Correspondence Address:
Kalyan Goswami
Department of Biochemistry, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha - 442 102, Maharashtra
India

Full Text

Sir,

In India due to popular usage, hair-dye poisoning is quite likely. Hair dye containing paraphenyldiamine (PPD) is commonly used for its lower cost. Such dye contains PPD (4%), cetasteryl alcohol, liquid paraffin, sodium-lauryl sulphate, di-sodium EDTA, resorcinol and propylene glycol. PPD, resorcinol and glycol derivative are quite known for nephrotoxicity; one Indian study confirmed that a formidable number of such cases developed renal toxicity. [1] Another study showed that majority of PPD poisoning cases is suicidal with a significant predominance of females from young adult group. More than 20% case fatalities found in this study is a matter of grave concern. [2]

In this case, a 19-year-old female was referred to our medical college hospital, who had consumed 50 ml of hair-dye oil in suicidal attempt. She developed drowsiness, shivering along with severe vomiting, swelling over face and neck and difficulty in breathing. Her urinary output decreased (~200 ml/day) with passage of chocolate brown-colored urine. Her blood pressure was recorded as 100/80 mm Hg, heart rate 92/min, respiratory rate 38/min. Patient had facial and bilateral pedal edema along with muscular weakness, sluggish reflexes and pinprick sensation in stocking and glove distribution area. Blood sample showed: hemoglobin 12.3 g/dl, total leucocyte count was 22600 per cmm. Differential leucocyte count was polymorphs-85%, lymphocytes-9%, eosinophils-1%, monocytes-5%; platelet count was 280000 per cmm, and reticulocyte count was 1.5%. Increased alanine aminotransferase and aspartate aminotransferase levels were found (420 and 566 IU/L respectively); however, both bilirubin and albumin levels were normal.

Chocolate brown-colored urine raised suspicion of hematuria or hemoglobinuria. In PPD poisoning rhabdomyolysis and intravascular hemolysis culminating in acute renal tubular damage was recorded. [3] In this case, increased level of creatine phosphokinase (22546 U/L) in blood with disproportionately lower contribution from myocardial fraction (220 U/L) indicates probable muscle damage. Consequently, enhanced excretion of myoglobin might be contemplated to cause acute kidney damage. Although there was decreased urine volume, both blood urea and creatinine and electrolytes levels being normal, diagnostic evidence of acute renal failure was absent. In this context it is worth mentioning that all these parameters of renal function remain unaltered until almost 50% of reduction in glomerular filtration rate. Urine microscopy showed occasional granular casts and degenerating renal epithelial cells and pus cells, suggestive of possible acute tubular necrosis. However, absence of red blood corpuscles ruled out the possibility of hematuria. Positive benzidine test (based on heme-associated peroxidation and consequent nascent oxygen-mediated color development with Benzidine in acidic media) with the urine sample reflected the presence of hemoglobin or myoglobin. Further treatment of sample by addition of potassium chloride in acidic media generated characteristic rhombic crystal (otherwise known as hemin crystal) and indicated presence of hemoglobin.

Specific lethal dose is not known for PPD: however, in this case consumption was around 2 g which was not fatal. In absence of specific antidote, patient responded with symptomatic and supportive management. Thus, evidence-based diagnostic workup confirmed hemoglobinuria with probable kidney damage in a case of PPD poisoning and underscored the crucial role of laboratory medicine in disease management.

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