An Atypical Cause of Gastrointestinal Bleeding
Nicolai Wennike, MRCP(UK); Tim Battcock, MBChB, FRCP; Andrew J. Bell, MA, MB, FRCP, FRCPath
Nicolai Wennike, MRCP(UK); Tim Battcock, MBChB, FRCP; Andrew J. Bell, MA, MB, FRCP, FRCPath
Background
A 53-year-old man who was diagnosed with multiple myeloma (IgAê) 18 months ago is admitted to the hospital via the emergency department (ED) with a 1-week history of melena, hematemesis, and lethargy. There is no associated weight loss, abdominal pain, dysphagia, or history of upper gastrointestinal (GI) hemorrhage. The patient has no risk factors for peptic ulcer disease, does not drink alcohol or smoke, and is not regularly taking any medications (including no recent nonsteroidal anti-inflammatory drugs [NSAIDs] or steroid use). He has no allergies of note, and his family history and social history are unremarkable. Other than multiple myeloma, which resulted in spinal cord compression that required radiotherapy (with full resolution of symptoms), the patient has no significant past medical history. He has not needed chemotherapy to date. On direct questioning, he does not describe any symptoms suggestive of active multiple myeloma and organ involvement.
On presentation, the patient appears clinically well, with no evidence of anemia, jaundice, lymphadenopathy, or peripheral signs of GI disease. He is hemodynamically stable, with a pulse of 90 bpm, blood pressure of 150/70 mm Hg (with no postural blood pressure drop), and a urine output of approximately 30 mL/hr. On examination, there is no evidence of active GI bleeding, his abdomen is soft and without any peritonitis or organomegaly, and a rectal examination shows evidence of melena, with no masses and a normal-sized prostate. His respiratory examination is unremarkable, with a clear chest and no evidence of aspiration pneumonia. The cardiac and neurologic examinations reveal nothing of significance.
The initial laboratory examinations show a hemoglobin of 8.5 g/L (0.85 g/dL); a low mean corpuscular volume (79 fL), with an iron deficiency picture; a normal international normalized ratio of 1.0; and mild dehydration, with urea nitrogen 10.1 mmol/L (28.29 mg/dL), creatinine 160 Gmol/L (1.81 mg/dL), sodium 136 mmol/L (136 mEq/L), and potassium 3.9 mmol/L (3.9 mEq/L). Liver tests showed a normal screen with alanine aminotransferase 30 U/L, albumin 40g/L (4 g/dL), alkaline phosphatase 50 U/L, and bilirubin 12 Gmol/L (0.70 mg/dL). The patient is treated with intravenous fluid and 2 units of blood. He remains hemodynamically stable and is subsequently able to undergo an esophagogastroduodenoscopy (see Figure 1).
Discussion
Biopsies of the polyps taken at the time of the endoscopy showed evidence of multiple myeloma type IgA ê. Multiple myeloma is a debilitating malignancy that is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. First documented in 1848, multiple myeloma is a disease characterized by a clonal proliferation of malignant B cells in the bone marrow (in which the predominant cell type is plasma cells) that results in an overabundance of monoclonal paraprotein. It is predominantly a disease of the elderly (median age: 60 years), with an incidence of 9.5 per 100,000 population and a slight male predominance.
It is the second most common hematologic cancer (10%), representing 1% of all cases of cancer; despite new advances,multiple myeloma still carries a poor prognosis, with a median survival of 2-3 years. The pathophysiology of multiple myeloma is that of a chromosomal translocation between the immunoglobulin heavy-chain gene (on the 14th chromosome, locus 14q32) and an oncogene (often 11q13, 4p16.3, 6p21, 16q23, or 20q11). This mutation results in dysregulation of the oncogene, which is thought to be an important initiating event in the pathogenesis of myeloma. The result of this mutation is proliferation of a plasma cell clone and genomic instability that leads to further mutations and translocations. The chromosome 14 abnormality is observed in about 50% of all myeloma cases; the other 50% of cases result from a deletion of (parts of) the 13th chromosome. The resulting plasma cells produce cytokines (especially interleukin [IL]-6) that cause osteopenia and create an environment for malignant cells to thrive.
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A 53-year-old man who was diagnosed with multiple myeloma (IgAê) 18 months ago is admitted to the hospital via the emergency department (ED) with a 1-week history of melena, hematemesis, and lethargy. There is no associated weight loss, abdominal pain, dysphagia, or history of upper gastrointestinal (GI) hemorrhage. The patient has no risk factors for peptic ulcer disease, does not drink alcohol or smoke, and is not regularly taking any medications (including no recent nonsteroidal anti-inflammatory drugs [NSAIDs] or steroid use). He has no allergies of note, and his family history and social history are unremarkable. Other than multiple myeloma, which resulted in spinal cord compression that required radiotherapy (with full resolution of symptoms), the patient has no significant past medical history. He has not needed chemotherapy to date. On direct questioning, he does not describe any symptoms suggestive of active multiple myeloma and organ involvement.
On presentation, the patient appears clinically well, with no evidence of anemia, jaundice, lymphadenopathy, or peripheral signs of GI disease. He is hemodynamically stable, with a pulse of 90 bpm, blood pressure of 150/70 mm Hg (with no postural blood pressure drop), and a urine output of approximately 30 mL/hr. On examination, there is no evidence of active GI bleeding, his abdomen is soft and without any peritonitis or organomegaly, and a rectal examination shows evidence of melena, with no masses and a normal-sized prostate. His respiratory examination is unremarkable, with a clear chest and no evidence of aspiration pneumonia. The cardiac and neurologic examinations reveal nothing of significance.
The initial laboratory examinations show a hemoglobin of 8.5 g/L (0.85 g/dL); a low mean corpuscular volume (79 fL), with an iron deficiency picture; a normal international normalized ratio of 1.0; and mild dehydration, with urea nitrogen 10.1 mmol/L (28.29 mg/dL), creatinine 160 Gmol/L (1.81 mg/dL), sodium 136 mmol/L (136 mEq/L), and potassium 3.9 mmol/L (3.9 mEq/L). Liver tests showed a normal screen with alanine aminotransferase 30 U/L, albumin 40g/L (4 g/dL), alkaline phosphatase 50 U/L, and bilirubin 12 Gmol/L (0.70 mg/dL). The patient is treated with intravenous fluid and 2 units of blood. He remains hemodynamically stable and is subsequently able to undergo an esophagogastroduodenoscopy (see Figure 1).
Discussion
Biopsies of the polyps taken at the time of the endoscopy showed evidence of multiple myeloma type IgA ê. Multiple myeloma is a debilitating malignancy that is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. First documented in 1848, multiple myeloma is a disease characterized by a clonal proliferation of malignant B cells in the bone marrow (in which the predominant cell type is plasma cells) that results in an overabundance of monoclonal paraprotein. It is predominantly a disease of the elderly (median age: 60 years), with an incidence of 9.5 per 100,000 population and a slight male predominance.
It is the second most common hematologic cancer (10%), representing 1% of all cases of cancer; despite new advances,multiple myeloma still carries a poor prognosis, with a median survival of 2-3 years. The pathophysiology of multiple myeloma is that of a chromosomal translocation between the immunoglobulin heavy-chain gene (on the 14th chromosome, locus 14q32) and an oncogene (often 11q13, 4p16.3, 6p21, 16q23, or 20q11). This mutation results in dysregulation of the oncogene, which is thought to be an important initiating event in the pathogenesis of myeloma. The result of this mutation is proliferation of a plasma cell clone and genomic instability that leads to further mutations and translocations. The chromosome 14 abnormality is observed in about 50% of all myeloma cases; the other 50% of cases result from a deletion of (parts of) the 13th chromosome. The resulting plasma cells produce cytokines (especially interleukin [IL]-6) that cause osteopenia and create an environment for malignant cells to thrive.
DOWNLOAD COMPLETE PDF HERE
oh i think this thing is serious, imagine if we all have that! we should always be aware