Clear As Mud: A Case of Peripheral Neuropathy and Weakness in an Hiv Patient

1UTHSCSA, San Antonio, TX

Meeting: Hospital Medicine 2015, March 29-April 1, National Harbor, Md.

Abstract number: 549


Case Presentation:
31 year-old Hispanic male with history of HIV presented to the hospital with a 5-month history of progressive pain and weakness in bilateral upper and lower extremities. Review of systems was also significant for subjective fevers, chills, weight loss, loss of hair in his forearms as well as alopecia, hearing loss, and stiffness in his fingers and ankles. He had become so weak that he was unable to ambulate on presentation.
Physical exam revealed scaling of his scalp, desquamation of the palms, and contractures of his distal interphalangeal joints. He had diffuse symmetric weakness in his upper and lower extremities, worst in his legs with bilateral foot drop. He had diminished deep tendon reflexes, and diminished sensation in symmetric stocking-glove pattern.
On laboratory studies, patient’s CD4 count and viral load were 210 and 145K. His RPR was reactive with 1:4096 titer with a positive treponemal antibody.  LP was remarkable for low glucose (26mg/dL), high protein (156mg/dL), with 47 total WBC’s (lymphocytic predominant at 95%), negative gram stain/culture, and +VDRL with 1:16 titer. CT head without contrast and MRI with and without contrast were normal. 
Patient was started on treatment for neurosyphilis with IV Penicillin G 24 million units continuous infusion. However, given how extensive his weakness was, EMG was done and showed electrodiagnostic evidence of a profound generalized axonal and demyelinative sensorimotor peripheral polyneuropathy. Neurology was consulted, began treatment with IVIG, and patient received 2 doses prior to discharge. His symptoms were thought to be due to chronic inflammatory demyelinating polyneuropathy, and with treatment, had partial remission with ability to walk at 2-month follow-up.
Chronic inflammatory demyelinating polyneuropathy is thought to be immunologically based, and has a well-established association with systemic disease such as HIV. Compared with AIDP, which reaches its peak illness in 3-4 weeks, CIDP continues to progress or have relapses for more than 8 weeks.  AIDP occurs most often at the time of HIV seroconversion while CIDP can occur at any phase of HIV disease. The hallmark of CIDP is symmetric weakness in both proximal and distal muscle groups, with a larger motor than sensory deficit. Sensory involvement tends to follow a distal to proximal gradient, with painful dysesthesias in some cases. A critical component of CIDP evaluation is electrodiagnostic testing to assess for demyelination. In severe cases, IVIG has the largest trials showing efficacy in treatment, with recommended dose of 2g/kg over 2-5 days. 
When neurologic symptoms are not fully explained by presumed diagnosis of neurosyphilis in a patient with HIV, other diagnoses such as CIDP should be considered. An EMG showing demyelination in these cases could be very helpful, benign, and in our case, saved our patient from permanent debility.

To cite this abstract:

Jamaleddine R, Crawford G. Clear As Mud: A Case of Peripheral Neuropathy and Weakness in an Hiv Patient. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 549. Journal of Hospital Medicine. 2015; 10 (suppl 2). Accessed March 28, 2020.

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