A Case of Liquorice-Infused Marijuana Causing Syndrome of Apparent Mineralocorticoid Excess.

Marijuana has long been used both for recreational and medicinal purposes. Most of the available forms of marijuana contain additives such as liquorice to enhance its flavour. Liquorice increases the amounts of cortisol in the body and produces metabolic abnormalities seen in primary hyperaldosteronism[1]. Liquorice extracts are mixed with marijuana in the same way as for tobacco[2,3]. We describe a case of apparent mineralocorticoid excess due to excessive smoking of liquorice-laced marijuana. To our knowledge, this is the first reported case of apparent mineralocorticoid excess caused by marijuana use. LEARNING POINTS: First report of liquorice-laced marijuana causing syndrome of apparent mineralocorticoid excess (SAME).Since its legalisation, marijuana is reported to be the most used substance second only to alcohol. With the increased availability of marijuana, the health care providers and consumers must be cognisant of its side effects.It is a dose-dependent phenomenon. The effects vary from minor clinical symptoms to fatal arrhythmias based on the amount consumed.

Pleurisy secondary to nonthrombotic pulmonary emboli in a patient with intravenous drug use.

Patients with injection drug use can have nonthrombotic pulmonary emboli (NTPE) of foreign insoluble particles that are either parts of the equipment used or mixed with the drug as an additive. These foreign particles can become a nidus for infection and inflammation. We present a case of a 31-year-old man with active intravenous drug use who initially presented with signs and symptoms of pleurisy and was found to have NTPE of septic refractile crystalline material as seen on bronchial wash and brush biopsy. We believe our patient likely had embolism of either crack particles, needle fragments or cotton-wool fragments that led to a localized inflammatory reaction and infection. This highlights the importance of obtaining detailed history and diagnostic workup. Once the diagnoses of bacterial endocarditis and thrombophlebitis are ruled out with blood cultures, transthoracic echocardiogram, trans-esophageal echocardiogram and/or CT scan (depending on the suspicion), NTPE should be considered and bronchoscopy with bronchoalveolar lavage with biopsy should be performed.

A Rare Case of Pancreatic Ascites Secondary to Chronic Pancreatitis.

Pancreatic ascites refer to continuous leakage of pancreatic secretions in the peritoneum leading to accumulation of pancreatic fluid in the peritoneal cavity. Although literature on the incidence of pancreatic ascites and presenting signs and symptoms is scarce, it may be seen in patients with chronic alcoholic pancreatitis. Patients typically present with acute chronic pancreatitis and new-onset ascites, with or without abdominal pain. A diagnostic paracentesis is usually the first step to determine the etiology of the ascites. Mild cases may resolve with conservative management. Optimization of nutrition status is an important factor to reduce morbidity and mortality. More severe cases or cases refractory to conservative management may require endoscopic or surgical intervention. This case report describes a rare presentation of pancreatic ascites in a 35-year-old female.

Fibroid degeneration in a postmenopausal woman presenting as an acute abdomen.

Uterine fibroid, one of the most common tumors in women, is estrogen dependent, which commonly regresses after menopause. Fibroid degeneration after menopause, therefore, is rare. Here the authors report a case of 56-year-old postmenopausal woman who presented with acute abdominal pain, low grade fever, and leukocytosis as a result of fibroid degeneration.

IgM Myeloma or Waldenstrom's Macroglobulinemia Is the Big Question?

ABSTRACT: Although critical from therapeutic and prognostic perspectives, differentiating IgM Myeloma (MM) from Waldenstrom's macroglobulinemia (WM) is fraught with failure. WM can usually be distinguished from IgM MM by the lymphoplasmacytic versus pure plasmacytic morphology, absent versus present lytic bone lesions, and immunophenotypic findings. However, all these features have their own limitations; hence, it requires constant vigilance and periodic re-evaluation. Here we describe a case of a 70-year-old woman initially diagnosed as smoldering IgM MM, who eventually turned out to have WM.

T cell acute lymphoblastic leukaemia presenting with sudden onset right oculomotor nerve palsy with normal neuroradiography and cerebrospinal fluid studies.

Leptomeningeal disease presenting with neurological dysfunction is not uncommon in leukaemia. However, it is often accompanied by abnormalities in cerebrospinal fluid (CSF) studies and/or neuroradiography. Here, the authors describe a case of a young patient presenting with sudden onset right oculomotor nerve palsy with normal neuroradiography and CSF studies, who was subsequently diagnosed to have T cell acute lymphoblastic leukaemia (T-ALL). This case highlights that neurological manifestations can be the initial presenting feature of T-ALL and can occur suddenly despite normal neuroradiography and initial CSF studies.

A 20-year-old Chinese man with recurrent hypokalemic periodic paralysis and delayed diagnosis.

Periodic paralysis in the setting of hypokalemia can be the result of several underlying conditions, requiring systematic evaluation. Thyrotoxic periodic paralysis (TPP), a curable cause of hypokalemic periodic paralysis, can often be the first manifestation of thyrotoxicosis. Because the signs and symptoms of thyrotoxicosis can be subtle and clouded by the clinical distress of the patient, the diagnosis of the underlying metabolic disorder can be overlooked. The authors report a case of TPP in a young Chinese man in whom the diagnosis of thyrotoxicosis was initially missed. This case illustrates the lack of awareness of TPP among many physicians, delay in the diagnosis of TPP and the importance of performing thyroid function testing in all cases of periodic paralysis.

Serum lipoprotein levels in takotsubo cardiomyopathy vs. myocardial infarction.

BACKGROUND: In the setting of myocardial infarction (MI) or acute coronary syndrome (ACS), current guidelines recommend early and aggressive lipid lowering therapy with statins, irrespective of the baseline lipoprotein levels. Takotsubo cardiomyopathy (TCM) patients have a clinical presentation similar to myocardial infarction and thus receive early and aggressive statin therapy during their initial hospitalization. However, the pathology of TCM is not atherosclerotic coronary artery disease and hence we assumed the lipid profiles in TCM would be healthier than coronary artery disease patients. METHODS: In this retrospective study, we assessed fasting serum lipoprotein levels of ten TCM patients and compared them with forty, age and sex-matched myocardial infarction (MI) patients. RESULTS: Comparing serum lipoprotein levels of TCM with MI group, there was no significant difference in mean total cholesterol between the two groups (174.5 mg/dL vs. 197.6 mg/dL, p = 0.12). However, in the TCM group, mean HDL-C was significantly higher (66.87 mg/dL vs. 36.5 mg/dL, p = 0.008), the mean LDL-C was significantly lower (89.7 mg/dL vs. 128.9 mg/dL, p = 0.0002), and mean triglycerides was also significantly lower (65.2 mg/dL vs. 166.8 mg/dL, p < 0.0001). CONCLUSIONS: In this study, TCM patients in comparison to MI patients had significantly higher levels of HDL-C, lower levels of LDL-C levels and triglycerides. The lipid profiles in TCM were consistent with the underlying pathology of non-atherosclerotic, non-obstructive coronary artery disease. As lipoproteins in most TCM patients were within the optimal range, we recommend an individual assessment of lipid profiles along with their coronary heart disease risk factors for considering long term lipid-lowering therapy. A finding of hyperalphalipoproteinemia or hypotriglyceridemia in 40% of TCM patients is novel but this association needs to be confirmed in future studies with larger sample sizes. These findings may provide clues in understanding the pathogenesis of takotsubo cardiomyopathy.