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BACKGROUND: Liquorice consumption can cause pseudohyperaldosteronism and potentially lead to life-threatening complications. Besides correcting hypokalemia and hypertension, finding the triggering factor for pseudohyperaldosteronism is essential to prevent recurrence. CASE DESCRIPTION: A 68-year-old Syrian man presented in the Emergency Department with complaints of fatigue, weakness and exercise-related shortness of breath. Blood tests revealed severe hypokalemia for which suppletion and cardiac rhythm surveillance was necessary. Talking to the patient's son, it occurred that our patient drank copious amounts of Erk Sous, a thirst-quenching drink made from liquorice. The diagnosis pseudohyperaldosteronismwas confirmed by a high level of glycyrrhetinic acid in the patient's urine. After correction of the hypokalemia, our patient recovered successfully. CONCLUSION: Erk Sous is a thirst-quenching drink that can cause pseudohyperaldosteronism. The drink is popular in the Middle East during summer and Ramadan. If a patient from the Middle East presents with hypokalemia and/or hypertension, ask for consumption of Erk Sous.

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Chronic ingestion of liquorice induces a syndrome with findings similar to those in primary hyperaldosteronism. We describe a patient who, with a plasma K+ of 1.8 mmol/l, showed a paralysis and severe rhabdomyolysis after the habitual consumption of natural liquorice. Liquorice has become widely available as a flavouring agent in foods and drugs. It is important for physicians to keep liquorice consumption in mind as a cause for hypokalaemic paralysis and rhabdomyolysis.

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A 25-year-old schizophrenic man presented with abdominal pain, nausea, vomiting, weight loss and anaemia. He was noted to be malnourished with generalised muscle atrophy. Laboratory investigations showed Hb 4.7 mmol/L, MCV 80fl, bilirubin 75 micromol/L and reticulocyte count 93 percent. Peripheral blood films showed anisocytosis, basophilic stippling and Cabot's rings. Electromyography confirmed typical motor nerve neuropathy. The clinical and laboratory findings were that of lead poisoning. The patient was later found to be ingesting lead-containing paint. He was treated with lead-chelating agents.

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Bronchocentric granulomatosis is an unusual pathologic entity that is characterized by a necrotizing granulomatous inflammation surrounding the airways. The diagnosis is usually made retrospectively, after histopathologic examination of an open-lung biopsy or resection of a pulmonary lesion. Although the aetiology has not been fully elucidated, the current pathogenetic mechanism is considered to be an immunologic reaction against endobronchial antigens, since most patients exhibit signs of bronchial asthma, eosinophilia and allergic bronchopulmonary aspergillosis. However, non-asthmatic patients may develop bronchocentric granulomatosis without signs for endobronchial fungal infections, but probably as a consequence of other pulmonary infections. An 80-year-old female patient presented with high fever and bilateral pulmonary infiltrates and nodules. After extensive investigations and open-lung biopsy, the diagnosis bronchocentric granulomatosis was established that was possibly associated with an influenza-A virus infection. Treatment consisted of immunosuppressive drugs (prednisone and cyclophosphamide), which led to complete clinical and radiological recovery.

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CASE PRESENTATION: Despite chemoprophylaxis with isoniazid a 58-year-old Creole patient with mild rheumatoid arthritis developed disseminated tuberculosis, pulmonary aspergillosis and cutaneous herpes simplex infection during treatment with infliximab and methotrexate. TREATMENT: The patient received antituberculous drugs (ethambutol, isoniazid, pyrazinamide, rifampicin), amphotericin B, flucytosine, and valaciclovir, along with prolonged intensive care treatment and mechanical ventilation. CONCLUSIONS: The present case confirms that isoniazid prophylaxis (300 mg once daily, during 6 months) does not protect against the reactivation and dissemination of latent tuberculosis. It also shows that combined treatment with infliximab and methotrexate may induce severe immunosuppression with prolonged leukocytopenia and depressed cellular immunity, leading to multiple opportunistic infections. Extensive diagnostic testing, early start of antimicrobial therapy and enteral immunonutrition, and further infection prevention with selective decontamination of the digestive tract may have been the key to a good clinical outcome.

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In an 80-year-old woman septic shock and gas gangrene were diagnosed secondary to a perforated carcinoma of the coecum.

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A 67-year-old woman and a 22-year-old man, great aunt and great nephew, were examined because of hyperferritinaemia; both had been operated during adolescence for bilateral cataract. The clinical diagnosis 'hereditary hyperferritinaemia-cataract syndrome' (HHCS) was confirmed after DNA-analysis, which showed a point mutation in the L-ferritin gene on chromosome 19 (32G > A, the previously reported Pavia-1 mutation). The further supervision of the patients consisted of reassurance, providing an explanation about the background of HHCS and how it differs from HFE-gene related haemochromatosis, and informing other family members. Both patients were referred back to their general practitioners. HHCS is an autosomal dominant disorder that is characterised by elevated serum ferritin in the absence of iron overload. The dysregulation of ferritin production is caused by heterogenous mutations in the iron responsive element of the L-ferritin gene on chromosome 19, which reduce the binding of iron-regulatory proteins. This results in exaggerated L-ferritin mRNA translation, which is normally tightly controlled by the intracellular iron availability. The only relevant clinical symptom is early-onset, bilateral cataract, which is due to L-ferritin deposits in the stroma of the lens. Internists and haematologists should differentiate this syndrome from haemochromatosis in order to avoid invasive diagnostics and mistreatment. Ophthalmologists should consider this syndrome in patients with congenitial or juvenile cataract.

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A 25-year-old man with schizophrenia had abdominal complaints and haemolytic anaemia, basophilic stippling and Cabot's rings due to lead poisoning.

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A woman experienced recurrent attacks of angioedema from the age of 17 to 21 years and these appeared to be associated with the use of oestrogens. After stopping the medication her complaints disappeared, but they returned during her first pregnancy. Angioedema is a serious condition, which can lead to acute abdominal symptoms, oedema of the upper respiratory tract and death by asphyxiation. The most well-known cause is hereditary angioedema, an autosomal dominant disorder that is characterized by deficiency of C1 esterase inhibitor (C1-INH). Recently, a new type of hereditary angioedema (type 3) has been reported that occurs exclusively in women and is characterised by oestrogen dependency (both endogenous and exogenous), normal C1-INH concentrations and severe attacks of angioedema, which are clinically indistinguishable from the classic form.

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A 69-year-old woman was hospitalized because of a left-sided pneumothorax due to chronic obstructive pulmonary disease. During chest tube placement she developed hypotension and a decrease in peripheral oxygen saturation. A diagnosis of heart tamponade was made and the patient was treated successfully with pericardiocentesis and placement of a pericardial drain. Cardiac tamponade following chest tube placement is a rare and serious complication. When the clinical condition deteriorates following chest tube insertion, cardiac tamponade should be considered.

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A patient with giant-cell arteritis and non-bacterial thrombotic (marantic) endocarditis of the mitral valve is described. To our knowledge, this is the first case reported. The importance of revising the diagnosis of infective endocarditis when no pathogen can be demonstrated is emphasized.

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