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How To Handle Hepatitis B Patient

Posted at January 19th, 2023 | Categorised in Manage Diabetes

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How To Handle Hepatitis B Patient

Cite this article: Alemam A, Ata S, Shaikh D, et al. (May 02, 2021) Syphilitic Hepatitis: A Rare Cause of Traumatic Lesions. 13(5): e14800. doi:10.7759/.14800

Bone Health In Hiv And Hepatitis B Or C Infections

Syphilitic hepatitis represents a rare manifestation of treponemal disease. The diagnosis is made in the presence of specific signs and symptoms with good serological markers, high liver function tests, and there is no other reason for hepatobiliary damage. Here we report a case of a patient with recent syphilis causing liver failure. With the increasing incidence of infectious diseases in the United States, this case highlights the importance of recognizing syphilis as a differential diagnosis for liver lesions.

. This disease is often associated with high sexual activity, especially in men, accounting for 86% of syphilis cases [1]. Syphilis will progress from primary to secondary and finally to advanced stage if untreated. Primary syphilis usually consists of a single painless lesion that resolves on its own. Secondary syphilis is accompanied by physical symptoms weeks to months after the initial infection, with a rash that often affects the hands and feet. Advanced Syphilis occurs in the years after the primary infection and can be manifested by serious diseases and heart [1]. Since 2001, primary and secondary syphilis has been increasing year by year [2]. In 2018, a total of 35,063 cases of primary and secondary syphilis were reported in the United States, resulting in a rate of 10.8 cases per 100,000 people [2]. Here we present an unusual case of syphilitic hepatitis.

A 42-year-old African American man with a history of gout, hypertension, and recurrent genital herpes presented to our Emergency Department complaining of right upper quadrant pain. body with epigastric abdominal pain and nausea and indigestion, not a person’s blood. – a long day. Epigastric pain appeared after eating a meal containing lobster and steak. It was defined as severe, sudden, unrelieved pain of moderate intensity without complications or reduction. He denies fever, chills, diarrhea, hematochezia, yellow skin, genital ulcers, or heartburn. He has no recent travel or illness. He started taking allopurinol (100 mg, once daily) 10 days before admission for chronic gout and was taking valacyclovir (500 mg, once daily) for genital herpes. A detailed medical history also revealed the use of poison ivy (poisonous flower) approximately three months prior to the injection. He reported frequent marijuana use but denied tobacco use, excessive alcohol consumption, acetaminophen use, or other drug use. He denied any family history of hepatobiliary disease. He had a history of previous discectomy and fusion (ACDF) surgery for disc degeneration secondary to a motor vehicle accident two years prior to presentation.

Vital signs showed blood pressure of 126/68 mm Hg, pulse of 73 beats per minute, temperature of 99.1°C, and respiratory rate of 15 breaths per minute with oxygen saturation of 100% on room air. Physical examination showed age-appropriate skin changes and no major problems. He had a past scar from a distant trauma in his childhood and a neck scar from ACDF. He had a hyperkeratotic papular rash on the arms, trunk, and legs (Figure 1), and lesions on the penis. Cardiac and pulmonary examinations showed results within normal limits. Abdominal examination showed a tender epigastrium and the rest of the abdomen was smooth, without disease, no organs or organomegaly. Neurological examination was within completely normal limits.

A Call For Advocacy And Patient Voice To Eliminate Hepatitis B Virus Infection

Initial studies revealed cholestatic liver injury and serum alkaline phosphatase (ALP) at 659 IU/L (normal: 52-128 IU/L), aspartate transaminase (AST) at 103 IU/L (normal: 9- 48 IU/L ), alanine transaminase (ALT) at 152 IU/L (normal: 5-40 IU/L), gamma glutamyl transferase (GGT) at 802 IU/L (normal: 8-54 IU/L), albumin at 3.3 g/dL (normal: 3.4-4.8 g/dL), total bilirubin at 0.5 mg/dL (normal: 0.2-1.1 mg/dL), and direct bilirubin at 0.3 mg/dL (normal: 0.0-0.3 mg/dL). Abdominal examination showed increased echogenicity of the liver without hepatomegaly, normal gallbladder, normal uncomplicated bile ducts, normal pancreas, and patent hepatic ducts.

The patient was admitted to the hospital for further investigation of liver damage. At that time, various diagnoses included drug-induced liver injury (DILI) secondary to allopurinol, autoimmune hepatitis, or biliary disease. Allopurinol was stopped because of concern about DILI and drug reaction and eosinophilia and systemic symptoms (DRESS). Viral hepatitis serology showed positive hepatitis A total antibody, negative hepatitis C antibody, high hepatitis B antibody, and herpes simplex virus (HSV) IgM polymerase chain reaction (PCR) negative. Autologous liver biopsy showed normal levels of immunoglobulin G and absence of nuclear, liver, kidney microsomal, smooth muscle, and anti-mitochondrial antibodies. The acetaminophen level was <14.9 ug/mL, below the normal toxic level.

Upon further questioning, the patient revealed that a week prior to presentation, he was diagnosed with syphilis by his former physician. Her initial diagnosis of syphilis two months ago was polyarthralgia, widespread pruritus, right upper quadrant pain, sore throat, fatigue, “cognac” colored urine, and weight loss. The patient received a single dose of penicillin G benzathine (2.4 million units intramuscularly). Its diagnosis was confirmed by nontreponemal (RPR titer 1:64) and treponemal (IgM fluorescent T pallidum absorbance antibody [FTA-Abs]) tests. The patient underwent blood tests in his primary care office and was noted to have abnormal liver function tests prior to admission (ALP of 722 IU/L, AST of 82 IU/L, ALT of 157 IU/L, albumin of 2.7 g/dL) that preceded the recent initiation of allopurinol, and had normal liver function tests with albumin of 4.2 g/dL, AST of 18 IU/L, ALT of 32 IU/L, and ALP of 55 IU/L in one year. first. Based on these data, DILI secondary to allopurinol was excluded, and syphilitic hepatitis became our primary diagnosis.

The patient’s liver function tests were monitored daily, and the decline in therapy was recorded. He was discharged after six days in the hospital with a final hospital ALP of 461 IU/L, AST of 43 IU/L, and ALT of 79 IU./L (Table 1). The patient was instructed to complete syphilis treatment by his primary care physician who scheduled his remaining two doses in two weeks. He was advised to follow up at our gastroenterology and hepatology clinic to repeat liver function tests and monitor resolution of syphilitic hepatitis.

A Roadmap For Serum Biomarkers For Hepatitis B Virus: Current Status And Future Outlook

Syphilitic hepatitis can be interpreted as a cholestatic pattern of high liver enzymes and serological evidence of treponemal in the absence of other causes of liver failure. The most common cause of liver failure is secondary syphilis. About 3% of cases of secondary syphilis may manifest as syphilitic hepatitis, but among all patients with syphilis, hepatitis occurs in 0.2% to 3% of the population. A literature review of 97 articles by Huang et al. in 2018 it was shown that the most common manifestations of syphilitic hepatitis are itching (78%), fatigue / lack of appetite (57%), icterus (35%), fever (26%), weight loss (23%), stomach . pain (22%), phallodynia (13.4%), sore throat (8.2%), and headache 7.2%. Physical examination revealed hepatomegaly (54%) and lymphadenopathy (31%). Liver tests showed total bilirubin of 8.2 mg/dL, ALT of 314.5 U/L, AST of 253 U/L, ALP of 84.5 U/L, and GGT was 561.8 U/L [5]. Although no clear evidence exists, Mullick et al. A positive diagnosis without disease can be explained by abnormal liver enzyme levels in a cholestatic sample, serological evidence of syphilis, exclusion of other causes of liver disease, and liver enzyme levels returning to normal after therapy. appropriate antibiotic [6] . Our patient showed all four criteria; however, the patient was lost to follow-up before complete results were shown. It is shown that the cholestasis of the liver injury seen in syphilitic hepatitis can be caused by infection through intercourse and the subsequent migration to the portal system and the consumption of fat by causing pericholangial inflammation [3, 7, 8]. This is indirectly supported by evidence showing that syphilitic hepatitis occurs in sexually active HIV-infected individuals (MSM) and syphilitic proctitis is a primary event in some patients [5, 8]. Most cases of syphilitic hepatitis resolve after syphilis treatment. Chronic hepatitis is rare, and a review of the literature shows two cases of liver failure due to syphilis leading to its progression and death [9, 10]. In our case, the patient started syphilis treatment before giving birth, and with the previous data as a baseline (Table 2) we observed a downward trend in liver infection. The patient was subsequently lost to follow-up.

Syphilitic hepatitis is a rare but important cause of abnormal liver enzymes. Syphilis infection should be considered in high-risk patients (with HIV, MSM, and multiple sex partners) with abnormal alkaline levels. The importance of identifying syphilis as a cause of increased liver enzymes is there

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