Murrah and Sunn herbs induced liver failure

To the Editor: Our patient was a 69-year-old Saudi female with diabetes mellitus complicated by peripheral arterial disease, which resulted in an above knee amputation of her left lower limb one year ago. She complained of pus discharge from a sinus at the stump. A course of oral cefalexin was prescribed for her two months prior to presentation, with no benefit. She was only taking insulin for diabetes. The patient was using herbal medications; Murrah and Sunn (composed of the feces of wild rabbits and other unknown components) for the last two months (Figure 1). S he used to dissolve 3-5 g of Murrah, in 1-2 L of water with 8-10 g of Sunn. After simple filtration, about 200 mL of the solution was taken orally three to five times a day, continuously, for two months. She presented to King Abdulaziz Medical City with complaints of nausea, vomiting, fatigue, and right hypochondriac abdominal pain. On examination, she was found to have normal vital signs with mild dehydration. There were no stigmata of chronic liver disease or encephalopathy, and she previously had a completely normal liver biochemistry. Initial laboratory results revealed leukocytosis and transaminitis with increased INR 4.3 (Table 1). HBs Ag, HAV IgM, and HCV-RNA were negative, as well as serology for Herpes virus, Cytomegalovirus (CMV), EpsteinBarr virus (EBV), Legionella, and mycoplasma. Autoimmune markers; ANA, ASMA, and AMA and metabolic screens: s.ceruloplasmin, alpha1 antitrypsin, and iron studies were all normal. Renal function, electrocardiogram (EKG), and echocardiography were unremarkable. Transjugular liver biopsy revealed prominent hepatocyte necrosis, >60%, predominantly involved zone 3, associated with marked congestion of the perivenularhepatic sinusoids (Figure 2). The central vein and portal tracts were unremarkable. Occasional eosinophilic bodies were noted in the uninvolved hepatic parenchyma (Figure 3). These histological features were consistent with either drugor herbal-induced centrilobular hepatic necrosis. The patient was rehydrated and was placed on insulin, intravenous Vitamin K, and cefuroxime (after wound swab culture), and was

signs with mild dehydration. There were no stigmata of chronic liver disease or encephalopathy, and she previously had a completely normal liver biochemistry. Initial laboratory results revealed leukocytosis and transaminitis with increased INR 4.3 (Table 1). HBs Ag, HAV IgM, and HCV-RNA were negative, as well as serology for Herpes virus, Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Legionella, and mycoplasma. Autoimmune markers; ANA, ASMA, and AMA and metabolic screens: s.ceruloplasmin, alpha 1 antitrypsin, and iron studies were all normal.
Renal function, electrocardiogram (EKG), and echocardiography were unremarkable. Transjugular liver biopsy revealed prominent hepatocyte necrosis, >60%, predominantly involved zone 3, associated with marked congestion of the perivenularhepatic sinusoids ( Figure 2). The central vein and portal tracts were unremarkable. Occasional eosinophilic bodies were noted in the uninvolved hepatic parenchyma ( Figure 3).
These histological features were consistent with either drugor herbal-induced centrilobular hepatic necrosis.
The patient was rehydrated and was placed on insulin, intravenous Vitamin K, and cefuroxime (after wound swab culture), and was  letters asked to stop taking herbs. The patient showed great improvement, clinically and biochemically over the following days.
The toxicology report from King Faisal Specialist Hospital and Research Center and the analysis of the samples, concluded that only  with a normal EKG, unremarkable echocardiography, and normal renal function. Furthermore, she was taking only insulin and previously had a normal liver biochemistry, excluding the possibility of either chronic liver injury or other druginduced hepatitis.
Herbal hepatotoxicity typically presents after several weeks or months of continuous herbal use, [3][4][5][6] such as in the case of our patient. People use Murrah for a few days without significant problems or perhaps develop subclinical hepatitis, which goes unrecognized. However, hepatotoxic injury varies from focal to extensive hepatocyte necrosis, chronic hepatitis, steatosis, cirrhosis, and veno-occlusive disease. 7 We believe, that our patient was taking these herbs in large doses for a long period, which led to hepatotoxicity and liver injury, as a result of contamination and accumulation of these toxic heavy metals and p-cresol, which was one of the organic compounds that was categorized as a phenol (sometimes called phenolics). Depending on the temperature, cresols could be solid or liquid because they had melting points not far from room temperature. Similar to other types of phenols, they were oxidized slowly by long exposure to air and the impurities often gave cresols a yellowish to brownish-red tint. Paracresol (p-cresol) was used to dissolve other chemicals, as a disinfectant, deodorizer, and to make specific chemicals as pesticide. It is known to cause multi-organ damage, including liver injury. 6,8 In addition, we could not rule out the possibility of interaction between these herbs, leading to more extensive liver necrosis and damage. We recommend health education addressing the risk of using herbs as medication, and health authorities must maintain sample No. 2, Sunn, was not suitable for human use, as it contained toxic quantities of lead and arsenic in addition to P-cresol, which is known to cause hepatotoxcity. 1,2 The patient did not have ischemic hepatitis, as she was having only mild dehydration and maintained her blood pressure, letters and supervise herbal shops with regard to the safety, preparation, storage, and dispensing. To the Editor: Cutis laxa (CL) is a group of inherited and acquired disorders characterized by loose and redundant skin with reduced elasticity. 1 Autosomal dominant, autosomal recessive, and X-linked recessive patterns have been noted in the inherited forms. [2][3][4] The autosomal dominant form has a benign course; primarily, skin involvement is present, with few, if any, systemic complications, and a normal life expectancy. It can be caused by mutations in the elastin gene, but molecular heterogeneity cannot be excluded. 2,3 Type I autosomal recessive CL is characterized by pulmonary emphysema, umbilical and inguinal hernias, and gastrointestinal and vesico-urinary tract diverticula, and has the poorest prognosis. The Type II recessive form is called CL and is associated with joint laxity and developmental delay. 4 The histopathology of the skin in patients with CL reveals loss and/or fragmentation of elastic fibers. 5,6 All forms are very rare and no precise data about their prevalence are available.

Congenital cutis laxa
We report an eight-year-old boy with congenital CL with umbilical and paraumbilical hernias, emphysema, and pulmonary artery branch stenosis. The child presented with fever and cough of seven days duration and four days of breathlessness of days duration. He was receiving treatment from a private practitioner, but was referred for increasing breathlessness. There was a history of recurrent episodes of cough and breathlessness since infancy, with an increase in the frequency and severity of the episodes in the past year. The patient had responded to oral medications in earlier episodes. This was the third child of nonconsanguineous parents with no similar family history. Early development was normal and the child was currently in the third grade and school performance was average. Increased laxity of the skin had been noticed six months of age, but a dermatology opinion was not sought. There was no history of skin rash or reaction to any drugs in the past. On examination, the child was febrile and had respiratory distress with intercostal and subcostal retractions. The respiratory rate was 88/min, heart rate 128/min, and blood pressure 100/70 mm Hg. There was no cyanosis or clubbing. The face had a senile appearance with an antimongoloid slant and slightly everted nostrils. The skin was loose and hanging in folds over the dorsum of the trunk and wrinkled over the face and on the dorsum of the hands. There was a left-sided, reducible, inguinal hernia and a small paraumbilical hernia (Figures 1 and 2); there was no laxity of joints. The weight and height were 20.5 kg and 118.5 cm, respectively, both at the fifth percentile for that age. Chest examination revealed an increased anteroposterior diameter with a Harrison sulcus. Rhonchi and coarse crepitations were heard bilaterally. There was