Most of the laboratory investigations for the diagnosis of amoebic liver abscess are non-specific. However, in many underdeveloped regions where no sophisticated investigations are available, they do have some place in the diagnosis of amoebic liver abscess.

Haemoglobin
Anaemia is very common in amoebic liver abscess. Wilmot¹ found it to be normocytic and normochromic in about half of his patients, and found that it was related to the duration of the symptoms and signs of the abscess. Also anaemia was severe when the size of the abscess was large.
In 1964, Mayet and Powell² carried out serial estimations of the haemoglobin, mean corpuscular haemoglobin concentration and serum iron and total iron binding capacity (TIBC) in 31 African adults with amoebic liver abscess. There was hypoferrimia and low TIBC level even in patients who were not anaemic.
Most authorities believe that this anaemia responds to specific amoebicidal agents and not to haematinics.

White cell count
There is usually a moderate leucocytosis accompanied by an absolute or relative increase in neutrophils. Although 25% of patients may have leucocyte counts below 10,000 per cu. mm., leucocytosis between 15,000 and 25,000 per cu. mm. is common, with neutrophil count upto 72-75%.' Higher counts may be present in secondarily infected abscesses. Eosinophil count is usually normal, unlike in other parasitic infections. Chaves,³ however, found normal leucocytic count in two-thirds of his patients and therefore believed that it cannot be taken as a very reliable diagnostic test in amoebic liver abscess.

Erythrocyte sedimentation rate
This is usually elevated. In 1966, Dacie⁴ established that leucocytosis is produced by factors independent of those causing an elevation in ESR. This would mean that these two haematological investigations are a measure of different functional derangements, both probably non-specific. Fibrinogen is an acute phase reactant and is elevated in hepatic amoebiasis⁵ giving a raised erythrocyte sedimentation rate. Chaves³ found it to be more than 100 mm. in the first hour in 50% of his patients. Ramachandran et al⁶ found it to be more than 20 mm. in 96% of his patients.

Stool examination
If it reveals cysts or vegetative forms of E. Histolytica, it becomes a valuable aid in the diagnosis. However, in endemic areas, where the incidence of carriers is high, presence of cysts of E. Histolytica should not be given too much importance.

Sigmoidoscopy
It is a useful investigation and may be positive in as many as 30 to 40% of cases. Any exudate seen on sigmoidoscopy must be obtained for parasitologic examination. It is importantto use a glass pipette or metal instrument since amoebae adhere to cotton swabs.⁷ If the diagnosis of amoebic ulcers is doubtful, a biopsy may also be taken to demonstrate E. Histolytica in the histopathological sections.

Liver function tests
These have to be mentioned at the cost of some repetition. One of the difficulties in the diagnosis of amoebic abscess of the liver is the absence of any hepatic function test which is specific for this condition.⁸

Serum proteins
It is interesting to note that there is nearly uniform hypoalbuminaemia, which occurs even in patients with symptoms of a few weeks' duration only. There is a fall of serum albumin and rise of certain globulin fractions. Reduction in serum albumin is due to multiple factors. Alper⁵ attributed this fall to the negative acute phase reactant property of albumin. According to him a low albumin level with an elevated gamma globulin would indicate the presence of an abscess of appreciable dimension and necessitate evacuation of the pus. In fact, presence of raised levels of gamma globulin during amoebic dysentery would be evidence of hepatic involvement due to intestinal amoebiasis. After treatment serum protein levels return gradually to normal. Serum immunoglobulins have been studied in patients with amoebic liver abscess.⁹ IGE levels are found to be slightly elevated.

Serum bilirubin
This has been discussed in detail in the previous chapter.

Bromsulphthalein test
This test is of particular value in assessing liver dysfunction in the absence of jaundice.
BSP is infused at two different rates and the plasma BSP level is estimated at intervals, later. The subsequent calculation allows the measurement of the two independent processes of BSP in the liver and its active secretion in the bile.¹⁰ The active secretory process has a maximal rate which is termed BSP transport maximum (Tm) and is measured in mg./min.⁸
In amoebic liver abscess, there is retention of bromsulphthalein and a lowering of its transport maximum (without alteration of storage or conjugation of the dye¹¹) due to an excretory defect following intrahepatic cholestasis. High BSP retention was found in 60% by May et al,¹² 62.5% by Brem,¹³ 90.5% by Viranuvatti et al,¹⁴ 93.3% by Kamat et al,¹⁵ and 100% by Magill. ¹⁶

Serum enzymes

1. S.G.O.T. and S.G.P.T. A mild rise in S.G.O.T. and S.G.P.T., although nonspecific, may be an aid in the diagnosis in conjunction with the clinical and other laboratory findings. However, many workers have found hepatic transaminases to be usually within normal limits. Santhagopalan et al¹⁷ found significant elevation of S.G.O.T. with a slight to moderate elevation of S.G.P.T.
2. Serum alkaline phosphatase. As far back as 1940, Guttman¹⁸ and his associates reported elevation of serum alkaline phosphatase in cases of live abscesses .

Brem¹³ found hepatic function tests in amoebic liver abscess to exhibit an unusual pattern consisting of elevation of the serum alkaline phosphatase and retention of bromsulphthalein associated with normal bilirubin levels and normal tests of hepato-cellular function.
In 1967, Salakos¹⁹ also reported that patients wit hepatic amoebiasis exhibit a consistent pattern of elevated serum alkaline phosphatase without a corresponding elevation of serum bilirubin.

3. Lactic acid dehydrogenase. This enzyme was found to be significantly elevated in 92% of case investigated by Mahajan et al.²⁰ The elevated level returned to normal within month following complete cure of the disease.

Thus, the authors recommended LDH enzyme determination as a useful index for cure of invasive hepatic amoebiasis.

4. Serum aldolase. Slight to moderate increase in levels of serum aldolase has been noted.¹⁷
5. Serum cholinesterase. Significant depression of serum cholinesterase in amoebic liver abscess has been reported.¹⁷

Other liver function tests
Serum mucoprotein levels have been found to be elevated.²¹
Serum alpha fetoproteins are very rarely, if ever present in an amoebic liver abscess.²² When detected it is usually in-the late stage of regeneration.
Cephalin cholesterol flocculation test in on study²³ was abnormal in 43.2% cases. Thymol turbidity test in the same study²³ was abnormal in 39.3% cases and zinc sulphate turbidity test in 68.53 %.

References

1. Wilmot, A J. Clinical Amoebiasis, Blackwell Scientific Publications, Oxford, 1962.
2. Mayet, F G. and Powell, S J. Am J. Trop Med. Hyg, 1964, 13, 790.
3. Chaves, F J Z. Am J. Gastroent., 1977, 68, 273.
4. Dacie, J V, and Lewis, S M, Practical Haematology, 4th Edition, Grune & Stratton, New York, 1968.
5. Alper, C A, New Eng. J. Med., 1974, 291, 287.
6. Ramachandran, S. Sivalingsam, S. et al, J. Trop. Med. Hyg., 1972, 75, 34.
7. Krogsstad, D J. Spencer, H C, et al, New Eng. J. Med., 1978, 298, 262.
8. Sherlock, S. Diseases of Liver and Biliary System, 5th Edition, Blackwell Scientific Publications, Oxford, 1975.
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12. May et al, 1967, as quoted by 11.
13. Brem, T H. Am. J. Med. Sci., 1955, 229, 135
14. Viranuvatti, V, Shuwanik, R. et al, Am. J. Gastroent., 1971, 55, 33.
15. Kamat, G R. Johri, B S. et al, J. Trop. Med. Hyg., 1968, 71, 111.
16. Magill, G B. and Killough, H. J. Lab. Clin. Med., 1958, 51, 333
17. Santhagopalan, T. Jayasekaran, S. et al, Ind. J. Path. Bact., 1968, 11, 61.
18. Guttman, 1940, as quoted by 19.
19. Salako, L A, J. Trop. Med. Hyg., 1967, 70, 19.
20. Mahajan, R C, Singh, K, et al, Ind. J. Med. Res., 1975, 63, 1006.
21. Ruas, A, Nunes, R. et al, Ann Trop. Med. Parasitol., 1967, 61, 21.
22. Damisah, M, Ajdukiewiz, A, et al, Brit. Med. J., 1976, 2, 529.
23. Viranuvatti, V, Harinasuta, T. et al, Am J. Gastroent., 1963, 39, 345.