Cases reported "Vitamin B 12 Deficiency"

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1/4. Recurrent urinary tract infections and genitourinary tract abnormalities in the Imerslund-Grasbeck syndrome.

    Two Imerslund-Grasbeck patients who presented with recurrent urinary tract infections and genitourinary abnormalities are described. The patients were evaluated with abdominal ultrasounds, voiding cystourethrograms, and Schilling tests. Each patient had large postvoid residual urine secondary to a motor-neurogenic bladder. One had a duplication of the distal urethra manifesting as two meatal openings. There was lack of urinary excretion of radioactive vitamin B12 on Schilling tests in both patients. patients with Imerslund-Grasbeck syndrome may be predisposed to urinary tract infections because of incomplete bladder emptying. Complete physical and radiological examinations of the genitourinary tract should be performed.
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2/4. Cases from the Osler Medical Service at Johns Hopkins University.

    A 50-year-old African American woman presented with bilateral lower extremity pain, a history of falls during the past several months, and personality and behavior changes. She had been in good health until approximately 5 months before admission, when she began to fall with increasing frequency, often while going down a flight of stairs. She described these falls as her "legs giving out" and feeling very heavy and unsteady. There was no head trauma or loss of consciousness. Her daughter noticed that her gait had become somewhat unsteady during the last several months. Her family also noted a change in her personality at this time. Previously, she had been a very tidy person who took great care with her appearance, who was working as a customer service representative. However, she had become less social and very withdrawn. She had been observed putting on dirty clothes after showering, as well as eating constantly. The patient denied any fevers, chills, night sweats, headaches, vision changes, or tinnitus. She also denied any rashes, muscle pain, or intolerance to heat or cold. There was no history of seizure disorder or depression. Her past medical history was notable only for hypertension and being a passenger in a motor vehicle crash 1 year before admission. She denied any alcohol, tobacco, or illicit drug use, and had no travel history other than coming to the united states, as she was originally from Trinidad.On physical examination, she was a moderately obese African American woman with a flat affect, psychomotor slowing, and alopecia of the scalp. She was alert and oriented to person, place, and time, but had a score of 26 out of 30 on the Mini-Mental State Examination. She lost points only for recall; she had no difficulty with serial 7s. Her cranial nerves were intact and her speech was fluent, although sparse, and she did not make any paraphasic errors. Her muscle strength was 5/5 in both the upper and lower extremities. Reflexes were 2 in the upper extremities and 1 in the lower extremities, and toes were downgoing bilaterally. She had intact sensation to light touch and pinprick, but markedly diminished proprioception of her lower extremities bilaterally. She had a wide-based gait with a positive Romberg sign and was markedly ataxic. Rectal examination yielded a positive guaiac test with brown stool, normal tone, and no masses. The remainder of the physical examination was normal.Laboratory studies revealed pancytopenia with a hematocrit of 22.7% and a mean corpuscular volume of 118.2 fL. A peripheral smear that was performed on admission, prior to transfusion, revealed macrocytic red cells and hypersegmented neutrophils.
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3/4. hyperhomocysteinemia masquerading as pulmonary embolism.

    We describe a 30-year-old male who presented with acute onset of breathlessness, tachycardia, and palpitations associated with distension of jugular vein and clear lungs on physical examination. The chest X-ray was normal and ECG was showing S1Q3T3 and right ventricular strain pattern. His 2-D echocardiography was showing dilated right atrium, right ventricular dilatation and moderate pulmonary arterial hypertension. He was found to have thrombosis involving left side of deep venous system with normal superficial venous system (Doppler proved). All routine blood investigations for etiology of recurrent DVT were normal except serum homocyteine level, which was significantly raised. Megaloblastic anemia on peripheral smear and hyperhomocysteinemia prompted us to search for its cause, which was subsequently found to be vitamin B12 deficiency. Such an association of megaloblastic anemia due to vitamin B12 deficiency leading to hyperhomocysteinemia and subsequent thrombosis in left venous system presenting as acute pulmonary embolism has not been described earlier in the medical literature.
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4/4. A case of encephalomyelopolyneuropathy in vitamin B12 deficiency.

    A case of a 44-years-old patient with unusual clinical presentation of encephalomyelopolyneuropathy in vitamin B12 deficiency is presented. The disease manifested itself with gastrointestinal bleeding, which necessitated emergency hospitalisation in surgical clinic. Clinical examinations revealed atrophic gastritis, pernicious anemia, neurological and mental complications. The diagnosis was made according to the following criteria: physical examination--smooth tongue, atrophic gastritis, mild hepatosplenomegaly; laboratory findings--pernicious anemia, low vitamin B12 serum levels; neurological examination--syndrome of combined damage of the posterior and lateral columns of the spinal cord; magnetic resonance imaging--typical hyperintense areas on T2-weighted images in the posterior columns in the cervical regions of the spinal cord; transcranial magnetic stimulation--prolonged central motor conduction time of the motor evoked potentials bilaterally; psychological examination--cognitive decline. After treatment with vitamin B12 an improvement of the hematological findings, neurological deficit and cognitive impairments was found. CONCLUSION: Neurological complications could be an early manifestation of vitamin B12 deficiency. In diagnostic aspect similar complaints require examination of the serum levels of vitamin B12. The delay in diagnosis and inadequate therapy bear the risk of incomplete recovery of the neurological deficit. The current problem of "cognitive decline" necessitates routine examination of the serum levels of vitamin Bl2 in all patients with initial cognitive impairments and their prompt and approapriate treatment.
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ranking = 12.434612698025
keywords = physical examination, physical
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