Dengue rhabdomyolysis successfully treated with hemoperfusion using CytoSorb® in combination with continuous renal replacement therapy: a case report.

BACKGROUND: Dengue fever is a mosquito-borne viral infection with a broad spectrum of clinical manifestations. Expanded dengue syndrome includes unusual manifestations that do not fall into the categories of dengue fever, dengue hemorrhagic fever, or dengue shock syndrome. Rhabdomyolysis causing acute renal failure in dengue is one such unusual manifestation, the pathophysiology of which is incompletely understood. CASE PRESENTATION: We describe a 21-year-old Sri Lankan man with dengue fever who developed severe rhabdomyolysis and acute kidney injury with extremely high creatinine phosphokinase levels (> 2 million U/L). Management of this patient was challenging as his creatinine phosphokinase kept rising with persistent anuria despite hydration, intermittent hemodialysis, and, later, continuous venovenous hemodiafiltration. Further therapeutic options were explored, and CytoSorb® adsorber was added as an adjunct to continuous venovenous hemodiafiltration, following which we observed a marked reduction in his creatinine phosphokinase and myoglobin levels over the next 12 hours and complete renal recovery over the next 5 weeks. CONCLUSION: We report a rare case of significant rhabdomyolysis secondary to dengue infection leading to acute kidney injury. Continuous venovenous hemodiafiltration performed with the hemofilter Pecopen 140 was ineffective, and the addition of CytoSorb® adsorber as an adjunct therapy to continuous venovenous hemodiafiltration may have a potential benefit in removing high-molecular-weight proteins such as myoglobin.

Uncommon triggers of insulin autoimmune syndrome: a case report.

BACKGROUND: Insulin autoantibody syndrome (IAS), or Hirata disease, is caused by high concentrations of insulin autoantibodies, which result in spontaneous, mainly post-prandial, hypoglycemic episodes. We report a case of a previously healthy 67-year-old man presenting with recurrent fasting hypoglycemia culminating in a diagnosis of insulin autoimmune syndrome linked to omeprazole and probably spices, namely, coriander, and ginger. CASE PRESENTATION: A previously healthy 67-year-old Sinhalese man presented with recurrent syncopal attacks for 3 months, which were found to be hypoglycemic episodes. He experienced mainly fasting hypoglycemic attacks, at a frequency gradually increasing to daily attacks. His cardiovascular, respiratory, abdominal, and neurologic examinations were normal. He was found to have insulin levels > 6000 mU/L and a post-polyethylene glycol insulin recovery of less than 9.5%. Contrast-enhanced computed tomography of the pancreas was normal. The diagnosis of insulin autoantibody syndrome was confirmed by testing for the insulin autoantibody level, yielding a level of > 300 U/mL. With regard to a possible trigger, he had a history of omeprazole intake for 2 weeks, 4 weeks prior to the onset of symptoms. He also consumed an herbal supplement containing coriander and ginger extracts daily for a period of 1 year, approximately 2 years prior to the onset of hypoglycemic attacks. He was commenced on prednisolone 30 mg daily, and hypoglycemic episodes responded dramatically, and thus he was tapered off corticosteroids. CONCLUSION: Omeprazole-induced insulin autoantibody syndrome is likely in this patient; however, the known hypoglycemic effects of coriander and ginger make it worthwhile to consider a possible association with insulin autoantibody syndrome. In addition, this case report highlights the need to consider insulin autoantibody syndrome even in patients presenting with fasting hypoglycemic attacks.

A rare case of Sweet syndrome secondary to melioidosis.

BACKGROUND: Melioidosis is an emerging infection in South Asia caused by Burkholderia pseudomallei with various clinical presentations that include pneumonia, bacteraemia, arthritis, and deep-seated abscesses. Various cutaneous manifestations have been described in association with melioidosis. However Sweet Syndrome secondary to melioidosis has not been reported in the literature. Herein we describe the first case of Sweet syndrome secondary to melioidosis. CASE PRESENTATION: A 53-year-old previously healthy Sri Lankan female presented with high-grade fever, painful oral ulcers, odynophagia and multiple bilateral cervical lymphadenopathies for 1 month. She also had a loss of appetite and weight. She had oral ulcers and bilateral blepharitis. Dermatological examination revealed multiple tender papules with a mamillated appearance and targetoid lesions with a yellowish centre over the face, upper trunk and upper limbs. She also had multiple tender subcutaneous nodules over the extensor aspect of upper limbs. Her inflammatory markers were significantly elevated. Aspirate from a submental lymph node abscess revealed the growth of Burkholderia pseudomallei. Melioidosis antibody titer was > 10,240. The histology of the skin lesions of the face and left forearm showed a prominent neutrophilic infiltrate in the dermis and the morphological features were in favour of Sweet syndrome with panniculitis. She was started on intravenous meropenem 2 g daily and showed rapid clinical improvement with the disappearance of skin lesions as well as a reduction in inflammatory markers. CONCLUSION: Sweet syndrome is an uncommon inflammatory disorder known to be associated with upper respiratory tract and gastrointestinal infections, malignancies and the use of certain drugs. Melioidosis is an emerging infection with various cutaneous manifestations. This is the first case of melioidosis causing the secondary sweet syndrome. It emphasizes the importance of considering melioidosis as a potential aetiology in patients with Sweet syndrome.

A Rare Cause of Ascites-Disseminated TB with Peritonitis in a Middle-Aged Female.

BACKGROUND: Disseminated tuberculosis (TB) has been increasingly recognized in adults in the recent times due to increased prevalence of immune suppression. Here we describe a case of 47-year-old female who presented with disproportionate ascites where the diagnosis of disseminated TB was delayed. CASE REPORT: A 47-year-old previously healthy female presented with generalised body swelling with disproportionate ascites and loss of appetite and weight for four-month duration. She denied any contact or past history of TB and reported no respiratory symptoms. Physical examination revealed significant ascites. There was no lymphadenopathy or hepatosplenomegaly. Respiratory system examination was normal. Her Erythrocyte Sedimentation Rate (ESR) was above 100. Tuberculin skin test was positive with 17mm. Contrast Enhanced Computed Tomography (CECT) abdomen revealed chronic liver disease with ascites. Diagnostic laparoscopy was in favour of miliary TB and the peritoneal biopsy revealed granulomatous inflammation with caseous necrosis, suggestive of TB. The patient was started on antituberculosis treatment and subsequently improved. CONCLUSION: TB peritonitis due to disseminated TB should be considered in the differential diagnosis of disproportionate ascites. Even though the diagnosis is difficult, diagnostic laparoscopy and biopsy is very helpful. It is important to have an early diagnosis since delay in treatment can be detrimental in most cases.

A phase II clinical trial to assess the safety of clonidine in acute organophosphorus pesticide poisoning.

BACKGROUND: An estimated 2-3 million people are acutely poisoned by organophosphorus pesticides each year, mostly in the developing world. There is a pressing need for new affordable antidotes and clonidine has been shown to be effective in animal studies. Our aim was to determine the safety of clonidine given as an antidote in adult patients presenting with signs or symptoms of acute organophosphate ingestion. METHODS: This study was a dose finding, open-label, multicentre, phase II trial. Forty eight patients with acute organophosphate poisoning were randomized to receive either clonidine or placebo: Four to receive placebo and twelve to receive clonidine at each dose level. The first dose level was an initial loading dose of 0.15 mg followed by an infusion of 0.5 mg of clonidine over 24 hours. The initial loading dose was increased to 0.3 mg, 0.45 and 0.6 mg. at all dosing levels however the subsequent infusion remained at 0.5 mg of clonidine over 24 hours. RESULTS: The baseline characteristics of both groups were similar. The trial was stopped after completion of the 3rd dosing level. At the 1st and 2nd dosing level there were no reported adverse drug reactions. At the 3rd dosing level 5 patients (42%) developed significant hypotension during clonidine treatment that responded to intravenous fluids. There were no statistical differences in ventilation rate, pre and post GCS, and mortality rates over all levels. CONCLUSION: Our findings suggest use of moderate doses of clonidine in acute organophosphate poisoning can be used without causing frequent clinical problems but that higher doses are associated with a high incidence of hypotension requiring intervention. Further studies are needed to study the efficacy of clonidine as an antidote in organophosphate poisoning.

Serotonin syndrome induced by fluvoxamine and oxycodone.

OBJECTIVE: To report a case of severe serotonergic symptoms following the addition of oxycodone to fluvoxamine. CASE SUMMARY: A 70-year-old woman developed severe serotonergic features, including confusion, nausea, fever, clonus, hyperreflexia, hypertonia, shivering, and tachycardia, following the addition of oxycodone 40 mg twice daily to fluvoxamine 200 mg/day, easily fulfilling diagnostic criteria for serotonin syndrome. Discontinuation of the offending drugs resulted in resolution of her symptoms over 48 hours, and no other cause of the syndrome was identified. Use of the Naranjo probability scale indicated a probable relationship between the serotonergic symptoms and the addition of oxycodone to fluvoxamine therapy. DISCUSSION: Serotonin syndrome is a serious adverse reaction usually due to interactions with serotonergic drugs. There have been only 3 previous reports involving oxycodone. Most previous reports of serotonin syndrome involving analgesics have been associated with meperidine, dextromethorphan, and tramadol. Unlike these synthetic opioids, however, oxycodone does not inhibit the reuptake of serotonin. In addition, there are a number of other possible pharmacologic mechanisms for the interaction we observed. CONCLUSIONS: Monitoring for serotonergic adverse events should be done when oxycodone is given to patients receiving serotonin-reuptake inhibitors.