الفهرس 
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Abstract
SUMMARY AND CONCLUSION
In Egypt approximately 20 million individuals, nearly
half of the population, are infected with schistosomal hepatic
fibrosis.
Hepatosplenomegaly is one of the main constant manifestations
of schistosoma mansoni infection. Schistosomiasis
is the main cause of portal hypertension in Egypt. Its
subsequent complication of variceal haemorrhage threatens
the life of the patient.
The main factor producing portal hypertension is the
pre-sinusoidal periportal fibrosis. Hypervolaemia was
suggested as a contributing factor for the production of
portal hypertension which was mainly attributed to salt and
water retension resulting from an increase in plasma aldosterone.
Another contributing factor is portal venospasm.
Until1 now management of portal hypertension is puzzling.
A portocaval shunt does not appear to prolong survival and
may be followed by encephalopathy and neuropsychiatric
syndromes, even in those patients with good liver function.
The complications of sclerotherapy include precipitation
or worsening of haemorrhage,oesophageal necrosis, perforation
or stenosing. Chest complications, dysphagia, fever and pains
are also reported. Medical management included the use of
drugs aiming at lowering portal hypertension and thus reducing
the possibility of bleeding or recurences. The aim of the
present study was to evaluate the different specific-Vasopressin,
glyperssin, propranolol and captopril - chemotherapeutic agents
as regard to their effects in lowering portal hypertension
and their effects on the haemostatic mechanisms especially
the fibrinolytic system. The study was carried out on
patients with schistosomal hepatic fibrosis and past history
of bleeding oesophageal varices.
The patients were classified into 4 groups each comprising
10 patients.
group ( A ) : received vasopressin in a dose of 20
U. in 100 ml. 5% dextrose over a period of
20 minutes.
group ( B ) : received 1 mg of glypressin intravenously
group ( C ) : received oral propranolol in a doses which
reduced heart rate by 25% (40 to 80 mg) twice
daily for one week and the investigations were
carried out before and after administration of
the drug as scheduled with other drugs.
group (D) : received captopril in a dose of 25 mg
three times daily one hour before meals for
one week and the investigations were carried
out before and after administration of the drug
as scheduled with other drugs.
The patients were subjected to the following:
1 - Complete history taking with special references
to schistosomiasis and other diseases known to produce portal
hypertension.
2- Complete clinical examination with special stress
on the liver, spleen, signs of portal hypertension, manifestations
of liver insufficiency, pulmonary hypertension, the
presence or absence of ascites and or jaundice.. Patients
with cardiac disease, pulmonary hypertension, chest diseases
and advanced hepatic insufficiency were excluded from the
study.
3- The following investigations were carried out:
- investigations to confirm the diagnosis of schistomiasis.
- investigations to confirm the diagnosis of portal
hypertension and oesophageal varices.
- blood pictures before and after 2 weeks of therapy
- Liver function tests before and after 2 weeks of
therapy.
- Euglobulin lysis time test before and after administration
of each drug then after 2 weeks.
- Systolic time Intervals before and after administration
of each drug 6 hours later then after 2 weeks.
- measurement of portal pressure before and after
administration of each drug 6 hours later then
after 2 weeks using the percutaneous trans-splenic
route.
Vasopressin lowers portal pressure for about an hour
after its administration may be due to constriction of the
splanchnic arterial bed causing an increase in resistance
to the inflow of blood to the gut. It controls haemorrhage
from oesophageal varices by lowering portal venous pressure
and this mechanism may be aided by contraction of the
smooth muscle fibres present in the lower third of the
oesophagus.
In our study vasopressin did not affect the blood
pictures and liver functions. It can be given in schistosoma1
hepatic fibrosis where the liver functions remain
intact until1 late stages of the disease.
Vasopressin was found to decrease pulse rate, to increase
the systemic arterial blood pressure and to decrease the
portal pressure for about one hour. The three items may be
benefit in cases of bleeding varices in patients with
schistosomal hepatic fibrosis. Although complications of
vasopressin are well known to occur rarely, but could not
be confirmed in our study.
Abdominal colicky discomfort and evacuation of the
bowels, together with facial pallor are usual side effects
during our study. These may decrease the incidence of
hepatic coma in cases of bleeding oesophageal varices.
Our study showed no effect of vasopressin on the left
ventricular performance. This may be attributed to our
selection of cases. We recommed utilization of vasopressin
in patients after doing E.C.G. or ST1.s if available to exclude
patients with cardiac lesions.
Vasopressin can be given with nitroglycerine to avoid
the coronary vasoconstriction as well as nitroglycerine was
known to enhance the decrease in the portal pressure.
The main disadvantage of vasopressin noticed in our
study is its stimulation to the plasminogen activator.
Plasminogen activator will accelerate the fibrinolysis
process which is not needed in cases of bleeding oesophageal
varices.
Vasopressin remains a useful initial, simple, cheap
emeregency method of controlling variceal bleeding due to
portal hypertension in schistosomal hepatic fibrosis.