Skin cancer is one of the most common cancers in the world and consists of melanoma and non-melanoma skin cancer (NMSC). Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are the most common non-melanoma skin cancers. The ideal surgical treatment for BCC is complete removal, and it can be achieved either with safety margins or with micrographic control. The currently accepted treatment for basal cell carcinoma is an elliptical excision with a 4-mm surgical margin of clinically normal skin. However, because of cosmetic and functional constraints on the face, a 4-mm surgical margin is often not feasible. We used PubMed, PubMed Central (PMC), and Google scholar as our main databases to search for the relevant published studies and used "Basal cell carcinoma" and "narrow excision margins" as Medical Subject Headings (MeSH) keywords. Fifteen studies were finalized for the review, which included 3843 lesions. The size of the lesions ranged from 3 to 30 mm, with a mean size of 11.7 mm. Surgical margins varied from 1 to 5 mm. This review was done to evaluate if small, well-defined primary BCCs can be excised using narrow surgical margins. Based on the reviewed literature, we found that for primary well-demarcated BCCs smaller than 2 cm, in the low-risk group, a safety margin of 3 mm gives satisfactory results. In the high-risk group, and for lesions larger than 2 cm, a 4-6 mm margin is suggested for getting clear margins. Mohs micrographic surgery is advocated for more complex and recurrent lesions where the clinical margin is not apparent. However, micrographic surgery is not readily available in many places and requires more training and experience. Therefore, excision with 2 mm margins for clinically well-defined lesions with close follow-up can be followed to preserve the healthy tissue in anatomic constraint lesions and avoid the need for complex reconstructive procedures.

Rahman et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Valproic acid (VPA) is an anti-epileptic drug (AED) used as a first-choice agent for most forms of epilepsy. It is used in the treatment of manic episodes, bipolar disorder, migraine prevention, and impulse control. Hence it is one of the most commonly prescribed drugs by physicians nowadays. VPA acts by increasing gama amino butyric acid (GABA) levels, and also reduces neuronal activation by blocking voltage-gated sodium, potassium, and calcium channels. VPA has various adverse effects like thrombocytopenia, hyperammonemia, teratogenicity causing spina bifida in newborns when exposed in utero. The focus of this review is to research one such easily overlooked adverse effect of VPA, which is VPA-induced Parkinsonism. We carried out a review of literature and gathered all comprehensive peer-reviewed articles from PubMed. The data for this research were collected ethically and legally after a thorough examination of the literature. Data obtained from the studies have suggested that Parkinsonism is an adverse effect of VPA. Chronic usage of VPA causes Parkinsonism. It occurs equally in males and females, more common in older people usually above the age of 55 years and not dose-dependent. According to the data obtained, all patients who developed Parkinsonism had serum levels in the therapeutic range (50-100 mcg/mL). Thus the chronic intake of maintenance dose of VPA seems to be the leading cause. The symptoms usually improve over a few weeks and fully resolve in a few months after stopping the drug. When the patient's symptoms do not improve, it means VPA has unmasked the underlying potential for developing Parkinson's disease. Such patients benefit from levodopa therapy. However, the mechanism of how VPA causes Parkinsonism remains unknown.

Xanthogranulomatous cholecystitis (XGC) is a rare inflammatory disease of the gallbladder characterized by severe proliferative fibrosis and the accumulation of lipid-laden macrophages in areas of destructive inflammation. Misdiagnosis is highly usual, and its macroscopic appearance may often be confused with gallbladder carcinoma. Here we discuss the case of a 56-year-old male who presented in the emergency room with fever, chills, and nausea. The routine laboratory investigations were normal except for elevated white blood cell counts. Abdominal ultrasound showed borderline gallbladder wall thickening. However, after CT scan findings, the suspect diagnosis of acute cholecystitis with possible perforation was made and the cholecystectomy was performed. The definitive diagnosis was delayed until the final pathology result came as a surprise, and later confirmed the histologic diagnosis of XGC. We consider this an important case because of the histopathologic finding of fibrotic thickened gallbladder wall with abundant histiocytes and pericholecystic fat stranding along with perforation and extensive inflammatory changes in the right upper quadrant of the abdomen which is highly suggestive and indicative of XGC in comparison to gallbladder carcinoma (GC). All things considered, clinically and grossly XGC presents in a similar fashion as GC; histopathology confirmed the diagnosis of XGC.