ABSTRACT
Hypertriglyceridemia is the third most common etiology for acute pancreatitis (AP), after alcohol and gallstones. Clinical evidence is relatively weak in its support of plasmapheresis for the treatment of hypertriglyceridemia-induced acute pancreatitis (HTG-AP). We report a case of severe HTG-AP in a young man who was successfully treated with plasmapheresis. The patient achieved full resolution of symptoms within 48 hours from presentation and was discharged two days later. To our knowledge, no other report in literatures shows such dramatic response to plasmapheresis.
ABSTRACT
Nephrogenic ascites is described as a clinical condition of refractory ascites in patients with end-stage renal disease (ESRD) on renal replacement therapy. This entity was first described in 1970. Many nephrologists do not believe in nephrogenic ascites. The underlying etiologies can be multifactorial including a combination of poor nutrition, inadequate dialysis and ultrafiltration, increased peritoneal membrane permeability, and overall uremia. The nephrogenic ascites is a rare syndrome and is often associated with a grave prognosis especially if it is not diagnosed early and treated. In the present study, we report a 27-year-old woman with past medical history of diabetes type 1 (diagnosed at age 11), ESRD secondary to diabetic nephropathy on hemodialysis (diagnosis in December 2017), bilateral diabetic retinopathy, ovarian cyst, hypertension, and anxiety who presented to the emergency department for evaluation of intractable abdominal pain, nausea and vomiting for 2-day duration. She was found to have large ascites. Diagnostic paracentesis was done and found to be exudative with serum ascites albumin gradient (SAAG) of 0.7. After detailed workup, hepatic, cardiac, infectious and malignant causes for ascites were ruled out. The diagnosis of ascites of nephrogenic origin was made. Given the patient's situation and her inability of self-care, she is not a good candidate for intra-abdominal dialysis. The patient has been treated conservatively with salt/fluid restriction and intensive hemodialysis with ultrafiltration.
ABSTRACT
In the present study, we report a case of multiple coronary artery ectasias (CAE) and multiple intracranial arterial dolichoectasias (IADEs). A 60-year-old female presented to the emergency department twice with chest pain and mild elevation of troponin and T-wave changes. Peripheral coronary angiography showed severe ectasia and stenosis of certain segments of the left main coronary artery (LMCA), left anterior descending (LAD), first obtuse marginal (OM1), distal left circumflex (LCX), and bilateral subclavian arteries. The patient was treated medically. Two weeks later, she presented with dizziness. Head computerized tomography (CT) angiography showed severe IADE involving the vertebrobasilar system, intracranial internal carotid arteries, and bilateral middle cerebral arteries. No neurovascular intervention was performed due to the complexity of the findings. CAE is an abnormal dilatation of a coronary artery segment of at least 1.5 times the size of a normal coronary artery. The slow flow phenomenon may lead to ischemia and thrombosis, which can result in acute coronary syndrome. IADE comprises a dilatation and elongation of the arteries that affects both the anterior and posterior cerebral circulation, often causing neurological complications such as ischemic stroke, intracranial hemorrhage, or compression of surrounding neural structures. We report this case due to the rarity of coexisting IADE and CAE. A rarefaction of elastic tissue of the media with degeneration of the internal elastic lamina, in addition to matrix metalloproteinase dysfunction, is a common pathological mechanism for this condition. The management of CAE and IADE is mostly conservative, essentially treating the risk factors and administering antiplatelet and anticoagulant agents. In some patients, angioplasty vs. surgical treatment may be applied.
ABSTRACT
Seventeen year old girl, a known case of Wilson disease presented to us with a non-healing skin ulcer followed by appearance of jaundice, ascites and progressive fatigue of 1 month duration. She was diagnosed to have Wilson disease 5 years back and had been well controlled on d-penicillamine. On enquiry, she was found to be noncompliant with her medication in the preceding 6 months. On examination, she had severe pallor, icterus with moderate ascites and oedema feet. Investigations revealed severe haemolytic anemia and deranged liver function. The lesion was diagnosed to be pyoderma gangrenosum on skin biopsy. The appearance of a cutaneous lesion followed by deterioration in the liver disease and hemolysis suggested uncontrolled Wilson disease as the triggering factor. Chelation therapy improved her haemoglobin and liver function as well as led to healing of the ulcer. We describe pyoderma gangrenosum as a new manifestation of Wilson disease.
