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Commentary case. By Prof / Fawzy Megahed. A 39-year-old man was admitted to this hospital because of night sweats and abdominal pain. The patient had been well until 1 week before admission, when night sweats developed, which he attributed to the summer heat.
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Commentary case By Prof / Fawzy Megahed
A 39-year-old man was admitted to this hospital because of night sweats and abdominal pain.
The patient had been well until 1 week before admission, when night sweats developed, which he attributed to the summer heat.
Three days before admission,episodes of sharp abdominal pain developed; the pain was greatest at the costal margin on the right side, and the patient rated it at up to 7 on a scale of 0 to 10(with 10 indicating the most severe pain).
The pain lasted up to 2.5 hours, increased with deep breaths, was worse 1 to 2 hours after meals, and was associated with mild nausea, belching, hiccups, bloating, and loose, gray stools. The symptoms did not improve with simethicone or ibuprofen.
On the day of admission,the pain recurred with increased severity, and the patient came to the emergency department at this hospital.
Two weeks before admission, the patient had had a sharp frontal headache for several days after having traveled to a coastal region in the northeastern United States.
He had had psoriasis since 10 years of age and, during the previous year, a few episodes of vertigo with ear fullness, for which he took meclizine, with improvement.
A diagnosis of erythema nodosum had been made 3 years beforeadmission, when he presented with raised, painful nodules on the shins and ankle pain;
1 month later, he had an episode of pain and erythema in the right knee (a synovial-fluid aspirate showed low cell counts and negative cultures).
He also had had cellulitis caused by methicillin-resistant Staphylococcus aureus, anappendectomy, a herniorrhaphy, and a turbinectomy.
He reported no fevers, chills,chest pain, dyspnea, vomiting, melena, hematochezia, new rashes, or bruises.
His only medication was topical clobetasol. He was allergic to trimethoprim–sulfamethoxazoleand hydrocodone. He drank alcohol in moderation and did notsmoke or use illicit drugs.
He was married and worked in a medical facility. His mother had diverticulitis, and his father had hypertension. His siblings werehealthy; he had no children.
the vital signs and oxygen saturation were normal. The abdomen was soft, without distention and with tenderness in the right upper quadrant.The spleen tip was palpable.
There were matted, firm lymph nodes in the inguinal region and hyperpigmented scaly plaques onthe lower legs and waist; the remainder of the examination was normal.
WBC was 5800 per cubic millimeter (reference range, 4500 to 11,000), with 73% neutrophils (reference range, 40 to 70), 14% lymphocytes (reference range, 22 to 44), 6% monocytes (reference range, 4 to 11), and 7% eosinophils(reference range, 0 to 8);
the blood level of C-reactive protein was 9.7 mg per liter (reference range, <8.0, negative for inflammation), and the blood level of (ACE) angiotensin-converting enzyme was 55 U per liter (reference range, 8 to 53).
The remainder of CBC, ESR, and urinalysis were normal, as were results of coagulation and renal and liver-function tests and blood levels of electrolytes, calcium, phosphorus, magnesium, glucose, lactate dehydrogenase, amylase, and lipase.
Testing for human immunodeficiency virus types 1 and 2, hepatitis C virus antibodies, and hepatitis B virus surface antigen was negative; testing for hepatitis B virus surface antibodies was positive.
An electrocardiogram (ECG) showednormal sinus rhythm, with a borderline early repolarizationabnormality and T-wave inversions in leads V1 and V2.
Ultrasonography of the abdomen revealed multiple rounded, hypoechoic areas in the spleen, which was not enlarged,with no evidence of cholelithiasis or cholecystitis.The patient was admitted to the hospital.
Computed tomographic (CT) scans of the abdomen and pelvis, obtained after the administration of contrast material,
showed numerous ill-defined, hypoattenuatinglesions, 1 to 2 cm in diameter in the spleen as well as bilateral, dependent atelectasisin the lungs. A hypoattenuating lesion in theliver, measuring less than 1 cm in diameter, wasslightly increased in size from a study 8 yearsearlier and was thought to represent a cyst;small, nonspecific retroperitoneal and mesenteric lymph nodes were also seen.
A chest radiographshowed an ill-defined opacity in the left apex, overlying the end of the first rib, and a rounded opacity in the left hilar region.
An ultrasound examination of the legs revealed benign- appearing enlarged inguinal lymph nodes,the largest of which was 1.5 cm by 0.6 cm.
The patient’s abdominal pain improved, and he was discharged on the second hospital day.
At a follow-up visit 2 days after discharge,a CT scan of the chest, obtained after the administration of contrast material, showedmediastinal lymphadenopathy, with lymph nodes as large as 1.8 cm in diameter.
The CT scan also showed bilateral hilar lymphadenopathy, an enlarged anterior diaphragmatic lymph node (1.2 cm in diameter), clustered nodular opacities withinthe lung in a perilymphatic distribution
multiple splenic lesions, a hypervascular lesion in the posterior right lobe of the liver, and a hypodense lesion (0.6 cm in diameter) in the leftlobe of the liver, which was thought to represent a hepatic cyst.
the differential diagnosis must focus on the lymphadenopathy detected on examination,the abnormal findings seen on CT scans, and the history.
1- Lymphoma2- Sarcoidosis3- Tuberculosis4- Endemic fungal infection5- Granulomatous polyangiitis
we need to include lymphoma inour differential diagnosis given the presence of widespread enlarged lymph nodes and the development of night sweats, and abnormal findings in the spleen,.
Also there were number of studies suggest that patients with psoriasis have an increased risk of lymphoma
the presence of lymphadenopathyand the history of erythema nodosum may point toward a diagnosis of sarcoidosis.
The combination of erythema nodosum and ankle pain shouldraise the possibility of a diagnosis of Löfgren’s syndrome, although the presence of hilar lymphadenopathyis generally also required for this diagnosis.
Löfgren’s syndrome is a form of sarcoidosis that is characterized by the triad of erythema nodosum, arthralgias, and hilar lymphadenopathy;it is usually self-limited, although its manifestations may persist for several years.
A small number of patients with Löfgren’s syndrome have normal chest radiographs at the time of diagnosis; most patients have hilar lymphadenopathy,13% of patients have respiratory symptoms, and 4% of patients have peripheral lymphadenopathy. Furthermore, 6% of patients have a recurrenceof sarcoidosis within 18 months to 20 yearsafter presenting with Löfgren’s syndrome.
Gastrointestinal manifestations of sarcoidosis primarily involve the stomach, and patients can present with abdominal pain, nausea, vomiting, and weight loss
Headaches, such as the one thispatient reportedly had during the weeks before admission, are sometimes a manifestation ofsarcoidosis.The patient’s hypoattenuating spleniclesions are consistent with sarcoidosis.
We still need to consider the minimally elevated blood level of ACE. When the ACE level is less than 25 U per liter, the likelihood ratio for sarcoidosis is 0.12; when the ACE level is between 25 and 71 U per liter, the likelihood ratio is 1.31; and when the ACE level is greater than 71 U per liter, the likelihood ratio increases to7.15.
This patient had an ACE level of 55 U per liter, and therefore the probability of sarcoidosis was slightly increased, although the clinical and radiographic findings already made sarcoidosis an overwhelmingly likely diagnosis.
The diagnostic procedure in this case was bronchoscopy with endobronchial ultrasound- guided needle biopsies