Many tropical illnesses frequently show as fever and jaundice. Tropical infections can impact the liver in a variety of ways, ranging from a little, temporary increase of liver enzymes to acute liver failure (ALF). The use of paracetamol in individuals who have a fever and jaundice may exacerbate the damage or cause a delay in its resolution; however, the studies have never addressed this possibility. The most well-known instance of hepatic involvement in tropical illnesses is malarial hepatopathy; however, other tropical infections such as typhoid fever, dengue fever, leptospirosis, amoebic liver abscess, and other bacterial and fungal infections can also present with similar symptoms.

A number of non-hepatotropic viruses, bacteria, protozoa and fungal infections can damage the liver in addition to hepatotropic viruses (Hepatitis A to E), which can cause abrupt liver failure. These infections can manifest clinically as fever, jaundice and encephalopathy. Common tropical illnesses that resemble ALF include jaundice and altered sensorium  such as typhoid fever, dengue, malaria and leptospira.

Given that HAV and HEV are hyperendemic in India, viral hepatitis is a serious public health concern there. 90%–100% of the population develop anti-HAV antibodies and become immune by adolescence according to seroprevalence studies. Numerous HEV outbreaks have been documented in India. In India, HAV-related liver illness is rare and mostly affects young people. ALF and sporadic adult acute viral hepatitis are likewise mostly caused by HEV. Patients with CLD and pregnant women are at a heightened risk of contracting HEV infection. The high mortality rate associated with HEV infection in these populations emphasizes the importance of preventative treatments for these populations.

HAV belongs to the Picornaviridae family of single-stranded RNA viruses. It has been linked for many years to "infectious hepatitis" epidemics that result from fecal contamination of food and water, especially in unsanitary nations. Nonetheless, infections are not uncommon in developed countries, and they frequently arise from outbreaks connected to sloppy food handling in eateries [1].

HAV infection can present as asymptomatic illness, especially in younger patients, or as fulminant hepatic failure requiring liver transplantation. The majority of adults exhibit symptoms, with 70% experiencing jaundice; nevertheless, infections are often minor and self-limiting and no persistent carrier condition has been found [2].

HBV is a member of the Hepadnaviridae family of viruses. It has circular, relaxed, and partly double-stranded DNA. Its virologic and clinical characteristics have been thoroughly studied since Blumberg et al. identified it as the "Australia antigen" around 35 years ago. Abrupt HBV infection, like HAV, can occur with no symptoms at all, although 30% of individuals experience icteric hepatitis, and some experience abrupt liver failure (20). Chronic hepatitis, cirrhosis, HCC and an asymptomatic carrier status are among the clinical manifestations of persistent HBV infection [3].

Study Settings: Nilratan Sircar Medical College, Kolkata, Department of General Medicine.

Study Population: Patients were admitted in general medicine ward through opd and emergency in Nilratan Sircar Medical College and hospital. Patients were included in the study only if they could fulfil the inclusion &exclusion criteria proposed.

Inclusion Criteria:

1. Fever (oral temp >99 degree Fahrenheit) for less than 7 days
2. Jaundice (total bilirubin >2.5 mg/dl) for less than 7 days.

Exclusion Criteria:

1. Fever for more than 7 days
2. Jaundice for more than 7 days
3. Chronic liver disease patient
4. Surgical jaundice
5. Liver malignancy (primary and secondary)
6. Alcoholic hepatitis

Study Period:  From February 2023 upto 1st May 2024.

Sample Size: 50 Cases

Study Design: Single centre Prospective and Observational Study.

METHODS:

The patients admitted in general medicine ward with history of fever with jaundice for less than 7 days to be evaluated for causes and outcome of the patients with details of clinical history, examination and related investigations. All patients enrolled will be followed up in 28 days after discharge. Biochemical parameters are compared with initial to 1wk and 4wk after admission and bio statistical analysis done with chi square chart and p value less than 0.05 was considered statistically significant.

Table 1: Cases found in study

Table 2: Bilirubin level, after 1 week, after 4 weeks

Table No 3: Initial Prothombin Time (sec), after 1 weeks (sec), after 4 weeks (sec)

Table No 4: Initial SGOT/SGPT level (U/L), after 1 week (U/L), after 4 weeks(U/L)

Figure No 1: Initial SGOT/SGPT level (U/L), after 1 week (U/L), after 4 weeks(U/L)

In a study of 50 patients, the most common diagnoses were Hepatitis A (28%), Hepatitis E (22%), and Leptospirosis (18%), followed by Dengue Fever (12%), Hepatitis B (12%), and Sepsis with MODS (8%). Initial total bilirubin levels were highest in Hepatitis A, B, and E, with the majority of patients in these groups having levels >10 mg. In contrast, patients with Dengue, Leptospirosis, and Sepsis with MODS predominantly had bilirubin levels <5 mg. After one week, a trend toward improvement was observed in all groups, particularly in Hepatitis A, B, and E, where more patients shifted to lower bilirubin categories, indicating clinical progress.

After one week, all Dengue Fever patients (6) had <5 mg total bilirubin, indicating early resolution. In Leptospirosis, bilirubin levels worsened, with only 1 patient <5 mg, and the rest split evenly between 5–10 mg and >10 mg. Sepsis with MODS showed improvement, with 3 patients <5 mg and 1 between 5–10 mg. By the fourth week, most patients across all groups had improved bilirubin levels: 12 of 14 Hepatitis A, 4 of 6 Hepatitis B, and 9 of 11 Hepatitis E patients had <5 mg, with only 1 patient in each group remaining >10 mg. All Dengue Fever patients continued to have <5 mg bilirubin at four weeks, reflecting sustained recovery.

By the fourth week, most patients showed improvement in total bilirubin and prothrombin time. In Leptospirosis, only 1 of 9 patients had <5 mg bilirubin, while 4 had 5–10 mg and 3 had >10 mg; in Sepsis with MODS, 3 of 4 had <5 mg bilirubin. Prothrombin time initially was >17 seconds in the majority of Hepatitis A (9/14), B (3/6), and E (8/11) patients, while Leptospirosis and Sepsis cases had milder elevations. At one week, prothrombin time remained prolonged (>17 sec) in most Hep A, B, and E patients but showed slight improvements. By four weeks, significant recovery was observed: in Hepatitis A, 12 patients had normalized prothrombin time (13–14.9 sec), with similar trends in Hepatitis E (9/11) and moderate improvement in Hepatitis B (3/6). This indicates a general trend of clinical recovery over time, particularly in viral hepatitis cases.

By the fourth week, most Dengue Fever patients showed normalized prothrombin time, with 5 out of 6 at 13–14.9 seconds, and similar improvements were seen in Sepsis with MODS. Leptospirosis patients, however, continued to have prolonged prothrombin time, with nearly half (4/9) remaining >17 seconds. Initial SGOT/SGPT levels were markedly elevated (>1000 U/L) in the majority of Hepatitis A (10/14), B (4/6), and E (7/11) cases, indicating acute hepatic injury, while levels were mostly normal (<150 U/L) in Leptospirosis and Sepsis. After one week, there was partial improvement in liver enzymes across all groups, though some patients in viral hepatitis groups still had levels >1000 U/L. By the fourth week, most Hepatitis A patients (12/14) had normalized SGOT/SGPT levels (<150 U/L), reflecting significant hepatic recovery.

By the fourth week, liver enzyme levels (SGOT/SGPT) had normalized (<150 U/L) in the majority of patients across all groups, indicating significant hepatic recovery. All Dengue Fever patients (6/6) and most Hepatitis E (9/11), Hepatitis B (4/6), Leptospirosis (7/9), and Sepsis with MODS (3/4) patients had normalized levels. A small number of patients in Hepatitis B, Hepatitis E, and Leptospirosis groups still had mildly elevated (150–1000 U/L) or markedly elevated (>1000 U/L) enzyme levels, suggesting ongoing liver involvement in a few cases.

In my study population, 30 patients (60%) male and 20 patients (40%) are female .So males are more prone to develop viral hepatitis and jaundice.

There were fifty patients examined in all in this investigation.The age group of 20–30 years old had the highest number of patients, followed by <20 years old and 30–40 years old. A total of 170 individuals were examined in the investigation on febrile jaundice carried out by Mokta J et al. [4] in a tertiary care setting.The maximum number of patients in the age category under 30 years was 50, or 39.4%, and the ratio of female to male patients was 1.8:1.

In a research on malarial hepatopathy by Shah et al. [5], the patients' ages (mean 26+/- 8.33) varied from 13 to 48 years. Every patient had an icteric fever.

In total number of patients 50, 14 patients (28%) were diagnosed hepatitis A; 11 (22%) were Hepatitis E; 9(18%) were Leptospirosis, 6 (12%) were Dengue Fever and Hepatitis B each and 4 (12%) were Sepsis with MODS.

In a tertiary care research, K. Vasanthan et al. reported febrile jaundice [7]. Thirteen individuals each with hepatitis A and B and three with hepatitis E were reported to have viral hepatitis in Tamil Nadu, India.Thirty-two individuals were undiagnosed, nine had clinical malaria, seven had leptospirosis.

Studying viral hepatitis in India, Abraham P [8] In India, HEV is the most frequent cause of sporadic hepatitis. According to a study by Mokta J et al. [4] on febrile jaundice at a tertiary care hospital in the Himalayan State, the most prevalent cause was scrub typhus, which affected 103 patients (or 60% of the total), followed by hepatitis E in 36 patients (21%), and leptospirosis in 9 patients (5.3%).

In our study all patients liver enzymes (AST/ALT) was elevated in the course of the disease, more rise in Hepatitis A, HepatitisB & Hepatitis E but mild rise of AST, ALT Level in patients diagnosed Leptospirosis.

In all hepatitis patients (HepA, HepB, and HepE), bilirubin levels were elevated; however, in instances of dengue fever and sepsis, there was only a little increase. In every patient in my research group, the level of conjugated bilirubin exceeded 30% of total bilirubin. The liver enzyme (AST/ALT) and bilirubin level was gradually lowered in the majority of instances of Hepatitis E, Hepatitis A, and HepB, and the patients recovered and their appetite improved. Thus, viral hepatitis had a positive result (p value <0.05).One patient with Hepatitis E experienced full-blown hepatic failure, but they eventually recovered.

In my study 30 patients (60%) was developed Hepatosplenomegaly; 100% of HepB, 85% of HepA; 63% of HepE; 33% Dengue fever; 25% of sepsis and 22% of Leptospirosis developed Hepatosplenomegaly.

According to a research by Vasanthan et al. [7] on febrile jaundice in a tertiary care setting, all patients had increased liver enzymes (AST/ALT), but none of them had elevations greater than three times normal, or 8.3% of patients with elevations greater than 65 units. With a direct bilirubin elevation more than 30% of total bilirubin, all patients had increased bilirubin.Clinically, 4 individuals in the hepatitis B group (7.7%) and 11 (21.2%) in the hepatitis A group had hepatomegaly. Hepatomegaly was present in two hepatitis E patients. One patient from the hepatitis A group and three from the hepatitis B group had splenomegaly based on clinical observations. Amir A. Shah et colleagues. found that elevated liver enzymes in an emergency medical situation may be a sign of improved survival in elderly individuals with bacterial sepsis. In my study, all four sepsis patients experienced elevated liver enzymes and jaundice; three of them survived, while one patient passed away.

In my study ,22% patients(11) had bleeding manifestation in the form of melena, gum bleeding, epistaxis, hematemesis or hemoptysis .4 patients(44%) of leptospirosis, 4 patients(66%) of Dengue Fever ,2(14%) of Hepatitis A and 1(9%) of HepatitisE had bleeding tendency.So Dengue Hemorrhagic Fever patients had severe Thrombocytopenia (<10,000/cmm) and platelet tranfusion needed in all patients and one of then needed pRBC tranfusion. Patients with leptospirosis experienced hemoptysis, acute dyspnea, and pulmonary bleeding.Additionally, those with viral hepatitis (Hep A & E) had bleeding, primarily from the gums, melena, a prolonged prothrombin time, the requirement for an FFP transfusion, and vitamin K administration.

Gouveia EL et al., Leptospirosis associated severe pulmonary hemorrhage syndrome [9] Between 2003 and 2005, 47 cases were found; the case mortality rate was 74%.By 2005, 55% of leptospirosis-related deaths were attributable to SPHS.

In my study two patients of Dengue Fever and 4 patients of DHF present .Liver enzymes (AST/ALT) was raised in 5 patients (83%); Hepatosplenomegaly present in 2 patients(33.3%); Ascites present in 4 (66.6%); AKI developed in 5(83%);Leukocytosis observed in 2 patients (33.3%); and all patients had thrombocytopenia.AST was more raised than ALT.

Iqtadar S et al.'s profile of hepatic involvement in adult dengue infections[10] reveals that around 60% of DHF patients exhibited hepatomegaly; 40 (18.2%) had hyperbilirubinemia; and all DHF patients had elevated AST levels.

In my investigation, thrombocytopenia was observed in every leptospirosis patient; however, in a prospective study of human leptospirosis, which Edwards CN did, thrombocytopenia was found in 54% of 24 cases.

In another research by Salvador et al. [9], case deaths were 15% and 24.1%. Two patients had died in my study: one from leptospirosis owing to severe lung bleeding and encephalopathy, and the other from sepsis with mods due to persistent septic shock.

In my study, 10 patients (20%) presented with jaundice and encephalopathy. Among them 4 parients (44%) of Leptospirosis, 3(75%) of sepsis, 1(7%) of Hepatitis A, 1 (9%) of Hepatitis E was present.A study Approach to clinical syndrome of jaundice and encephalopathy in Tropics conducted by Anil C Anand show most common etiology in India are viral Hepatitis (HepE>HepB>HepA), and a similar presentation can also see in Dengue fever, typhoid fever, Leptospirosis and bacterial infection.

Of the fifty patients, fourteen had Anti-HAV IgM positivity; peak ALT and peak bilirubin were 5500 u/l and 17.8 mg/dl, respectively; two patients (14%) had thrombocytopenia, two patients (14%) had leukocytosis, one patient (7%) had acute renal failure, and seven percent of Hepatitis A patients developed fulminant hepatic failure.

A study on Clinical characteristics and outcomes of acute Hepatitis A multicenter study conducted by So Young Kwon et al show- mean peak ALT was 2963 IU/L with a mean peak bilirubin of 7.3 mg/dl.Fulminant hepatic failure developed in 0.91% of Hepatitis A patients, 10 patients died due to fulminant hepatic failure.

We find that the most prevalent causes of fever and jaundice lasting fewer than seven days are hepatitis A and hepatitis E. Other causes include sepsis with MODS, dengue fever, and leptospirosis. Thrombocytopenia is often linked to people with dengue fever and leptospirosis. Leptospirosis and sepsis are more strongly associated with leukocytosis and severe renal damage. In tertiary care facilities, the prognosis for viral hepatitis is favorable.The prognosis for leptospirosis with bleeding symptoms and encephalopathy is poor.

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