Biomedical subjects
Publications and source records attributed to A Koshy.
A case of retroperitoneal cystic lymphangioma is reported. Added to the 42 cases of retroperitoneal lymphangioma found from the English literature, this brings up the total of cases reported to date to 43. A critical review of the clinical picture and management of this condition is presented on the basis of these reported cases.
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An epidemic of jaundice probably due to toxic hepatitis occurred in three adjoining districts of Northwest India during the period November and December, 1974. The dogs of the villages were affected first, then the human beings. Detailed clinical features, appropriate laboratory tests, and liver biopsies were studied. A retrospective epidemiological survey was carried out. The disease had a subacute onset starting with high fever, followed by rapidly progressive jaundice. Ascites appeared simultaneously and soon became quite massive. Hepatomegaly was recorded when ascites decreased. Liver function tests suggested cholestatic jaundice. The mortality rate in the hospital was 10%. Clinical features in dogs were similar, but mortality was almost 100%. Liver histology was characterized by (1) edema and collagenization of the central veins, never with thrombosis, (2) cholangiolar proliferation, (3) moderate to severe ballooning of the hepatocytes, (4) perisinusoidal fibrosis, (5) cholestasis, and finally, (6) cirrhosis with reverse lobulation. Etiology of this epidemic of hepatitis could not be unequivocally established. Critical analysis of the data suggests that some food toxin may have been a factor in the outbreak of this unusual epidemic of toxic hepatitis.
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In animals, there may exist a hyperemic response in the portal circulation during intravenous administration of hypertonic glucose, but a hemodynamic response of this kind has never been described in man. This study was designed to evaluate if hyperglycemia itself could induce systemic or splanchnic hemodynamic changes in patients with cirrhosis. Sixteen patients with cirrhosis were studied before and during i.v. infusions of hypertonic (900 mOsmoles per liter) glucose (n = 8), mannitol (n = 4) or saline (n = 4) at 2 ml per min. In the group receiving glucose, there were significant increases in hepatic venous pressure gradient (+12%), azygos blood flow (+27%) and pulmonary capillary pressure (+32%), while calf blood flow decreased (-26%). No changes occurred in the mannitol or saline groups. Changes in plasma osmolality, plasma volume, splanchnic oxygen extraction and vasoactive hormones, including vasoactive intestinal polypeptide and glucagon, did not appear to be involved in the mechanism of these vasoactive phenomena. It is suggested that the possible deleterious effects of increase in portal pressure and azygos blood flow should be taken into consideration when administering hypertonic glucose to patients with portal hypertension.
To delineate the circulatory effects of glucagon in cirrhosis, we infused two moderately supraphysiological doses of this hormone into 19 patients with cirrhosis and determined hemodynamic responses. Patients were divided into a group with good liver function (Pugh Class A, n = 8) and poorer function (Pugh Class B and C, n = 11). All patients received glucagon at 10 ng per kg per min for 20 min, then 20 ng per kg per min for a further 20 min. These doses raised serum glucagon levels to a similar degree in both groups of patients. Serum glucose levels also rose in both groups but to a lesser degree in Class BC patients. Serum noradrenaline and adrenaline remained unchanged in both groups. Heart rate, mean arterial pressure, cardiac index, systemic vascular resistance, hepatic venous pressure gradient and hepatic blood flow were measured basally and during the second glucagon infusion. None of these measurements significantly changed in either group of patients. Azygos and renal venous blood flow were measured basally and during the first and second infusions. Azygos flow increased significantly only in Group A patients: basal, 0.32 +/- 0.03 liter per min; first infusion, 0.40 +/- 0.06 liter per min; second infusion, 0.49 +/- 0.07 liter per min. Corresponding values in Group BC patients were: 0.54 +/- 0.08, 0.54 +/- 0.08 and 0.52 +/- 0.08 liter per min. Renal blood flow did not change significantly. One patient with a portacaval shunt increased superior mesenteric venous flow from 0.78 liter per min to 0.95 liter per min with glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)
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In order to study the acute effects of pharmacological agents on the vascular resistance of portal-systemic collaterals, a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the conscious rat. The haemodynamic effects of several vaso-active substances were evaluated in this model and compared with those obtained after saline administration. Prazosin (0.5 mg), an alpha 1-adrenergic antagonist, significantly reduced mean arterial pressure by 29%, portal pressure from 13.8 +/- 1.0(mean +/- s.e.m.) to 10.1 +/- 0.4 mmHg and portal tributary blood flow (radioactive microspheres) from 13.6 +/- 2.1 to 11.7 +/- 1.2 mL/min. It also decreased portal-systemic vascular resistance from 95 +/- 16 to 73 +/- 9 dyn s/cm5 x 10(3). Propranolol (4 mg), a beta-adrenergic antagonist, significantly reduced mean arterial pressure by 12% and portal pressure from 15.5 +/- 1.2 to 13.3 +/- 0.9 mmHg while reducing portal tributary blood flow from 14.6 +/- 1.5 to 11.0 +/- 1.7 mL/min and increasing portal systemic collateral vascular resistance from 88 +/- 7 to 103 +/- 8 dyn s/cm5 x 10(3). Ketanserin (0.25 mg/kg), a 5-hydroxytryptamine receptor antagonist, reduced portal pressure from 15.8 +/- 1.0 to 13.3 +/- 0.7 mmHg at a dose that did not alter mean arterial pressure or portal tributary blood flow. It achieved this by reducing portal-systemic collateral vascular resistance from 90 +/- 14 to 74 +/- 13 dyn s/cm5 x 10(3). Saline had no significant effect on systemic and splanchnic haemodynamics. This study shows that ketanserin decreases vascular resistance of portal-systemic collaterals while propranolol increases it. Thus, it is suggested that collateral vascular resistance is accessible to pharmacological manipulation.
Pharmacotherapy of portal hypertension started with the use of intravenous vasopressin in the 1960s. However, the short half life of the drug and the non-availability of an oral preparation limited its use to acute variceal bleeding. It was two decades later that propranolol, a beta blocker was shown to decrease portal pressure. However, the usefulness of beta blockers in the treatment of recurrent variceal bleeding remains controversial with controlled trials showing both benefit and lack of benefit. This review is aimed to bring into perspective, current knowledge of the effect of beta blockers on the splanchnic circulation in man and animals, its clinical usefulness in portal hypertension and its place in the therapeutic armamentarium against portal hypertension.
Nine patients of leprosy, 5 BL and 4 LL who developed jaundice during the course of disease were investigated. Two LL patients developed jaundice during ENL reaction. There was slight hepatomegaly in 5 patients and moderate splenomegaly in 3 only. There was significant alterations in liver enzymes and serum bilirubin in all patients. The abnormalities of the enzymes levels persisted for abnormally long periods even when the serum bilirubin had come down and the patients had become asymptomatic. Blood for HBsAg and anti-HAV IgM was negative in all the patients except one in whom HBsAg was positive. Drugs could not be implicated as the cause of jaundice, all patients maintained recovery even after restarting antileprosy drugs. The possibility of non A, non B viruses producing hepatitis during the course of disease is brought out. Course of prolonged jaundice in leprosy is compared with other diseases which could result in a similar situation.
We studied the role of portosystemic shunt development in the maintenance of portal hypertension in a prehepatic portal hypertension rat model. A first group was studied two days after partial portal vein ligation. When portosystemic shunts were negligible; the second group was studied 3 weeks after the partial portal vein ligation, when large portosystemic shunts were present. Portal pressure was significantly higher in the first group than in the second group (19.9 +/- 0.8 mmHg (mean +/- 1 SD) and 12.8 +/- 2.3 mmHg, respectively; p less than 0.001). When compared with sham operated rats: a) portal tributary blood flow (measured with the radioactive microspheres method) was decreased in the first group (- 34 p. 100; p less than 0.01) and increased in the second group (+ 32 p. 100; p less than 0.02); b) portal system vascular resistance was markedly increased in the first group (+ 269 p. 100; p less than 0.001) and did not significantly change in the second group (+ 30 p. 100). These results suggest that portosystemic shunt development decreases portal pressure but not to normal value because portal tributary blood flow is increased. Moreover the increase in portal system vascular resistance and in portal tributary blood flow play different roles in the maintenance of portal hypertension depending on the stage of evolution of portal hypertension.