Hepatitis B is a global problem and approximately there are 248 global carriers and 60,000 among them die every year because of liver-related diseases. Although the overall prevalence of HBsAg is 3.6%, it varies according to the geographical area. Moreover, the prevalence of chronic HBV is less than 2% in low prevalence areas and 2-7% in areas with intermediate prevalence. It can transmit from the mother to the child, sexually, through transfusion, and transplant.
Furthermore, the clinical manifestation of HBV varies based on whether it is acute or chronic. The manifestations of the acute phase are subclinical or anicteric hepatitis to icteric hepatitis. However, in some cases, it can be fulminant hepatitis. The manifestations can range from asymptomatic carrier states to chronic hepatitis. In the chronic phase, it can also be cirrhosis and hepatocellular carcinoma.
Acute Icteric Hepatitis B
It is also possible for a serum-sickness-like syndrome to develop during the prodromal period in acute icteric hepatitis B. Moreover, constitutional symptoms are also seen. For example, anorexia, vomiting, nausea, and discomfort in the right upper quadrant. The signs of jaundice disappear in one to three months. However, fatigue may be seen even after the serum aminotransferase concentration is normalized.
Extrahepatic manifestations are also seen but they are more common with chronic hepatitis B infection. They are rarely seen in acute HBV in association with extrahepatic conditions. The conditions include serum sickness-like syndrome, polyarteritis nodosa, polyarthritis, dermatologic conditions, and cryoglobulinemia. Furthermore, neurological, and pathological conditions are also seen.
Relationship Between Acute Hepatitis B and Acute Myopathy
There is no literature on the relationship between acute Hepatitis B and acute myopathy. The systemic diseases causing myopathy are metabolic or inflammatory disorders. They also include paraneoplastic, drug, or endocrine-related diseases or infections. Moreover, viral infections can also commonly cause myopathies.
Approximately 5% of the patients suffer from the development of neuropathy with chronic HBV. It rarely happens in acute HBV infection. Furthermore, muscle disease is linked with inflammatory myopathy. Hence, this case that has been presented is the first one with acute Hep B, which coexists with acute myopathy.
A 57-year-old Iranian female was given referral to visit the infectious disease department at a local hospital for fever, jaundice, abdominal pain, body itch, muscle weakness that was progressive, in addition to pain for one week.
Doctors did a physical exam and found that she has an icteric sclera, pain in the right upper quadrant, and a reduction in muscle force. She had a ten-year history of diabetes mellitus. Moreover, she had hyperlipidemia, hypothyroidism, and diabetic foot around five months ago. She had also been using insulin for two years. Her admission to the hospital was based on the diagnosis of acute hepatitis and myopathy. However, due to strain consumption, she did not have serum creatinine kinase elevation.
The muscle strength was 4 out of 5 in the upper and 2 out of 5 in the lower limbs when she was admitted. However, a day into hospitalization, she developed urinary retention, requiring catheterization. It led to severe muscle weakness, and she could not walk or defecate. Neurological and rheumatological examination showed that the muscle force and strength are decreased in the gluteal muscle and external anal sphincter. Her initial diagnosis was acute hepatitis, rhabdomyolysis, and statin toxicity. Moreover, the labs were positive for HBV Ag and the viral load level was high. However, tests for other hepatitis viruses were negative. The first labs showed an increase in ALT, AST, alkaline phosphate, CK, bilirubin, LDH, ferritin, and aldolase. Although the results showed improvement without any medications after fourteen days.
Other Labs and Examinations
Ultrasound abdomen revealed mild hepatomegaly and splenomegaly. The urine analysis was negative for myoglobin and the EMG/NCV showed acute myopathic process and chronic sensorimotor polyneuropathy. Chronic sensorimotor polyneuropathy was due to diabetes mellitus.
Moreover, all rheumatological tests were negative. Furthermore, copper urine and blood, TIBC, and ceruloplasmin were within normal. Blood culture, Wright, and Coombs Wright were also negative. In addition, urine analysis for myoglobinuria was also negative, which ruled out rhabdomyolysis.
Doctors did not give the patient any treatment and her hepatitis along with her muscle strength gradually improved. Moreover, she could walk with a walker after being discharged. She was discharged on the 19th day with a good condition generally. The diagnosis at the discharge was coexisting acute hepatitis B and myopathy, which was a complication of viral hepatitis B.
She was followed up on day 30 and a year later. She showed complete recovery according to her test results.
Hepatitis B can trigger immune-mediated syndromes. For example, peripheral neuropathy and myopathy. It can invade the muscle fibres directly and cause myopathy.