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Misra, Misra, Singh, Kumar Pati, Kumar Kar, Kumar Panigrahi, Seba Das, Ranjan Panda, Misra, Narayan Mallik, and Prasad Singh: Hepatic sarcoidosis masquerading as tuberculosis


Hepatic involvement is common in sarcoidosis. Hepatic sarcoidosis is usually asymptomatic, and hence is rarely reported in India because of the prevalence of more commonly recognized granulomatous diseases, such as tuberculosis and Hansen’s disease. We report a case of hepatic sarcoidosis with no systemic manifestations, and which was initially incorrectly diagnosed and treated as tuberculosis of the liver, significantly delaying correct diagnosis and treatment.

Case report

A 50-year-old woman presented with a 2-week history of pain in the upper-right abdomen, fatigability, fever, vomiting and loss of appetite. The patient also reported yellow discoloration of the eyes and dark-coloured urine for the previous 7 days. There was no history of cough, dysuria, gastrointestinal bleeding, pruritus or clay-coloured stools.

The patient was diagnosed with type 2 diabetes mellitus 10 years previously. Her blood sugar was well controlled using oral hypoglycaemic agents (glimepiride). For the previous 5 years, the patient had been taking telmisartan (Micardis®, Boehringer Ingelheim, Ingelheim am Rhein, Germany) for hypertension and thyroxine for hypothyroidism. Seven months before, the patient had undergone laparoscopic cholecystectomy for cholelithiasis, during which the surgeon noticed multiple nodules over the liver surface and took a biopsy from the nodular regions. A diagnosis of tuberculosis was made on histopathological study and the patient was put on antitubercular drugs for 6 months. There was no history of herbal or hepatotoxic drug use.

On examination, the patient was pale and exhibited icterus, mild facial puffiness and pedal oedema. There was no lymphadenopathy or thyroid enlargement. Abdominal examination revealed an enlarged liver palpable 10 cm below the right costal margin, which was firm and non-tender with a nodular surface. The spleen was enlarged 5 cm below the left costal margin and was firm and non-tender. There was minimal free fluid in the abdomen, and no other masses were detected. Examination of other systems did not reveal any abnormalities.

On investigation, haematological investigations were normal, except for anaemia (haemoglobin 8 g/dl; total leucocyte count 5990 cells/mm3 with 72% neutrophils). Urinanalysis revealed more than 50 pus cells per high-powered field, but urine culture was negative for bacteria. Blood glucose values were normal (fasting 71 mg/dl; postprandial 96 mg/dl), as was renal function (serum urea 25 mg/dl, creatinine 0.7 mg/dl, sodium 130 mEq/l and potassium 2.6 mEq/l). All the viral markers (IgM antihepatitis A virus, IgM antihepatitis E virus, hepatitis B surface antigen and antibodies to hepatitis C) were negative. Tests for antinuclear antibodies, anti-liver/kidney microsomal antibodies and anti-smooth muscle antibodies were also negative. Liver function tests showed elevated bilirubin and alkaline phosphatase levels (serum bilirubin 6.2 mg/dl, aspartate aminotransferase 36 IU/l, alanine transaminase 48 IU/l, alkaline phosphatase 1696 IU/l, serum protein 6.7 mg/dl, albumin 3.0 mg/dl). Prothrombin time was 11.6 (control)/17.8 (test) with an international normalized ratio of 1.4. A thyroid function test revealed the patient to be in a hypothyroid state [free triiodothyronine (T3) 1.87 pmol/l, free thyroxine (T4) 0.89 pmol/l and thyroid-stimulating hormone 8.14 pmol/l] with serum alpha-fetoprotein 3.88 ng/ml and calcium 19-9 was 511.20 U/ml. Serum cortisol was 615 nmol/l and serum calcium was 8.20 g/dl. An ascitic fluid study revealed the following: total leucocyte count 1320/mm3, lymphocytes 70%, neutrophils 30%, serum protein 0.8 mg/dl and albinum 0.5 mg/dl; serum–ascites albumin gradient >1.1 g/dl.

Ultrasonography revealed hepatosplenomegaly with fatty change in liver, minimal ascites and uterine fibroid. Computerized tomography (CT) and magnetic resonance imaging of the abdomen revealed an enlarged liver (17.2 cm) with increased density under normal enhancement. Intrahepatic biliary radicles were not dilated, and the portal vein and common bile duct were normal. There was splenomegaly (14 cm), but splenic density and the pancreas were normal, and the uterus was bulky and contained a fibroma measuring 5.6 × 5.8 cm. However, there was minimal ascites with multiple small peripancreatic and para-aortic nodes, the largest being 1 × 1.1 cm (Figure 1A, B and C).


CT scan and magnetic resonance cholangiopancreatography (MRCP) of liver and biliary tree. (A) Enlarged liver and spleen. (B) MRCP showing normal biliary tree. (C) CT sagittal section showing hepatosplenomegaly with fibroid of uterus. (D) High-resolution CT showing pulmonary nodule and basal fibrosis.


A liver biopsy was repeated to determine the cause of liver injury. Histopathology revealed moderate macrovesicular steatosis, hepatocellular degeneration and intracellular as well as cholangiolar bile stasis, focal lobular inflammation and portal inflammation comprising neutrophils, eosinophils, lymphocytes and macrophages with bile duct destruction. Moderate piecemeal necrosis was found around the portal tracts with fibrous expansion. The patient was diagnosed with drug-induced liver injury leading to moderate chronic active hepatitis (Histology Activity Index 9, stage 2) (Figure 2A).


Liver histology done at different times. (A) Drug-induced liver injury. (B) Granulomatous hepatitis. (C) Naked granulomas with asteroid body. (D) High-power view showing asteroid body.


The patient was treated with modified ATT (levofloxacin, ethambutol and streptomycin), along with ursodeoxycholic acid and thyroid hormone supplement, and discharged after 3 weeks. Regular follow-up visits were advised.

After 2 months, the patient reported a 15-day history of severe fatigability, lethargy and loose mucoid stools. Examination did not reveal any new finding. Haematological findings, renal function tests and a blood glucose test were all within normal limits. However, liver function tests showed high alkaline phosphatase (1680 IU/l). A stool occult blood test was negative. An ascitic fluid study revealed a high serum–ascites albumin gradient (1.1 g/dl). A repeat liver biopsy was carried out, and histopathology revealed macrovesicular steatosis, focal circumscribed aggregates of epithelioid cells with occasional Langhans giant cells, sparse lymphocytes, plasma cells and eosinophils in these granulomas. Granulomatous hepatitis was suspected (Figure 2B).

As the patient was not responding to ATT, an evaluation for sarcoidosis was carried out. The serum calcium level was assayed and found to be higher than normal (8.20 g/dl), and the angiotensin-converting enzyme level was 207 u/l (normal 8.65 u/l). High-resolution CT revealed multiple hilar and mediastinal adenopathy, pulmonary nodules and basal fibrosis, the results of which led to a diagnosis of sarcoidosis stage II (Figure 1D).

Following these developments, a review of all the liver biopsy slides was deemed necessary, which was carried out by a senior and experienced histopathologist. Histopathological examination of the first liver biopsy, taken during laparoscopic cholecystectomy, revealed numerous small, discrete, granulomas with sharp well-defined edges consisting of epithelioid cells, without any stromal response. These were naked granulomas without caseous necrosis. An asteroid body was seen in the centre of one granuloma and a histopathological diagnosis of hepatic sarcoidosis was made (Figure 2C and D).

The patient was diagnosed with sarcoidosis. ATT was stopped and the patient was treated with glucocorticoid at a dose of 1 mg/kg body weight. The patient’s liver reduced to normal size. The patient’s condition has continued to show significant improvement on regular follow-up.


Sarcoidosis is a systemic granulomatous disease of unknown aetiology. It affects people of all races, of all ages and of both sexes. Hepatic involvement in sarcoidosis is common and is usually asymptomatic.13 Only 5–30% of patients present with symptoms such as nausea, vomiting, abdominal pain, fever with night sweats, myalgia and weight loss.4 Approximately 50–80% of patients with systemic sarcoidosis have hepatic involvement.5 It is rarely reported in India because of the prevalence of more commonly recognized granulomatous diseases, such as tuberculosis and Hansen’s disease.6 Diagnosis can be delayed if the patient does not have any other system involvement, or if the patient undergoes unnecessary diagnostic testing and inappropriate treatment prior to diagnosis.7

This case proved to be unexpectedly enlightening. When dealing with a case of granulomatous hepatitis in a region where tuberculosis is endemic, one should consider tuberculosis first; however, if the patient does not respond to therapy despite good compliance then other possibilities, such as sarcoidosis and amyloidosis, should be kept in mind, and the histopathology should be reviewed to garner clues for diagnosis and possible revision of diagnosis, as in our case. Clinicians and pathologists in the developing world should be aware of these possibilities.



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