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Isoniazid (INH) is the mainstay of management against Mycobacterium tuberculosis. INH-induced acute pancreatitis is an uncommon association and with dearth of literature on it. We are reporting a case of an 11 years old girl who developed acute pancreatitis after 2 weeks of antituberculous therapy. An INH free regimen was started. She was discharge...
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... had normal liver functions; however, serum amylase was high (2862 IU/L (normal 25 -100), serum lipase was 1379 IU/L (normal 28 -100). Her CT abdomen (Figure 2) showed swollen head, body and tail of pancreas with signs of acute pancreatitis. Her ATT and levetiracetam was stopped, considering drug induced pancreatitis. ...
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Dyslipidemia constitutes a well-known factor that can lead to acute pancreatitis. Hypertrigliceridemia and hypercholesterolemia are part of dyslipidemia. In a prospecitve study, we analyzed the role of hypercholesterolemia in
triggering episodes of acute pancreatitis and the capacity of cholesterol blood level to predict the severity and the
evolut...
Background /Aim: Acute pancreatitis (AP) is a complex disease with various etiology, most frequent biliary and alcoholic. Clinical presentation shows different degree of severity with biphasic evolution. The aim of this study is to evaluate the surgical procedures with mini-invasive approach as preferred choice in patients with pancreatitis.
Citations
... Isoniazid has been associated with pancreatitis in several patients, either during chemoprophylaxis or the treatment of tuberculosis [102][103][104][105][106][107][108][109][110][111][112][113][114]. A positive rechallenge was described in a total of seven patients, with other causes excluded in seven patients. ...
Acute pancreatitis (AP) is an acute inflammation of the pancreas caused by the activation of digestive enzymes in the pancreatic tissue. The main causes of AP are cholelithiasis and alcohol abuse; less commonly, it can be caused by drugs, with a prevalence of up to 5%. Causal associations between drugs and pancreatitis are largely based on case reports or case series with limited evidence. We reviewed the available data on drug-induced AP, focusing on antimicrobial drugs and antivirals, and discussed the current evidence in relation to the classification systems available in the literature. We found 51 suspected associations between antimicrobial and antiviral drugs and AP. The drugs with the most evidence of correlation are didanosine, protease inhibitors, and metronidazole. In addition, other drugs have been described in case reports demonstrating positive rechallenge. However, there are major differences between the various classifications available, where the same drug being assigned to different probability classes. It is likely that the presence in multiple case reports of an association between acute pancreatitis and a drug should serve as a basis for conducting prospective randomized controlled trials to improve the quality of the evidence.
... В литературе сообщается о 12 случаях изониазид-индуцированного панкреатита [90][91][92][93][94][95][96][97][98][99][100][101]. При этом в большинстве случаев изониазид был единственным противотуберкулезным препаратом, который принимали пациенты [102,103]. ...
More than 500 medicines are included in the database of the World Health Organization as drugs that can cause acute inflammation of the pancreas. Drug-induced acute pancreatitis develops against the background of taking many medications (statins, antitumor drugs, drugs for the treatment of diseases of the gastrointestinal tract, analgesics and anti-inflammatory drugs, antimicrobial, antiparasitic and antiviral drugs, drugs for the treatment of tuberculosis, diseases of the central nervous system, estrogens, calcium preparations, etc.) from different classes, while the clinical picture does not differ from pancreatitis of other etiology. Based on this, it is worth paying attention to the reasons that contributed to the development of this pathology. Therefore, one of the main principles of the diagnosis of drug-induced pancreatitis is a thorough collection of a pharmacological history. If you suspect that pancreatitis was caused by a drug, you should immediately stop using it and start traditional therapeutic treatment.
... The most notable adverse effect is hepatitis. The estimated rate of clinical hepatitis in patients given INH alone is approximately 0.6% (Wallace and Griffiths, 2009;Farrah 2015). Isoniazid is a component of the Directly Observed Therapy Short Course (DOTS) for treatment of The study was aimed at evaluating the effect of aqueous extract of Brysocarpus (Connaracea) on oxidative stress biomarkers in isoniazid induced oxidative stress in adult male Wistar rats. ...
The study was aimed at evaluating the effect of aqueous extract of
(Connaracea) on oxidative stress biomarkers in isoniazid induced
Wistar rats. Adult male Wistar rats (n = 36), weighing 80g rats each and treated as follows:
Group I received 1ml/kg normal saline;
group II: received
27mg/kg isoniazid (INH);
group II received 27mg/kg isoniazid (INH) + 20mg/kg Livolin forte
group IV: received 27mg/kg isoniazid (INH) + 200mg/kg B.
isoniazid (INH) + 400mg/kg B.
800mg/kg B. coccineus. Administration was done orally twice a day for a period of 30days;
isoniazid was administered at 0900hrs while livolin forte and B.
1800hrs daily. At the end of the experiment, the male Wistar rats were sacrificed and the was collected for assay of oxidative stress biomarkers. significant (p ≤ 0.05) increase in serum Malondialdehyde in the Isoniazid group and an insignificant (p ≤ 0.05) decrease in serum Malondialdehyde aqueous extracts of B. coccineus, the extracts also caused an insignificant (p
both the serum Superoxide dismutase at 200mg/kg and serum Catalase at 400mg/kg when
compared to the control andLivolin forte. Th
has anti-oxidant effects in isoniazid induced oxidative stress in adult male Wistar rats.
Keywords: Isoniazid, Oxidative stress, Brysocarpus
Objective
A current assessment of case reports of possible drug-induced pancreatitis is needed. We systematically reviewed the case report literature to identify drugs with potential associations with acute pancreatitis and the burden of evidence supporting these associations.
Methods
A protocol was developed a priori (PROSPERO CRD42017060473). We searched MEDLINE, Embase, the Cochrane Library, and additional sources to identify cases of drug-induced pancreatitis that met accepted diagnostic criteria of acute pancreatitis. Cases caused by multiple drugs or combination therapy were excluded. Established systematic review methods were used for screening and data extraction. A classification system for associated drugs was developed a priori based upon the number of cases, re-challenge, exclusion of non-drug causes of acute pancreatitis, and consistency of latency.
Results
Seven-hundred and thirteen cases of potential drug-induced pancreatitis were identified, implicating 213 unique drugs. The evidence base was poor: exclusion of non-drug causes of acute pancreatitis was incomplete or poorly reported in all cases, 47% had at least one underlying condition predisposing to acute pancreatitis, and causality assessment was not conducted in 81%. Forty-five drugs (21%) were classified as having the highest level of evidence regarding their association with acute pancreatitis; causality was deemed to be probable or definite for 19 of these drugs (42%). Fifty-seven drugs (27%) had the lowest level of evidence regarding an association with acute pancreatitis, being implicated in single case reports, without exclusion of other causes of acute pancreatitis.
Discussion
Much of the case report evidence upon which drug-induced pancreatitis associations are based is tenuous. A greater emphasis on exclusion of all non-drug causes of acute pancreatitis and on quality reporting would improve the evidence base. It should be recognized that reviews of case reports, are valuable scoping tools but have limited strength to establish drug-induced pancreatitis associations.
Registration
CRD42017060473.
Background: Cases of acute pancreatitis (AP) have increased among pediatric populations worldwide; however, the natural course of this condition in Saudi Arabia was unknown.
Aim: To report the characteristics as well as outcomes of pediatric AP.
Patients and methods: A retrospective chart review study was conducted to include acute pancreatitis in patients ≤ 19 years. The period was from 1994 until 2015. Demographic, clinical, laboratory, imaging and outcome data were collected and analyzed.
Results: 50 patients (n = 26; 52% males vs. n = 24; 48% females) were included. The mean age at diagnosis was 11.6 years. The mean length of hospital stay was 10.5 days. 9 (18%) patients had a recurrence of AP and 4 (8%) had complications. Idiopathic AP was the most frequent etiology (n = 21; 42%), followed by cholelithiasis (n = 11; 22%). 2 patients (4%) had drug-induced AP, where one was taking isoniazid and the other had taken a large amount of erythromycin, amoxicillin and ibuprofen. 2 choledochal cysts complicated by AP (4%). Pancreaticobiliary diseases, as a complete entity, accounted for 34% (n = 17). Clinically, abdominal pain (n = 47; 94%) and vomiting (n = 38; 76%) were most commonly encountered. KUB was non-diagnostic in all patients. No patient died during their admission.
Conclusion: Although still relatively uncommon in Saudi Arabia, there are on average 2–3 cases of pediatric AP diagnosed annually in our institution. Idiopathic AP was the most common cause. Isoniazid and choledochal cysts are rare causes of AP and were reported in the study.
With the rise of multiple-drug resistant tuberculosis (MDR-TB) and extensive drug resistant tuberculosis (XDR-TB), varieties of anti-TB drug combinations and doses have been used clinically worldwide. Long-term therapy with one or more anti-TB drugs and their concomitant use with other medications such as retroviral drugs and schizophrenia medications have resulted in many adverse effects. This chapter mainly focuses on summarizing new and emerging adverse effects of anti-mycobacterial drugs reported in the year of 2015. While common side effects of drugs are briefly covered in this section, the focus was on summarizing rare adverse effects of drugs and mechanisms and genetic predispositions associated with toxicity of selected drugs. Drugs covered in this chapter include rifamycins, bedaquiline, linezolid, isoniazid, ethambutol, fluoroquinolones, pyrazinamide, clofazimine, cycloserine, delamanid, dapsone and streptomycin.
