A 30-year-old man comes to the office with fatigue and lethargy that has worsened over the last 2 weeks. He has been forgetful lately and feels "exhausted" at the end of the day. The patient works as a contractor and is currently renovating old houses for sale. He describes feeling "clumsy" and dropping things at work, as well as tripping multiple times while climbing stairs. He also has abdominal pain that he attributes to constipation. The patient drinks 1 or 2 beers each weekend and does not use tobacco or illicit drugs. His mother was diagnosed with lupus and his older sister had thyroid surgery. Blood pressure is 120/80 mm Hg, and pulse is 76/min. Examination shows normal jugular venous pressure, no thyromegaly, clear lung fields, and normal first and second heart sounds. The abdomen is soft and nontender. There is no hepatomegaly or splenomegaly. There is weakness on dorsiflexion of bilateral wrists and feet. Upper and lower limb deep tendon reflexes are 1+. Laboratory results are as follows: Creatine phosphokinase levels are normal. Which of the following is most likely to improve this patient's symptoms?

Question

A 30-year-old man comes to the office with fatigue and lethargy that has worsened over the last 2 weeks.  He has been forgetful lately and feels "exhausted" at the end of the day.  The patient works as a contractor and is currently renovating old houses for sale.  He describes feeling "clumsy" and dropping things at work, as well as tripping multiple times while climbing stairs.  He also has abdominal pain that he attributes to constipation.  The patient drinks 1 or 2 beers each weekend and does not use tobacco or illicit drugs.  His mother was diagnosed with lupus and his older sister had thyroid surgery.  Blood pressure is 120/80 mm Hg, and pulse is 76/min.  Examination shows normal jugular venous pressure, no thyromegaly, clear lung fields, and normal first and second heart sounds.  The abdomen is soft and nontender.  There is no hepatomegaly or splenomegaly.  There is weakness on dorsiflexion of bilateral wrists and feet.  Upper and lower limb deep tendon reflexes are 1+.  Laboratory results are as follows:  Creatine phosphokinase levels are normal.  Which of the following is most likely to improve this patient's symptoms?

Quizplus · Accepted Answer

Explanation: 11ec25c8_d0f9_2b99_bc81_abe111d620ab_MD0003_00 This patient likely has acute lead toxicity from exposure to lead-based paint given his recent work renovating old houses. His constellation of clinical manifestations, including nonspecific findings (eg, fatigue), consists of: Gastrointestinal manifestations: Constipation Neuropsychiatric manifestations: Sensorimotor neuropathy (eg, weakness with dorsiflexion), short-term memory loss Hematologic manifestations: Microcytic anemia (often with basophilic stippling on peripheral smear), hyperuricemia (due to impaired purine metabolism) Chronic lead toxicity can cause hypertension, nephropathy, and more pronounced neuropsychiatric symptoms (eg, psychosis). Lead is absorbed predominantly via the lungs in adults. It is stored predominantly in the skeleton and is released slowly, exerting its pathologic effects over decades. Diagnosis depends on establishing a history of lead exposure accompanied by corroborating physical examination findings (eg, neurologic manifestations) and elevated blood lead levels. The treatment for symptomatic lead poisoning is chelation therapy with an agent such as calcium disodium EDTA. It is important to separate the patient from further lead exposure as the chelating agent may otherwise increase lead absorption from the source. (Choice A) Allopurinol is a xanthine oxidase inhibitor used as urate-lowering therapy to prevent recurrent gout. This patient has hyperuricemia from lead-induced inhibition of purine synthesis, but no inflammatory arthritis suggestive of gout. Urate-lowering therapy would be unlikely to improve the neuropsychiatric and other symptoms related to lead toxicity. (Choices C and F) Cobalamin (vitamin B₁₂) deficiency (pernicious anemia, post-gastrectomy syndrome, intestinal malabsorption) causes macrocytic (not microcytic) anemia and subacute combined degeneration (eg, spasticity, incontinence, paraplegia). Thiamine (vitamin B₁) deficiency, seen with alcohol abuse and white rice/cereal-based diets, manifests as Wernicke-Korsakoff syndrome (eg, nystagmus, ophthalmoplegia, ataxia, confabulation) or beriberi (eg, distal and symmetric peripheral neuropathy, cardiomyopathy). ₁₂ ₁ (Choice D) Hypothyroidism can cause a sensory neuropathy and may be associated with motor weakness and hyperuricemia. However, anemia due to hypothyroidism is generally either normocytic or macrocytic, without reticulocytosis. (Choice E) Plasmapheresis improves outcomes in patients with severe Guillain-Barré syndrome. Although the syndrome presents with progressive motor neuropathy and decreased/absent deep-tendon reflexes, the sensory and cognitive deficits are usually milder than those in this patient, and there is no direct association with hyperuricemia or microcytic anemia. Educational objective: Chronic lead toxicity presents in adults with neuropsychiatric, gastrointestinal, and general symptoms, including peripheral sensorimotor neuropathy, fatigue, abdominal pain, and constipation. It can lead to hypertension, nephropathy, hyperuricemia, and microcytic anemia with basophilic stippling seen on peripheral smear. Treatment for symptomatic patients involves chelation therapy with an agent such as calcium disodium EDTA. References: Evaluation and management of lead exposure. (http://www.ncbi.nlm.nih.gov/pubmed/26677413)

A 30-Year-Old Man Comes to the Office with Fatigue and Lethargy