pozdrav i sve najbolje!!
Jedno (mozda) nepristojno pitanje: Koliko imas godina?
I mi smo bili kod nje, i stvarno mislim da je ona pun pogodak!!! Ali, ako sto ti rekoh, UZ je samo jedna od metoda za dijagnosticiranje....na kojoj se mogu videti promene na porti, samoj jetri, protoku krvi, nekim ostecenjima.......Probaj, vidi sta ce ona da kaze, ali svakako idi i kod infektologa, a za pocetak, obavezna dijeta......
Pozdrav i sve najbolje!!
Jedno (mozda) nepristojno pitanje: Koliko imas godina?
hey majo,
hepatitis je kao sto rekoh upala jetre, u slucaju koriscenja alkohola ili droge u velikim kolicinama , jednostavno jetra vise ne moze da cisti toksine i onda dodje do upale. dda se razumemo, ne svako ko pije ili koristi lekove ( imas gore listu lekova) i droge , dobije hepatitis. koliko ja znam , ne postoji lek za ovaj hepatitis. najcesce lekari preporucuju da osoba prestane da koristi alkohol ili drogu. i posle odredjenog vremena jetra se potpuno regenerise ako nema ciroze. jetra je jedini organ u telu koji moze totalno da se regenerise. osim ovog hepatitisa iam i auto imuni, taj bas i nije jako dobar.
sto se tice odkrivanja, analiza krvi plus biopsija. najcescece su uvecani jetreni rezultati, alt ast itd
hepatitis je kao sto rekoh upala jetre, u slucaju koriscenja alkohola ili droge u velikim kolicinama , jednostavno jetra vise ne moze da cisti toksine i onda dodje do upale. dda se razumemo, ne svako ko pije ili koristi lekove ( imas gore listu lekova) i droge , dobije hepatitis. koliko ja znam , ne postoji lek za ovaj hepatitis. najcesce lekari preporucuju da osoba prestane da koristi alkohol ili drogu. i posle odredjenog vremena jetra se potpuno regenerise ako nema ciroze. jetra je jedini organ u telu koji moze totalno da se regenerise. osim ovog hepatitisa iam i auto imuni, taj bas i nije jako dobar.
sto se tice odkrivanja, analiza krvi plus biopsija. najcescece su uvecani jetreni rezultati, alt ast itd
-
majja
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- Pridružio se: Čet Jan 26, 2006 10:57 pm
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Da, da, pitanje je bilo upuceno Vama ...........nista posebno, samo me je zanimalo zbog ciroze......i alkohola.........MM ima hep C, a Bogami je dugi niz godina (15-16) posteno zalivao (da ne kazem nalivao 
), jetru, ali njemu je jetra sa ovim virusom na 1. stepenu ostecenja, ali koliko sam uspela da vidim i procitam...nema to tako mnogo veze... 
.......
Javite nam se kada zavrsite sa doktorom na tu temu, da vidimo sta ce da kaze!!
Pozdrav i sve najbolje!
...........nista posebno, samo me je zanimalo zbog ciroze......i alkohola.........MM ima hep C, a Bogami je dugi niz godina (15-16) posteno zalivao (da ne kazem nalivao ), jetru, ali njemu je jetra sa ovim virusom na 1. stepenu ostecenja, ali koliko sam uspela da vidim i procitam...nema to tako mnogo veze... .......Javite nam se kada zavrsite sa doktorom na tu temu, da vidimo sta ce da kaze!!
Pozdrav i sve najbolje!
pozdrav svima koji su pomagali
Bili smo na UZ i nema ciroze, stavise zacudjujuce dobar izgled jetre cak nije ni uvecana, samo je masna, sto nije kazu opasno.
Naravno to nista ne znaci , uglavnom se sve svelo na to da mora da prestane da pije,
i da od 01.08.pocinjemo lecenje u Palmpticevoj
Vise nemama
Bili smo na UZ i nema ciroze, stavise zacudjujuce dobar izgled jetre cak nije ni uvecana, samo je masna, sto nije kazu opasno.
Naravno to nista ne znaci , uglavnom se sve svelo na to da mora da prestane da pije,
i da od 01.08.pocinjemo lecenje u Palmpticevoj Vise nemama
izvinjenje , poslao je poruku moj komp bez moje volje i pre nego sam zavrsila.
Dakle sada nam predstoji cisto psihijatrisko lecenje , i naravno malo uredniji zivot i hrana , da se oporavi jetra, kazu nije jos najgore, sacuvao se , a pije skoro 30 g i to svakodnevno i to samo zastoko i to do 1 l dnevno, pitam se cesto od cega je .
jos jednom hvala svima na razumevanju
Nadam se da vise necu morati da se bavim ovakvim analizama
Dakle sada nam predstoji cisto psihijatrisko lecenje , i naravno malo uredniji zivot i hrana , da se oporavi jetra, kazu nije jos najgore, sacuvao se , a pije skoro 30 g i to svakodnevno i to samo zastoko i to do 1 l dnevno, pitam se cesto od cega je .
jos jednom hvala svima na razumevanju
Nadam se da vise necu morati da se bavim ovakvim analizama