Fulminant hepatic failure caused by tuberculosis.
ABSTRACT A 54 year old Asian woman developed fulminant hepatic failure followed by renal failure. Because of a past history of possible tuberculosis, she was given antituberculous drugs. The chest x ray was normal. A transjugular liver biopsy showed caseating necrosis, granulomas, and acid fast bacilli indicative of miliary tuberculosis. Despite full supportive therapy, her condition deteriorated and she died. Postmortem examination showed widespread miliary tuberculosis; culture confirmed the presence of Mycobacterium tuberculosis. Tuberculosis causes fulminant hepatic failure rarely and only three cases have been described. In this, as with the other cases, hyponatraemia and hepatomegaly were features at presentation. This is the first report of treatment being given before death.
- Journal of thoracic disease. 02/2013; 5(1):E1-E4.
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ABSTRACT: To present and discuss 28 female cases with abdominopelvic tuberculosis (TB) and abnormal CA125 levels to better distinguish this disease from advanced ovarian cancer (AOC) and pelvic inflammatory disease (PID). Abdominopelvic tuberculosis (APTB) is one of the extrapulmonary tuberculosis (TB) sites, usually misdiagnosed as AOC and PID and then has to undergo surgery. However, the treatment of APTB is totally based on medical therapy other than surgery except biopsy. This article aims to present and discuss 28 female APTB cases with abnormal CA125 levels to better distinguish this disease from AOC and PID so as to find out non-invasive APTB diagnosis methods. 28 APTB patients diagnosed between January 2000 and January 2010 in our gynecologic department of Nanjing Jinling hospital were reviewed retrospectively and compared with AOC and PID. The mean age was 38.24 ± 11 (range 15-64) years. Elevated levels of serum CA125 were determined in all 28 patients (100 %). Other common findings were ascites in 20 (71.43 %, 20/28), pelvic mass in 21(75 %, 21/28), slight fever with night sweat in 13 (46.43 %, 13/28), cough and pleural effusion in nine (32.14 %, 9/28), high fever more than 39 °C combined with abdominal pain and elevated white blood count in five (17.86 %, 5/28), weight loss more than 5 kg at admission in six (21.43 %, 6/28). Diagnoses were made based on biopsy from laparotomy in 14 (50 %) patients, from laparoscopy in nine (32.14 %), from diagnostic curettage because of primary infertility in two (7.14 %), and only from clinical suspicion in three patients. Histopathology revealed that caseating granulomatous lesions were seen in 25 patients, positive anti-acid staining in 11 patients. Totally 26 patients completed anti-TB therapy successfully and were cured, two patients died of the disease because of long-term immune inhibitor used. Although it is difficult to exactly distinguish APTB from AOC and PID without operation, it is important because the treatment of APTB is totally based on medical therapy other than surgery. Some difference may be found out if clinical manifestation, physical examination, laboratory tests and imaging findings are carefully analyzed to avoid unnecessary extensive surgery and improve the prognosis.Archives of Gynecology 10/2013; · 0.91 Impact Factor
Article: Hepatobiliary tuberculosis.[Show abstract] [Hide abstract]
ABSTRACT: Hepatobiliary tuberculosis is a rare manifestation of Mycobacterium tuberculosis infection and is usually secondary to tuberculosis of the lungs or gastrointestinal tract. Diagnosis is difficult pre-operatively in local (focal and tubular) forms because of its rarity and presentation in the form of non-specific symptoms and signs and lack of any defined criteria on imaging studies. Histopathological examination is necessary for definite diagnosis but in cases where there is suspicion of hepatobiliary tuberculosis, with PCR assay diagnosis it is possible pre-operatively. Recommended treatment is with conventional antituberculous drugs and surgical intervention in tuberculous abscess or granulomas. The disease is usually associated with good prognosis under complete antituberculous treatment. The author encountered 4 cases of hepatobiliary tuberculosis over 5 years. The aim of this article is to present current knowledge of hepatobiliary tuberculosis and to comprehensively review all the available literature.Annals of gastroenterology : quarterly publication of the Hellenic Society of Gastroenterology. 01/2014; 27(3):207-211.
Gut 1995; 36: 792-794
Fulminant hepatic failure caused by tuberculosis
W Hussain, D Mutimer, R Harrison, S Hubscher, J Neuberger
A 54 year old Asian woman developed
renal failure. Because of a past history of
possible tuberculosis, she was given anti-
tuberculous drugs. The chest x ray was
showed caseating necrosis, granulomas,
and acid fast bacilli indicative of miliary
tuberculosis. Despite full supportive ther-
apy, her condition deteriorated and she
died. Postmortem examination showed
widespread miliary tuberculosis; culture
confirmed the presence ofMycobacterium
tuberculosis. Tuberculosis causes fulmi-
nant hepatic failure rarely and only three
cases have been described. In this, as
with the other cases, hyponatraemia and
hepatomegaly were features at presenta-
tion. This is the first report of treatment
being given before death.
(Gut 1995; 36: 792-794)
Keywords: fulminant hepatic failure, tuberculosis.
The Liver Unit
and Department of
Dr JNeuberger, Liver Unit,
Queen Elizabeth Hospital,
Birmingham B15 2TH.
Accepted for publication
15 July 1994
Most cases of fulminant hepatic failure result
from viral infection
treatment ofsuch patients is largely supportive,
with liver transplantation being indicated for
those with a poor prognosis. It is important,
however, to make an early diagnosis of the
cause of the fulminant hepatic failure because
treatment may be affected. For instance, the
prognosis and the use of prognostic markers
are dependant on the aetiology; early diagnosis
can allow for
transplantation to be made before the onset of
the correct diagnosis will lead to alternative
hepatic failure associated with pregnancy, or
may contraindicate liver transplantation
in fulminant hepatic failure resulting from
malignant infiltration of the liver.
fulminant hepatic failure and usually results
from Gram negative septicaemia,
association with pregnancy. Treatment with
appropriate antibiotics is usually followed by
prompt recovery. We report a woman with
disseminated tuberculosis who presented with
fulminant hepatic failure and despite early
or drug toxicity.' The
a decision on the need for
case of fulminant
A 54 year old Kenyan Asian woman, who had
lived in the United Kingdom since 1968,
presented on the 10 November 1993 to her
vomiting and right upper quadrant abdominal
five day history
pain. She had been admitted two months
earlier for investigation ofchest pain, for which
no cause had been found. Liver tests at that
time were normal.
Between 1971 and 1973 she had been
treated for presumed pulmonary tuberculosis
on the basis of abnormal chest x ray and a
raised erythrocyte sedimentation rate; sputum
clinical details are not available. Treatment
was rifampicin 450 mg once daily, isoniazid
100 mg three times daily, and pyridoxine
10 mg daily.
There was a history ofmild asthma for many
years for which she took salbutamol inhaler as
amlodipine 5 mg once daily for more than a
year. She was not taking any other drugs.
There was no history of alcohol consumption
or use of recreational drugs. Her sister had
been diagnosed as suffering from tuberculosis.
On examination she was mildly jaundiced,
with a fever of 39°C. She was tender in the
right upper quadrant of the abdomen, there
were no cutaneous stigmata of chronic liver
disease. The chest was normal on clinical
examination. Investigations showed a raised
bilirubin of 66 pumol/l (NR 1-26), alkaline
phosphatase 695 U/l (NR 70-380), aspartate
transaminase 151 U/1 (NR 5-30), albumin of
24 g/dl (NR 34-51), and a serum sodium of
126 mmol/l (NR 134-146). The prothrombin
time was prolonged with an INR of 1-6 (NR
0.8-1.2). Paracetamol was undetectable and
subsequent investigations showed that tests for
hepatitis A IgM, hepatitis B surface antigen,
anti-hepatitis B core (IgM and IgG), and
hepatitis C RNA were all negative. The chest
x ray was normal, abdominal ultrasound
showed a slightly enlarged liver but no other
deteriorated over the next eight days. The
serum aspartate transaminase reached 1790
U/1 and serum sodium fell to 114 mmol/l, so
she was transferred to the Queen Elizabeth
Hospital on 19 November 1993 for considera-
tion for possible transplantation. On arrival she
was in grade I hepatic encephalopathy but
her condition deteriorated over the next 12
hours to grade IV. Mechanical ventilation
and inotropes were required. Renal failure
developed - the serum creatinine rose to
341 Rmol/l (NR 50-101) and the urea to
29 mmol/l (NR 3-2-7.6). Repeat ultrasound
scan showed a homogenously enlarged liver.
The chest x ray was again normal.
Because of the possibility that the liver
failure was caused by tuberculosis, treatment
with rifampicin 600 mg, isoniazid 300 mg,
daily was started; a decision to list her for
g, and pyridoxine
group.bmj.com on July 15, 2011 - Published by gut.bmj.com Downloaded from
Fulminant hepaticfailure caused by tuberculosis
(A) Liver at postmortem examination containing numerous irregular areas ofcaseation
necrosis. Areas ofsurviving liverparenchyma appear unremarkable (haematoxylin and
eosin); (B) higher power view ofliver at postmortem examination showing an area of
caseation necrosis with a poorlyformed granulomatous reaction at the periphery. A solitary
giant cell is present.
transplantation was deferred until the diagno-
sis was confirmed or refuted. Two days later a
showed caseating epithelioid granulomata and
acid fast bacilli. Subsequent culture proved
measures the patient's condition continued to
deteriorate and she died on the 23 November
1993, 13 days after her initial admission to
Postmortem examination showed multiple
caseating granulomas in the liver, lungs, medi-
astinal lymph nodes,
Occasional acid fast bacilli were still demon-
strable by Ziehl Neelsen staining. The liver
also contained scattered areas of coagulative
necrosis in keeping with preterminal hypo-
tension and ischaemia. Overall, more than 50/O
ofthe liver parenchyma was destroyed, predom-
inantly by caseating necrosis. Surviving liver
parenchyma showed mild patchy changes of
cholestasis, but was otherwise unremarkable.
There was no significant inflammation and no
other features were present to suggest recent
viral hepatitis ofany other cause for liver failure.
Culture of the liver specimen confirmed the
presence ofMycobacterium tuberculosis.
Although fulminant hepatic failure may occur
as part of a systemic illness resulting from
failure has been
We believe that this patient's liver failure was
caused by tuberculosis for a number ofreasons.
Viral causes have, as far as possible, been
excluded serologically although it is by defini-
tion impossible to exclude the putative non-A
non-B non-C virus. Furthermore, the histo-
logical features, both attransjugularbiopsy and
at necropsy, did not show features characteris-
tic of fulminant viral hepatitis.6 A drug related
aetiology is unlikely because treatment had
been unchanged for over a year.7 Postmortem
failed to show other possible
causes of fulminant hepatic failure such as
hepatic biliary obstruction. The liver biopsy
and postmortem examination both showed
features of hepatic necrosis, granulomatous
infiltration, and on staining acid fast bacilli.
The degree of hepatocyte necrosis is sufficient
to cause the clinical picture of liver failure.
It is well established that miliary tuber-
culosis can affect the liver. One series reported
hepatic granulomata in all cases of miliary
tuberculosis studied.8 Although microscopic
involvement of the liver is common, clinical
1748 patients hospitalised for tuberculosis.
Hyponatraemia is not uncommon, however, in
patients with disseminated tuberculosis1o; this
was not a prominent feature of this case. Cases
hepatic failure have been reported. Godwin3
reported a case of a 67 year old man who
presented with myalgia and upper respiratory
symptoms then developed fulminant hepatic
and renal failure who on postmortem examina-
tion was found to have miliary tuberculosis.
However, other potential causes of fulminant
hepatic failure, such as hepatitis C or drugs,
were not excluded.
There are also two case reports from Japan of
patients similar to the one reported here.45 The
time from admission to death was also very rapid
as with our own, the
viruses, drugs or toxins is usually associated with
a shrunken liver. The enlarged liver in this and
the other cases of miliary tuberculosis, together
with hyponatraemia, may be a useful pointer to
this unusual cause of fulminant hepatic failure.
The use of a transjugular liver biopsy permitted
early diagnosis. This resulted in what we believe
is the first case where the diagnosis was made
and treatment started before death. The clinical
and serological features suggested that the prog-
nosis was extremely poor and transplantation
was, therefore, considered. Because of the pres-
ence of active untreated tuberculosis, however,
it was felt that transplantation would be unsuc-
cessful as the effect ofsurgery and immunosup-
pression would make it highly probable that she
would die from disseminated tuberculosis. The
liver was enlarged.
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Hussain, Mutimer, Harrison, Hubscher, Neuberger
fact that viable mycobacteria were found on
postmortem examination even two days after
the start of appropriate antibiotic treatment,
suggests that there was active disease, which
would have become increasingly active after
Fulminant hepatic failure caused by tuber-
culosis is rare in this country, but the incidence
Although this patient died despite treatment,
this rare cause of fulminant hepatic failure
should be considered in patients at risk so
treatment can be started early.
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2 O'Grady J, Alexander GJM, Hayllar KM, Williams R. Early
indicators of prognosisin fulminant hepatic
Gastroenterology 1989; 97: 439-45.
3 Godwin JE, Coleman AA, Sahn SA. Miliary tuberculosis
presenting as hepatic and renal failure. Chest 1991; 99:
4 Asada Y, Hayashi T, Sumiyoshi A, Aburaya M, Shishime E.
Miliary tuberculosis presenting as fever and jaundice with
hepatic failure. Hum Pathol 1991; 22: 92-4.
5 Hosokawa K, Morita A, Imai T, Kitahara M, Kamegaya K,
Tanaka M, et al. A case of miliary tuberculosis presenting
as fever and jaundice with hepatic failure, looking like the
course offulminant hepatitis. Kansenshogaku Zasshi 1992;
6 Scheuer PJ. Acute hepatitis. In: Wight DGD, ed. Systemic
pathology.3rd ed. Vol
7 Danan G. Concensus meeting. Criteria of drug induced
liver disorders. Jf Hepatol 1990; 11: 272-6.
8 Cucin RL, Coleman M, Eckhardt JJ, Silvet RT. The diag-
nosis of miliary tuberculosis: utility of peripheral blood
abnormalities, bone marrow and liver biopsy. Journal of
Chronic Diseases 1974; 26: 355-61.
9 Cruise JM. Jaundice in tuberculosis. Am Y Med Sci 1974;
10 Munt RW. Miliary tuberculosis in the chemotherapy era:
with a clinical review in 69 American adults. Medicine
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1995 36: 792-794Gut
W Hussain, D Mutimer, R Harrison, et al.
Fulminant hepatic failure caused by
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